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Would ovoviparous to viviparous mutation have been gradual? How would that work?

Would ovoviparous to viviparous mutation have been gradual? How would that work?



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It seems unlikely that an ovoviparous ancestor of mammals long ago could have had a viviparous offspring in a sharp one-generation dividing line, but what would be the gradual steps between egg birth and live birth? Are there any examples of answers to the first question today? It seems that marsupials are a different thing altogether, not something in between egg laying and live birth (no modern mammal's ancestors aren't believed to have marsupial-style birth in their evolutionary history, right?)?


I happen to have seen a talk by an anthropologist who was working on this (i can't reference them here i'm sorry to say - forgotten her name). I can only give an example from their work…

If you look at old world and new world primates, there is a large difference between the gestation time. If you look at the table in the link, lemurs have half the gestation time that humans and gorillas have.

What I can recall is that the lemurs placenta lacks many of the structures that primates have (see section 5). The lemur placenta is supposed to be primitive and a lot more like an egg sac which was internalized as opposed to a more articulated womb that primates have. So her thesis was that eggs would start out being internalized and subsisting only on their own internal structures, still isolated from the mother, then later placental structures would come about that nourish the fetus and enable it to enjoy longer gestation and better development pre-partum.

The stage I'm describing is only the divergence between primitive wombs and 'more advanced' wombs in the sense that they were capable of supporting the fetus for 9 months rather than just 4. That development happened over about 30 million years. The divergence of mammals is thought to have happened about 270 million years ago.

So the rough answer would be hundreds of millions of years for the whole shebang, but internalized eggs and live birth would be a relatively smaller amount of time.


Developing a theoretical evolutionary framework to solve the mystery of parturition initiation

Eutherian mammals have characteristic lengths of gestation that are key for reproductive success, but relatively little is known about the processes that determine the timing of parturition, the process of birth, and how they are coordinated with fetal developmental programs. This issue remains one of biology's great unsolved mysteries and has significant clinical relevance because preterm birth is the leading cause of infant and under 5 year old child mortality worldwide. Here, we consider the evolutionary influences and potential signaling mechanisms that maintain or end pregnancy in eutherian mammals and use this knowledge to formulate general theoretical evolutionary models. These models can be tested through evolutionary species comparisons, studies of experimental manipulation of gestation period and birth timing, and human clinical studies. Understanding how gestation time and parturition are determined will shed light on this fundamental biological process and improve human health through the development of therapies to prevent preterm birth.


Chapter 27. Vertebrates: Fishes, Amphibians, Reptiles, and Mammals

- Gnathostomes are a diverse clade of vertebrates that include fishes, amphibians, reptiles, and mammals.

a. great diversity of organs

c. multiple clusters of Hox genes

1- Actinopterygii, or Ray-Finned Fish - The most species-rich clade of bony fishes

- fins are supported by skeletal extensions of the pectoral and pelvic areas that are moved by muscles within the fins.

The chondrichthyans (sharks, skates, and rays) have a skeleton composed of flexible cartilage and powerful appendages called fins. They are active predators with acute senses and were among the earliest fishes to develop teeth

Bony fishes consist of the Actinopterygii (ray-finned fishes, the most species-rich clade) and the lobe-finned fishes, which include the Actinistia (coelacanths) and the Dipnoi (lungfishes). In Actinopterygii, the fins are supported by thin, flexible rays and moved by muscles inside the body

Tetrapods = Amphibians + Amniotes (Reptiles, Birds, Mammals)

- 4 Legs, Bony Endoskeleton
- Stronger Respiratory and Circulatory Systems
- Better Vision, Hearing, Balance, Expanded Brain
- Land: 20 x's more O2 1000x's less buoyant
-unstable body temperature habitat diversity
- Internal Fertilization

They have successfully invaded the land, but most must return to the water to reproduce.

Ectothermic
- 3 chambered heart (2A/1V - pulmocutaneous & systemic circuits)
Very thin, porous skin
Gills/Lungs
- positive pressure = buccal pumping
Stronger bony skeleton,
- 4 limbs, webbed feet
Lay eggs in water Eggs with jelly-like membrane (shell-less)
Development involves metamorphosis

Amphibians live on land but return to the water to reproduce. In frogs and toads, the larval stage undergoes metamorphosis, losing gills and tail and gaining lungs and limbs

Along with the amniotic egg, other critical innovations that enabled the conquest of land include the following:

Desiccation-resistant skin. Skin of amniotes is thicker and water-resistant and contains keratin, a tough protein. As a result, most gas exchange takes place through the lungs.

Thoracic breathing. Amniotes use thoracic breathing, in which coordinated contractions of muscles expand the rib cage, creating a negative pressure to suck air in and then forcing it out later. This results in a greater volume of air being displaced with each breath than with buccal pumping.

Water-conserving kidneys. The ability to concentrate waste prior to elimination and thus conserve water is an important role of the amniotic kidneys.


RESULTS

The IEF analysis revealed that adult lizards express four distinct isoHb components (Fig. 3), and the MS/MS analysis revealed that each of the subunit components represent products of the previously annotated α- and β-like globin genes in the Anolis genome assembly (Fig. 4). There were no peptide matches corresponding to the products of genes other than the α A -, α D -, β I - and β II -globin genes of Anolis. The MS/MS analysis revealed that adult lizards express each of the four possible tetrameric α2β2 subunit isoHb combinations, which were present in the following rank order of protein abundance: α A 2β I 2>α D 2β II 2≥α D 2β I 2>α A 2β II 2. In the mature erythrocytes of adult lizards, the mean ratio of α D /α A -chain isoHbs was 1.13 (range=1.09-1.17), and the mean ratio of β I /β II -chain isoHbs was 1.38 (range=1.30-1.52 N=4 individuals)

In the case of the developmental study, results of the MS/MS analysis revealed that the α- and β-globin genes of the green anole are differentially expressed during the course of embryonic development (Fig. 5). However, the same subunit isoHbs that were identified in the mature erythrocytes of adult lizards were also expressed throughout the entire course of prenatal development. Thus, although expression levels undergo subtle changes during the course of development, the MS/MS data demonstrate that the α A -, α D -, β I - and β II -globin genes were expressed in both primitive and definitive erythroid cells.

With regard to the α-like globin genes, the α D -chain isoHbs were most highly expressed during the earliest stages of embryogenesis, and the relative abundance of α D -chain isoHbs consistently exceeded that of α A -chain isoHbs over the course of development (Fig. 5). The ratio of α D /α A -chain isoHbs decreased from 1.44 at day 1 post-oviposition (stage 5) to 1.03 at day 21 (stage 17). Compared with the embryos at stage 17, the ratio of the two α-chain isoHbs remained remarkably similar to the ratio measured in the mature erythrocytes of adult lizards.

With regard to the β-like globin genes, the β I -chain isoHbs were most highly expressed during the earliest stages of embryonic development, exhibiting a twofold increase in relative abundance at day 4 post-oviposition (stage 5/6), followed by a gradual decline up to the pre-hatching stage (stage 17). Aside from the early spike in the relative abundance of the β I -chain isoHb, the ratios of β I /β II -chain isoHbs during the remaining stages of embryonic development were quite similar to the ratio measured in the mature erythrocytes of adult lizards.


Evolution: The ramfications of multiple mutations And the necessity for Informatio.

Despite the current beliefs on the Evolution theory, this one's is not as stable as we were lead to believe. The following arguments are quite logic and do no require any specific scientific knowledge apart from bases in anatomy and biology.
The basis of the theory clearly state a starting point from where a mutation occurs and cause radical or simples changes in the individual. Due to Darwin lack of recent knowledge into anatomy, specifically the way that organs interact with each others, his mistakes are quite easy to understand. What we have come to learn recently is that no "simple" physical mutation may occur without a disregard to specifics from the said mutations or another organ that might be linked.
As a quick example to help understand what I mean:
If having a third arm would help to one's species survival and that some day, an individual would have one, he would therefore need new nerves connection to his brain that would fit EXACTLY the new arm, (Which would need to be a separate mutation, as nerves and arms are quite separated in the DNA) And then he would need new entries into the brain to "acknowledge" the new arm, which would require a new mutation (As again, brain functions and arm's are quite separated) and from now on, he would also need new ligaments and et cetera. As one's could imagine, the probability for all those mutations to concur into one's body and to "fit" with each other, not to mention that even with billions of years of tries, the fact that one's mutation without the others would render the 1st mutation useless is even more detrimental to the probabilities. And those are quite slim. So slim that mathematically speaking, we do have an appellation for it: Impossible.

My second point is referring to information. Most of you would agree that this one's needs to be generated by an intelligent organism, both for the encoding mechanism and for the decoding one, along with the fact that plain matter cannot create information.
Then again, most of you would agree to the fact that the DNA possess information which is decoded by ribosomes. However, information cannot be created by matter, and such as, do need an intelligent source. As the sole source on Earth known to be able to do something that might approach some day the DNA complexity and information is the human, and that is impossible that humanity, time's paradoxes forbid, is the source to humanity, or evolution for that matter, we must conclude that a form of intelligence have preceded us. And no matter what is that source, in each case it involves exterior involvement in the creation of life, leading into a falsified, or at least incomplete evolution theory.
Cordially,
SX23.

I thank my opponent, SX23 for initiating this debate. Unfortunately, it appears my opponent does not properly understand several key facets of evolution. I'll do my best to clear this up as well as provide my own arguments in support of the resolution. Hopefully, by the end of the debate we can arrive at a consensus.

C1 - Irreducible Complexity

CON's first argument is based on biochemist Michael Behe's contention that certain organ systems are sufficiently well-matched, with mutually interacting parts performing specific functions in such a way that the removal of any one of the parts would cause the system to cease functioning.[1]

Supposedly irreducibly complex systems, such wings or arms, evolve through useful intermediates. This is called the Mullerian Two-Step, named after Nobel Prize winning geneticist H.J. Muller. A feathered animal with no wings may not be able to fly, but the feathers are good for other things, such as insulation or trapping insects. The same could be said of wings without feathers, however they could work for gliding from tree to tree. Each trait evolves independently for different purposes, but they may later become co-opted. The wings and the feathers used in conjunction make sustained flight possible.[2]

Herein lies the misunderstanding. CON argues that life cannot come from non-living things. This has nothing to do with the process of of evolution, which merely explains changes in the gene pool of a population from generation to generation after life has already been formed.[3] What my opponent alludes to is an unrelated topic called abiogenesis.[4]

There is a staggering amount of evidence for evolution, but I will be focusing on two simple, but powerful examples that fit in perfectly with an evolutionary model, but pose serious explanatory problems for Young-Earth Creationists.

Many animals have nonfunctioning evolutionary remnants. Snakes have vestigial pelvises. The pelvis is detached from the vertebrae and simply floats in the abdominal cavity, serving no purpose. This fits perfectly with the evolutionary belief that snakes descended from earlier, legged reptiles. Certain beetles have useless wings tucked beneath fused wing covers. Dandelions reproduce without pollination, yet retain both pollen and flower.[5] It's difficult to imagine why an omniscient creator would bother to make such useless structures, yet easy to understand from an evolutionary perspective.

C2 - Observed Instances of Speciation

Even at low concentration, copper is toxic to many plants. The Yellow Monkey Flower (Mimulus guttatus), however, produced offspring with a tolerance to the metal. When researched attempted to crossbreed the copper resistant flower with the non-copper resistant flower, the offspring was found to be inviable. The two plants were reproductively isolated two separate species.[6]

There have been other cases as well, such as the fruit fly, Drosophila melanogaster. Researchers experimented with exposing different populations to different humidty and temperature conditions. After several generations of isolated breeding, the offspring of the separate populations were found to be sterile in many instances.[7]

I've demonstrated my case. The evidence for evolution is unequivocal it is a fact as well established as gravity. I wish my opponent luck in the ensuing rounds.

The resolution is AFFIRMED.

2. Theobald, Douglas, Ph.D. "The Mullerian Two-Step: Add a part, make it necessary." 2007. http://talkorigins.org.

5. Theobald, Douglas, Ph.D. "29+ Evidences for Macroevolution" 2004. http://www.talkorigins.org.

6. Macnair, M. R. and P. Christie. "Reproductive isolation as a pleiotropic effect of copper tolerance in Mimulus guttatus." Heredity. 50:295-302. 1983.

7. Kilias, G., S. N. Alahiotis and M. Delecanos. "A multifactorial investigation of speciation theory using Drosophila melanogaster." Evolution. 34:730-737. 1980.

"Quote"
C1 - Irreducible Complexity

CON's first argument is based on biochemist Michael Behe's contention that certain organ systems are sufficiently well-matched, with mutually interacting parts performing specific functions in such a way that the removal of any one of the parts would cause the system to cease functioning.[1]

Supposedly irreducibly complex systems, such wings or arms, evolve through useful intermediates. This is called the Mullerian Two-Step, named after Nobel Prize winning geneticist H.J. Muller. A feathered animal with no wings may not be able to fly, but the feathers are good for other things, such as insulation or trapping insects. The same could be said of wings without feathers, however they could work for gliding from tree to tree. Each trait evolves independently for different purposes, but they may later become co-opted. The wings and the feathers used in conjunction make sustained flight possible.[2]

You do assume that mutations might come in a single handily matter. However you did fail to see the fact that despite a wing to serve a purpose with another characteristic, such as the feather, and serving sole purposes, such as your gliding, a wing without nerve connections would serve no purpose at all, as you would not be able to either move or feel it. As I already, I believe, clearly stated, this will lead to an important use of resource to maintain an "chunk" off the body, therefor depriving the individual survival's chances due to resource being wasted. The fact is, that despite how "simple" a mutation will appear, it will require another one, perhaps more (and a lot, especially on the molecular level) in most of the case, to be actually useful.
Let me give you an example for the mammal's reproduction process. To achieve it, you need three "majors" mutations. (That already includes hundreds of smaller one's). First of all, you need a mother being able to carry a baby. Then, and that is my point, you need breast's for the baby's nourishment. However, the baby must have a psychological pattern for the reflex to actually feed. Which concludes into two mutations, in separate individual, each one alone giving a death sentence, as you have a baby which is unable to feed or a mother which is unable to give to his babies, due to lack of breasts.

As for "vestigial" structures, my answer is simple: we did not found anything yet. Or are scientists arrogant to the point that they would assume to know all about life?
This has been proven false on some degree. As for the human, the appendix (along with some others) were thought to be one of those "vestigial" structures. However, we have recently found that the appendix has a role in immunity system.
And if I do understand your second example, you state that obtaining different characteristics with reproduction is impossible as it gives sterile infants. On the other hand, we have remarked some interesting mutation that did promote survival single handily, such as hemophilia, which makes you immune to malaria. However, in the process, information is lost and therefor they bleed out quite easily and as such, die easily. This does not, in overall, promote survival.

I'm glad CON has abandoned his argument from abiogenesis, unfortunately, he seems to have misunderstood the explanation I gave about useful intermediates and the examples of observed macroevolution taking place. I'll try to make my meaning more apparent. Hopefully by clarifying these issues, I can convince my opponent of my position.

C1- Irreducible Complexity

My opponent writes: "a wing without nerve connections would serve no purpose at all." Complex structures, such as limbs, do not suddenly emerge fully formed they develop from earlier, simpler structures. Arms are believed to have evolved from fins, specifically from pectoral fins. The pectoral fin evolved through a repositioning of pre-existing pelvic fins through a mutation of its homeotic gene.[1] Pelvic fins, in turn, evolved from simpler pelvic flaps.

In the gradual process from pelvic flap to pectoral fin, the necessary bones, muscles, tendons were each developed gradually. Though it's impossible to be sure exactly how it happened, it probably occurred something like this: first came nerves that allowed the fish to receive sensory input from the appendage. Muscles were then adapted from other purposes to allow a limited manipulation of it. Cartilage formed within the structure, giving it greater rigidity. Eventually, the cartilage became bone. The sarcolemma of the muscle fibers became elongated, making them more effective. These later became tendons. With all this in place, the transition from pectoral fin to leg was rather simple, in fact, we have transitionary fossils showing it.[2] Tiktaalik roseae is a prehistoric fish with several traits found in reptiles, among these, tiny feet in the pectoral region.

This brings us to CON's second objection, the development of mammalian reproduction. CON names three important traits: live birth, mammary glands, and feeding instincts. CON claims that having any one of these, without the others, would cause the animal to die out quickly. This is must certainly not true. The platypus does not give birth to live offspring, yet it possesses mammary glands that its young feed off of.[3] Moreover, there is no reason to believe that live birth would necessitate breast feeding.

Of these three traits, it's believed that mammary glands came first. Endothermic reptiles, possibly with hair or fur -- precursors to modern mammals -- probably developed bare, vascularized patches of skin used to facilitate the incubation of their eggs. These warm blooded animals likely had various skin glands used to radiate heat and keep their fur soft and pliable. With the development of internal body heat, the risk of bacterial growth increased, so it seems logical that these glands adapted to produce antibacterial and antiviral secretions to protect the skin and the eggs. At some point, these secretions may have supplemented the nutrients contained in the developing embryo's yolk sack. Over time, they may have grown and become more specialized, allowing the hatchlings to nurse.[4]

Viviparity may or may not have developed in conjunction with breastfeeding. Regardless, we have a pretty good idea of how it happened. Chicken eggs typically spend one day in utero, followed by 21 days of external maturation. Platypus eggs, by contrast, spend 28 days in tract and only 10 in external incubation.[5] The evolution of live birth is simply a matter of eggs spending more time developing in the uterus.

Saiphos equalis, or the common skink, a small snake-like reptile from southeastern Australia appears to be in the process of developing viviparity before our very eyes. Skinks living in the highland regions give birth oviparously, while skinks in the coastal region give birth viviparously. Even the viviparous skinks have not completely left behind their oviparous past -- baby skinks are born encased in a gelatinous membrane that they break out of within about 36 hours.[6]

I'll be brief here, since my opponent's objection is a simple matter of misunderstanding. It is not that scientists cannot conceive of a purpose for structures such as the tiny femur bone found on whale skeletons completely hidden from external view they did have a purpose sometime in the animal's evolutionary past. The issue is that they no longer serve that purpose, they remain merely as reminders of their former use. It does not require omniscience to see this these remnants of hind limbs are immobile, bound by strong ligaments and with the hip joint fused into one piece.[7] In the rare instances (about 1 in 100,000) where they protrude visibly form the body, the drag they create in the water actually hinders the animal.[8]

C2 - Observed Instances of Speciation

Again my opponent's objection is merely a misunderstanding. He writes: "if I do understand your second example, you state that obtaining different characteristics with reproduction is impossible as it gives sterile infants." This is incorrect. In the study I cited, the copper resistant plants were perfectly capable of reproducing with other copper resistant plants it was when attempts were made to crossbreed them with the non-resistant plants that problems arose. The same is true of the fruit fly example. Flies that were bred together for multiple generations under similar temperature and humidity conditions were able to breed with eachother, but were not able to interbreed with populations bred for multiple generations under different conditions.

By explaining the development of limbs, viviparity, nursing, and other processes, I have dismantled my opponent's primary argument from irreducible complexity. In doing this, I have also given examples of transitionary fossils and instances of evolution taking place in the world today, thus strengthening the affirmative case. I eagerly await my opponent's reply.

Thank you, the resolution has been AFFIRMED.

1. Young et al. "Cdx and Hox genes differentially regulate posterior axial growth in mammalian embryos." Dev. Cell 17 (4): 516󈞆. October 2009.

2. Shubin et al. "The pectoral fin of Tiktaalik roseae and the origin of the tetrapod limb. Nature 440(6): 764-771. 2006.

3. "Platypus." Environmental Protection Agency/Queensland Parks and Wildlife Service. 2006. http://www.epa.qld.gov.au. .

4. Blackburn et al. "The origins of lactation and the evolution of milk: a review with new hypotheses." Mammal Review 19: 1- 26. 1989.

5. Cromer, Erica. "Monotreme Reproductive Biology and Behavior." Iowa State University. 2004. http://www.biology.iastate.edu. .

6. Stewart, et al. "Uterine and eggshell structure and histochemistry in a lizard with prolonged uterine egg retention." Journal of Morphology, n/a. doi: 10.1002/jmor.10877

7. Struthers, John, M.D. "On the Bones, Articulations, and Muscles of The Rudimentary Hind-Limb of the Greenland Right-Whale (Balaena mysticetus)." Journal of Anatomy and Physiology (London), Vol. 15, p. 141-321. 1881.

8. Wilford, John. "Whales' Hind Feet Show Up in Fossils." The New York Times. 1990. http://www.nytimes.com.

"Quote"
In the gradual process from pelvic flap to pectoral fin, the necessary bones, muscles, tendons were each developed gradually. Though it's impossible to be sure exactly how it happened, it probably occurred something like this: first came nerves that allowed the fish to receive sensory input from the appendage. Muscles were then adapted from other purposes to allow a limited manipulation of it. Cartilage formed within the structure, giving it greater rigidity. Eventually, the cartilage became bone. The sarcolemma of the muscle fibers became elongated, making them more effective. These later became tendons. With all this in place, the transition from pectoral fin to leg was rather simple, in fact, we have transitionary fossils showing it.[2] Tiktaalik roseae is a prehistoric fish with several traits found in reptiles, among these, tiny feet in the pectoral region.
"End of Quote"

First of all, thank you for this quite interesting answer.

Of course, but as you apparently failed to see, my whole case is based on the fact that having a "chunk" of an arm is of no useful purpose, and as such, stating one of evolution rule's: "The mutation may enable the mutant organism to withstand particular environmental stresses better than wild-type organisms, or reproduce more quickly." However, having smaller increments do not increase chances of survival. As a matter of fact, if I may say something: 99% of proteins mutation do have a negative effect of the individual, due to a loss of information or useless duplicates that use energy to no real purpose. As per your theory, an individual will have a small increment, the first being nerves. However, as I stated, having nerves STILL requires other factors to be of use, or they are a characteristic that will be lost to the individual by the mere probabilities law's that were first stated: If a mutation has no real purpose other than using energy, and therefore hampering the specie's to reproduce with the mutation, and it is then lost.

As for the second point, stating mammalian reproduction, I was mentioning in the case of a "transition". As the evolution theory stated, reptilians came first and mutated through time to get to mammalians. However, if one reptilian have mammary glands that produce the necessary "food" through a mutation, he will not be able to pass on this characteristic, unless it had very precise survival goals, either it will just disappear through time, his only use being to drain energy. What I was referring to was the first mammal or transition between the two's. Having babies that develop in an exterior habitat without protection requires babies that have a mutation to live through it. Resulting again in multiple mutation that needs each other to bring a survival aspect.

For the mutation's odds to happen in concurrence, I believe I can share an interesting insight on the numbers:

The mathematical problem for evolution comes when you want a series of related mutations. The odds of getting two mutations that are related to one another is the product of the separate probabilities: one in 107 x 107, or 1014. That's a one followed by 14 zeros, a hundred trillion! Any two mutations might produce no more than a fly with a wavy edge on a bent wing. That's a long way from producing a truly new structure, and certainly a long way from changing a fly into some new kind of organism. You need more mutations for that. So, what are the odds of getting three mutations in a row? That's one in a billion trillion (1021). Suddenly, the ocean isn't big enough to hold enough bacteria to make it likely for you to find a bacterium with three simultaneous or sequential related mutations.

What about trying for four related mutations? One in 1028. Suddenly, the earth isn't big enough to hold enough organisms to make that very likely. And we're talking about only four mutations. It would take many more than that to change a fish into a philosopher, or even a fish into a frog.

Contrary to popular opinion, drug resistance in bacteria does not demonstrate evolution. It doesn't even demonstrate the production of favourable mutations. It does demonstrate natural selection (or a sort of artificial selection, in this case), but only selection among already existing variations within a kind. It also demonstrates that when the odds that a particular process will produce a given effect get too low, good scientists normally look for a better explanation, such as the plasmid explanation for resistance to multiple antibiotics.

In result to these odds, I believe another quotation is needed:

Way back in 1967, a prestigious group of internationally known biologists and mathematicians gathered at the Wistar Institute to consider Mathematical Challenges to the Neo-Darwinian Interpretation of Evolution Way back in 1967, a prestigious group of internationally known biologists and mathematicians gathered at the Wistar Institute to consider Mathematical Challenges to the Neo-Darwinian Interpretation of Evolution.10 All present were evolutionists, and they agreed, as the preface clearly states, that no one would be questioning evolution itself. The only question was, could mutations serve as the basis—with natural selection—as a mechanism for evolutionary change? The answer of the mathematicians: no. Just plain no!

As for your last point, "observed instances of Speciation"
You will forgive me if I do not see the link between it and the actual matter, as no mutation of some sort are involved.
And as a last comment: I had though that origin of life was a matter in link with the theory of evolution. Therefore, having a supposition about how it appeared would be quite logic for the theory. As I was apparently mistaken, the point is another one to debate. However, if you want to pursue it here, feel free and be pleased to do so.

P.S: You will forgive me for not having cited any sources earlier on.
Here they are:

# 1 Novick, Richard, Plasmids, Scientific American, December 1980.
# 2 Moorehead, Paul A., and Martin M. Kaplan, Mathematical Challenges to the Neo-Darwinian Interpretation of Evolution, Wistar Symposium No. 5, Wistar Institute Press,Philadelphia, 1967.
# 3 Denton, Michael, Evolution: A Theory in Crisis, Burnett Books, London, 1985.
# 4 http://www.answersingenesis.org.
# 5 Dobzhansky, Theodosius, F. Ayala, L. Stebbins, and J. Valentine, Evolution, W. H. Freeman and Co., San Francisco, 1977.
# 6 http://www.gate.net.
# 7 Ayala, Francisco, The Mechanisms of Evolution, Scientific American (and Scientific American book Evolution), September 1978.
# 8 Beadle, George W., The Ancestry of Corn, Scientific American, January 1980.
# 9 Ayala, Francisco, The Mechanisms of Evolution, Scientific American (and Scientific American book Evolution), September 1978.

My opponent brings up several new objections that are at best unpersuasive, and at their worst completely irrelevant. Before I address these, I'd like to make note of something. PRO has lifted large sections of his essay from this page: http://answersingenesis.org. Additionally, in a rather transparent effort to build ethos for his case, he copied every single reference from the article without so much as bothering to change the order or include numbered citations within his essay. Needless to say, I don't find this amusing and I don't think the voters will either.

Since my opponent has only one major contention divided into other, minor points, I'll address them each individually.

---> "The mutation [must] enable the mutant organism to withstand particular environmental stresses better than wild-type organisms, or reproduce more quickly."

This is not true. Many mutations are neutral, neither aiding nor hindering survival. These spread through populations by genetic drift.[1] While useless in and of themselves, when combined with other mutations, they may have a positive effect. I'll expand on this later.

---> "Having nerves STILL requires other factors to be of use. "

Obviously. In explaining the devleopment of limbs, the animal in question is assumed already to have some basic nervous system in place. These pre-esxisting structures can easily be adapted for other purposes. If my opponent wishes for me to explain in minute detail ever single step in the evolutionary process from single celled microogranism to complex vertebrate, I'm afraid I must disappoint him it is simply impossible within the confines of 8,000 characters. Moreover, it would add nothing to the debate, I have already demonstrated that the argument from irreducible complexity is wholly unscientific. Finally, my opponent has not given any coherent, logical reason to believe why a nervous system *couldn't* have evolved by gradual increments in a naturalistic fashion. What is stated without evidence can be dismissed without evidence.

---> "If one reptilian (sic) have (sic) mammary glands that produce the necessary 'food' through a mutation, he will not be able to pass on this characteristic, unless it had very precise survival goals."

I already explained the precise survival goal that early mamary glands may have served. I suggest my opponent re-read my argument. Moreover, as I explained earlier, even if mammary glands conferred no survival advantage, there is no reason to suppose they wouldn't be passed on through neutral evolution, or genetic drift.

---> "The odds of getting two mutations that are related to one another is the product of the separate probabilities: one in 107 x 107, or 1014."

To begin with, 107^2 is most assuredly *not* 1014, but 11,449. More importantly, this statistic is ridiculous and completely irrelevant. Obviously, the odds of having three simulataneous complementary mutations are slim, but this is not how evolution works. This argument relies on several absurd assumptions:

1. - Mutations must be beneficial to be passed on

This is absolutely false. Many mutations on their own produce no noticeable difference in an organism, however when paired with other mutations, they may cause drastic changes. These mutations do not not need to to be beneficial to be passed on, they can spread through a population by genetic drift. In some instances, organisms possessing favorable traits may even have mutations that hinder them, but by "hitch hiking" on the organism's good genes, these mutations can be passed on anyway.

1. - Mutations must occur sequentially or simultaneously

Again false. As I explained earlier, even mutations coferring no survival advantage can still spread through a population. Once a certain mutation becomes common, the odds of a complementary mutation occurring increase exponentially.

3. - Assumes that only one mutation occurs per generation

Off these three assumptions, this is perhaps the most baffling. An organism may have several mutations. Even if a majority of these mutations have no complementary mutations, a small number of them very well could. A simpler example of how this works is the birthday paradox.

In a room containing 23 people, the odds are slightly better than 50-50 that two of them will share a birthday. But if that were the case, doesn't it seem like you should meet more people who share your birthday? Not neccessarily. The odds of someone sharing YOUR birthday are much lower because it has to be on a SPECIFIC day. In a group of 23, the odds of any two people sharing a birthday are much higher because the match can occur on ANY day.[2]

This works the same way with mutations. While the chances of any one mutation having a complementary mutation are slim, given multiple mutations and multiple generations, the odds suddenly don't look so daunting.

---> "Drug resistance in bacteria does not demonstrate evolution."

I'm not sure why my opponent brought this up, since I never mentioned anything about it. The emergence of drug resistant bacteria is indeed evolution. New information is created by mutations in the genome. There is strong lab evidence of this.[3]

CON has apparently dropped this argument, therefore PRO should win by default.

C2 - Ovserved Instances of Speciation

My opponent writes: "you will forgive me if I do not see the link. as no mutation of some sort are (sic) involved."

Of course mutations were involved! How else would copper resistance and reproductive isolation occur?

My opponent's main objection involves ridiculously inflated statistics from an unreliable source. My main points remain virtually uncontested. I look forward to my opponent taking the time to write *his own* response in the next round.

The resolution is AFFIRMED.

1. Suzuki, et al. "An Introduction to Genetic Analysis." 4th ed. W.H. Freeman. p. 704. 1989

First of all, I would like to take a few moments to give a quick English vocabulary reminder.
I hope you appreciate the irony, as I am the one having a primary foreign language:

Quote:
--Verb (used with object)
1.
to repeat (a passage, phrase, etc.) from a book, speech, or the like, as by way of authority, illustration, etc.
2.
to repeat words from (a book, author, etc.).
3.
to cite, offer, or bring forward as evidence or support.

I believe I have clearly stated whereas I put a quote. And once again, they were to SUPPORT my argumentation, they were not to BE the argumentation.
This assertion : "He copied every single reference from the article without so much as bothering to change the order or include numbered citations within his essay. Needless to say, I don't find this amusing and I don't think the voters will either."
Is not only false, but can be considered as a personal attack. The required citations for my point are not only in three distinct location, their only link being that they refer to the same subject. The article itself containing more the 16000 characters. As for numbered citations, I was not aware that those were needed, but this is my first debate, and as such I believe that having a little indulgence towards those criteria would be appropriated. As for the amusing part, well whether the voters find amusing or not that you personally attack a newcomer to this site is of course their prerogative.

==================
Answers to specific points mentioned in the reply above:
==================

--------> The utility of mutations and their occurrence into generations:

You claim that many mutations are neutral, however, 70% of all mutations have a DIRECT negative effect on the individual, such as birth termination (death) or defects. The remainder is indeed either neutral or weakly beneficial.

In many cases the structure is of no direct harm, yet all structures DO require extra energy in terms of development, maintenance, and weight, and are also at risk in terms of disease (e.g., infection, cancer), providing some selective pressure for the removal of parts that do not contribute to an organism's fitness. A structure that is not harmful will take longer to be 'phased out' than one that is. In view to this, every single physical change, even with non-interfering result for the individual survival, is most likely to be wiped after a few thousand's generation. And the required time for a beneficial change is acknowledged to be much more:

If I may allow myself to quote one of your own sources:

Twenty years ago, evolutionary biologist Richard Lenski of Michigan State University in East Lansing, US, took a single Escherichia coli bacterium and used its descendants to found 12 laboratory populations.
The 12 have been growing ever since, gradually accumulating mutations and evolving for more than 44,000 generations, while Lenski watches what happens.

But sometime around the 31,500th generation, something dramatic happened in just ONE of the populations - the bacteria suddenly acquired the ability to metabolize citrate, a second nutrient in their culture medium that E. coli normally cannot use.

This means that an organism as simple as a single bacteria do need, more or less, 31,500 thousand generations to evolve an actually useful trait. And that has been observed in only 1 of the 12 population. A simple mathematical calculus should resolve the number of generations required to took in average: 31,500 x 12= 378000. That means we have observed 378,000 generations in a single bacteria before we have something useful. The odds to have beneficial mutations, followed by multiple evolutionary mutations, especially with organism that are incredibly more complex than a bacteria, such as a mammalian, which requires a considerable amount of time with a lot more generations due to their said complexity, are then lowered to an impossibility point. (Not to mention reptilian forms, insects, and etc.)

-------->Observed Instances of Speciation:

You do use to wrong ends the word Speciation:

Definition: Speciation is the evolutionary process by which new biological species arise. In the case of the copper resistant plants, there is no new species involved. Only a genetic change that allow the plant to better resist certain circumstances.

I did not dropped the subject, and my answer on it remains the same: Even if we might consider that an organ has lost his "primary" function from one specie to another, the fact remains that the organ, even considered as "vestigial" do still have an use on the other specie, even if less severe in terms or requirement for survival. A perfectly good example of it would be the humans vermiform appendix. Even if the require role is not the same as the precedents one observed, it does still have one.

I do have to acknowledge a severe mistake that made my source look as unreliable and fantasist. When I copied over several parts of the mathematical explanations that served my theory, I did not look over the exponential part:

The mathematical problem for evolution comes when you want a series of related mutations. The odds of getting two mutations that are related to one another is the product of the separate probabilities: one in 10^7 x 10^7, or 10^14. That's a one followed by 14 zeros, a hundred trillion! Any two mutations might produce no more than a fly with a wavy edge on a bent wing. That's a long way from producing a truly new structure, and certainly a long way from changing a fly into some new kind of organism. You need more mutations for that. So, what are the odds of getting three mutations in a row? That's one in a billion trillion (10^21). Suddenly, the ocean isn't big enough to hold enough bacteria to make it likely for you to find a bacterium with three simultaneous or sequential related mutations.

What about trying for four related mutations? One in 10^28. Suddenly, the earth isn't big enough to hold enough organisms to make that very likely. And we're talking about only four mutations. It would take many more than that to change a fish into a philosopher, or even a fish into a frog.

Contrary to popular opinion, drug resistance in bacteria demonstrate natural selection (or a sort of artificial selection, in this case), but only selection among already existing variations within a kind. It also demonstrates that when the odds that a particular process will produce a given effect get too low, good scientists normally look for a better explanation, such as the plasmid explanation for resistance to multiple antibiotics.

As you will probably notice, it is 10^7 x 10^7 that gives 10^14. You could review the original source before assuming that a slight copy-over mistake makes it unreliable. Due to the (revised) mathematical answers stated above, the insights giving by the probabilities impossibility is quite clear. Also, several exterior sources to the one I cited do acknowledge 1966's mathematical result:

You can now rest assured (Unless you discredit three different sources) that a symposium (Academic Conference) has been held in 1966 with this very precise question: Could mutations serve as the basis—with natural selection—as a mechanism for evolutionary change?
The answer of the mathematicians: No. Just plain No!

My opponent claims that the quotes he included were only to support his arguments, however, this hardly seems to be the case he lifted four entire paragraphs! However, he still did not include the entire article that he "quoted" and therefore cannot legitimately claim to have used all of its sources.

CON apparently has no grasp of the meaning of the word "species," which I will define later in C2 of my affirmative case. He has done little to answer my argument against his probability claim other than to repeat his prior statements. Indeed, he has brought up very little of substance, therefore I intend to keep this round very brief.

---> "70% of all mutations have a DIRECT negative effect on the individual."

Yes, and bad mutations much less likely to be passed on. l fail to see how this is at all relevant.

---> "In many cases the structure is of no direct harm, yet all structures DO require extra energy. "

This is a contradiction in terms if a mutation causes harm, direct or indirect, then it isn't neutral.

---> "An organism as simple as a single bacteria needs. 31,500 thousand generations to evolve [a] useful trait."

It took 20 years to develop the ability to metabolize citrate. Given that the earth is 4.54 billion years old,[1] and life has existed for at least 3.5 billion years,[2] does evolution really seem so improbable?

Moreover, there is no reason to arbitrarily distinguish between the 12 populations. Suppose Lenski had simply combined them into one large population? Remember that we are only dealing with a small lab population bacterial colonies are large and abundant in nature.

---> "The odds to have beneficial mutations, followed by multiple evolutionary mutations, especially with organism that are incredibly more complex than a bacteria, such as a mammalian, which requires a considerable amount of time with a lot more generations due to their said complexity, are then lowered to an impossibility point."

Here my opponent raises an important point. Ever since the development of sexual reproduction, evolution has progressed much more quickly.[3] This is because many favorable genetic combinations can be rapidly assimilated into one phenotype. Say animal A has a trait that allows it to run faster, while animal B has a trait that causes it to digest food more efficiently. Animal C has a mutation that strengthens its immune system, and animal D evolves better eyesight. All four traits are likely to be passed on because of the survival advantages they confer. As each favorable trait becomes more prevalent throughout a population, there's a good chance that some animal will come to possess all four of them, thanks to sexual reproduction.

---> Probability of multiple beneficial mutations

My opponent has not listed three independent sources verfying his claim, but three different articles citing the same original source. CON is merely repeating himself -- I have already fully refuted his probability claims and feel no need to do so a second time. In addition to all of my earlier objections, I also pointed out in this round that sexual reproduction greatly increases the rate at which evolution takes place. My opponent's argument truly holds no water.

The human appendix still retains some use, therefore it is not truly a vestigial structure. I pointed out that whale femurs can actually hinder the animal, and CON has made no attempt to refute this. Moreover, we have fossil evidence PROVING that the femur is an evolutionary remnant. Early whales had small feet and flippers that could also be used as forelimbs.[4] These animals were very similar to modern seals or walruses.

CON has also ignored the other examples I have given, such as the pelvises found in snakes, useless wings sealed beneath fused wing covers in certain beetles, and the flowers and pollen of the dandelion. There are literally thousands more similar examples, but it is useless to belabor the point.

C2 - Observed instances of speciation

Species: Taxonomic groups, usually defined by inability to interbreed and produce viable offspring. Species are reproductively isolated from each other. Genes in one species cannot combine with genes from another species and produce a successfully reproducing vehicle.[5]

The copper resistant monkey flowers were indeed a new species. Not only did they have a new, favorable trait, but they were reprodutively isolated from the non-resistant plants, as I stated quite clearly in my opening round.

My core contentions remain unrefuted. Unless CON can pull together some powerful evidence in his last round, I strongly urge you to vote PRO.

The resolution is AFFIRMED.

2. Schopf, J.W., Kudryavtsev, A.B., Agresti, D.G., Wdowiak, T.J., Czaja, A.D. "Laser--Raman imagery of Earth's earliest fossils." Nature 416: 73𔃄 . 2002

3. Colegrave, N. . "Sex releases the speed limit on evolution." Nature 420: 664-666. 2002

First of all, I merely took two paragraphs from the original source. I then separated them to give an easier reading. They do also refer to mathematics and therefor support my claims, and do not MAKE my claims.

As for your first rebuttal:
---> "70% of all mutations have a DIRECT negative effect on the individual."

Yes, and bad mutations much less likely to be passed on. l fail to see how this is at all relevant.

---> "In many cases the structure is of no direct harm, yet all structures DO require extra energy. "

I stated DIRECT impacts. As for secondary impacts, we lower the odds to less than 0.001% to have an impact free mutation with beneficial aspects only. This is quite low and remains with the other problems generated by the mutation, such as the need for support provided by other mutations.

You also assume that sexual reproduction slows the process of mutation. However, this has been proven false on numerous occasions, for a very specific reason:
It is the advantage of complementation (also known as hybrid vigor, heterosis or MASKING OF MUTATIONS) that happens to occur during sexual reproduction, lowering the odds to pass one on by half on each individuals.
This is not what I would call helpful to the odds.

Time Parameters for the Evolution:

As for the bacteria, we OBSERVED 378,000 generations in a laboratory stance with factors that enhanced the growth of mutations. It is reasonable to assume that a simple animal would need at least a dozen times this number, only due to differences in the length of the DNA strains. A hundred time this number would make 3,780,000 generations before having an actually useful trait. In other words, more or less 4 millions generation. Now, if we look at the fact that most of the animals needs around 5 years to achieve a generation, (And even then I'm being generous) we pass to 18,900,000 years to achieve a SINGLE useful trait. As the passage to one family to another requires at least a thousand (And more, in most of the cases) useful mutations, we go up to 18,900,000,000 years. We've already passed Earth existence (4,500,000,000). Don't seem that probable to me. Of course, we could continue on with every families (Not even species!) on Earth, and we will go further the creation of our solar system.
And just a small side-note, simple animal forms are believed to be of existence since (only) 600 millions years (1). Now, with luck, it would indeed be possible to slightly lower the year requirement without getting too much off the probability laws. Now, let's compare 18,900,000,000 years (For one new family!) to the best estimates of animal life: 600,000,000 years. I let you compare those odds, and if you have the slightest knowledge in mathematics, you would understand that it's an instance of what we call something impossible.

Probabilities of multiple beneficial mutations:
My three source do assert that they're was a symposium in 1966. Now, if you want other sources that describes the results: http://www.evolutionnews.org. (3 and 4)
I fear this one is quite credible, as it originates for a pro-evolution site.

If you want a description of the symposium:

(3)""""One of the best known mathematical forays into evolution was the 1966 Wistar Symposium, held in Philadelphia, where mathematicians and other scientists from related fields congregated to assess whether Neo-Darwinism is mathematically feasible. The conference was chaired by Nobel Laureate Sir Peter Medawar. The general consensus of many meeting participants was that Neo-Darwinism was simply not mathematically tenable. """"

(4)"""" "We (The participants) do not know any general principle which would explain how to match blueprints viewed as typographic objects and the things they are supposed to control. The only example we have of such a situation (apart from the evolution of life itself) is the attempt to build self-adapting programs by workers in the field of artificial intelligence. Their experience is quite conclusive to most of the observers: without some built-in matching, nothing interesting can occur. Thus, to conclude, we believe that there is a considerable gap in the neo-Darwinian theory of evolution, and we believe this gap to be of such a nature that it cannot be bridged within the current conception of biology." """"

To see some of the mathematical calculus that lead to some of those conclusions, please refer to my anterior posts or the resume stated at the end.

The human appendix was a mere example. It was long tough to be one of those vestigial structures. However, with studies versed into the subject, we discovered it wasn't. Now, my rebuttal to your argument will be in the form of a very simple question on which I would like a DIRECT (such as yes or no) answer:

Is it possible, that due to the current knowledge, that those "vestigial" structures have a primary or secondary purpose of which we have not discovered yet, such in the long believed case of the human appendix?

The cooper "resistant" plants: First of all, they do make a cryptic species complex 2-(In biology, a cryptic species complex is a group of species which satisfy the biological definition of species—that is, they are reproductively isolated from each other—but whose morphology is very similar (in some cases virtually identical), and are not completely dissociated from their original specie. The consideration on if it's really a speciation instance or just a diversification example is still under debate.

For those reasons, PRO's arguments can be considered as weak due to their bases on questionable and easy refutable data.

Quick resume and Conclusion:

Despite a few personal attacks and lack of research into the sources from PRO's part, leading into false accusations, this was a debate which I would qualify to be quite entertaining and rather interesting.
As for a quick resume for those who lack the time/will to read the whole argumentation:
My arguments are based on the fact that mutation do need several factors in order to be truly beneficial, such as support provided by other mutations or they will draw energy and make them literally useless, having multiple mutations, on the mathematical side, can be resumed through this:

The mathematical problem for evolution comes when you want a series of related mutations. The odds of getting two mutations that are related to one another is the product of the separate probabilities: one in 10^7 x 10^7, or 10^14. That's a one followed by 14 zeros, a hundred trillion! Any two mutations might produce no more than a fly with a wavy edge on a bent wing. That's a long way from producing a truly new structure, and certainly a long way from changing a fly into some new kind of organism. You need more mutations for that. So, what are the odds of getting three mutations in a row? That's one in a billion trillion (10^21). Suddenly, the ocean isn't big enough to hold enough bacteria to make it likely for you to find a bacterium with three simultaneous or sequential related mutations.
What about trying for four related mutations? One in 10^28. Suddenly, the earth isn't big enough to hold enough organisms to make that very likely. And we're talking about only four mutations. It would take many more than that to change a fish into a philosopher, or even a fish into a frog.

The time parameters for evolution and probabilities can be resumed through the calculus based up above in my thread.

And so we reach the end of the debate. Since my prior illustrations regarding probability seem to have fallen on deaf ears, I'll make one final attempt to convince my opponent of his error. Again, CON has decided merely to repeat his prior points without bothering to respond to my thorough rebuttals. Therefore, apart from a few short rebuttals and a last illustration regarding probability, I intend to use this round mainly as a summarization of the main points of the debate.

---> "As for secondary impacts, we lower the odds to less than 0.001% to have an impact free mutation with beneficial aspects only."

It's telling that CON hasn't bothered to source this, the reason being that it's blatantly false. Studies done with fruit flies (Drosophilia melanogaster) show that of the remaining 30% of mutations that aren't harmful, all are either neutral or weakly beneficial.[1] Studies done with yeast have shown that only a paltry 7% of mutations are actually harmful.[2] Moreover, my opponent has completely missed the mark: the fact that there are *any* beneficial mutations is sufficient to validate the evolutionary model. Harmful mutations will not be passed on neutral and beneficial mutations will.

---> "You also assume that sexual reproduction slows the process of mutation."

On the contrary, I stated quite clearly that sexual reproduction greatly increases the rate of evolution and gave a clear explanation why this is true.

---> "Now, if we look at the fact that most of the animals needs around 5 years to achieve a generation, we pass to 18,900,000 years to achieve a SINGLE useful trait."

Without bothering to check CON's math, it's easy to see why this is false. A great deal of evolutionary change took place with very simple life forms. Many modern organisms share several traits, to a greater or lesser extent depending on how closely they are related. Once certain shared characteristics had been developed, the process of differentiation could proceed much more quickly. CON also incorrectly assumes that there is no evolutionary overlap in the development of new traits. It is not as if, say, eyes, ears, and mouths all developed separately, starting with the eyes and then proceeding to the ears, and finally on to the mouth. All three structures likely evolved more or less simultaneously.

---> Probabilities of multiple beneficial mutations

Yes, CON's three sources assert that there was a symposium of mathematicians in 1966. Without access to their report, I can't offer any specific criticisms of their methods, however, I have already refuted CON's numerous assertions regarding probability ad nauseum and it is unnecessary to do so again.

In spite of this, for my opponent's benefit, I will offer one final explanation to help him understand the process. Let's say the odds of having a beneficial mutation are slim -- as rare as winning the lottery. Given enough people, however, we *know* one of them will win. Because of natural selection and recombination, every organism in the population will soon have a genetic "copy" of the lottery winnings. When it comes time for the next lottery, everybody entered will already be a previous winner, there the chances that someone will win twice and thus have *two* beneficial mutations are very good.[3]

I have explained at length how and why these structures are useless evolutionary relics. I have offered fossil evidence of the gradual transition. The simple answer to my opponents question is *yes,* we do know for a fact that these structures serve no purpose it is painfully obvious even to the casual observer.

C2 - Observed instances of speciation

Whether or not the Yellow Monkey Flower descendants represent a "cryptic species" or not is irrelevant. The point is to show that significant changes (macroevolution), caused by beneficial mutations can and do occur regularly.

I have given a great deal of evidence and logical support to my case while CON seems to be content to plagiarize others arguments and repeat himself endlessly without bothering to respond to my criticisms. For this reason,

The resolution has been strongly AFFIRMED. Thank you for reading, and vote PRO!


Birth timing

Parturition, and especially its timing, is a mission-critical event for the success of mammalian viviparity. Normal parturition occurs at a specific time referred to as term, when the fetus is sufficiently mature to survive as a neonate, and the mother is able to provide care for the neonate’s nutrition, protection and physiologic stability, while preserving her own fitness. Timing mechanisms for parturition have likely been selected to optimize reproductive fitness based on benefits to the mother and fetus for the current pregnancy, and benefits to the mother’s survival and future reproductive potential (note that these two are not always aligned). One important general association with birth timing is its correlation with body size at birth (Phillips et al., 2015). This association may reflect energy utilization particularly due to the developing fetal brain (Dunsworth et al., 2012) or physical constraints such as infant size related to the size of the birth canal (Rosenberg and Trevathan, 2002 Rosenberg and Trevathan, 2001).

Studies utilizing concordance in birth timing in offspring of twins, or family-based segregation or epidemiology, suggest that 30–40% of the variation in human birth timing is due to genetic factors, and these reside largely in the maternal genome (Kistka et al., 2008 Plunkett et al., 2009). The ‘compound genome’ of pregnancy is unique when considering the maternal-fetal unit during gestation, consisting of DNA composition of 3 distinct haplotypes. How these unique or shared haplotypes interact to produce the 30–40% variation in human gestation length is only beginning to be explored (Zhang et al., 2015 Zhang et al., 2018 Figure 2). The remaining 60–70% of the variation is thought to arise from environmental influences of uncertain origin. These may include nutrition, infectious disease, health behavior, and social circumstances/stress. Furthermore, recent genomic investigations have demonstrated a causal relationship between single nucleotide polymorphisms (SNPs) that associated with adult height and gestation length in humans such that taller maternal height and its genetic determinants leads to longer gestation (Zhang et al., 2015). Other maternal traits, such as fasting blood glucose and blood pressure, have also been shown to causally determine length of gestation or fetal size at birth in humans (Chen et al., 2020). Recent ability for GWAS comparison of those loci that uniquely determine gestational duration with those that have been associated with birth weight provide an interesting avenue moving forward to disentangle the underlying genetics responsible for the relationship of gestational duration and birth weight (Early Growth Genetics (EGG) Consortium et al., 2018 Zhang et al., 2017).

Do species other than humans exhibit a significant frequency of preterm birth? This question is difficult to answer since preterm birth in humans is an arbitrary definition. If we simply scale the assignment of preterm birth based upon duration of term gestation (37 out of 40 weeks, or 92.5% of gestation) then other eutherian mammals also experience preterm birth (Phillips et al., 2015). Frustratingly, the most commonly studied, genetically tractable animal model, the mouse, does not appear to exhibit spontaneous preterm birth (Phillips et al., 2015). Does this reflect laboratory selection in strains currently utilized or a fundamental trait of rodents? This question merits investigation. Other non-traditional animal models that demonstrate spontaneous preterm birth, such as mammals used in livestock (Nielsen et al., 2016 Fthenakis et al., 2012 Scott et al., 2008 Asher, 2007), could be utilized to investigate preterm birth and low birth weight pregnancies in the future.


Would ovoviparous to viviparous mutation have been gradual? How would that work? - Biology

Biol Res 43: 299-306, 2010

Omissions in the synthetic theory of evolution

Instituto de Entomología, Universidad Metropolitana de Ciencias de la Educación, Código Postal 7760197, Santiago. Chile, E-mail: [email protected]

The Synthetic Theory of Evolution is the most unifying theory of life science. This theory has dominated scientific thought in explaining the mechanisms involved in speciation. However, there are some omissions that have delayed the understanding of some aspects of the mechanisms of organic evolution, principally: 1) the bridge between somatic and germinal cells, especially in some phylum of invertebrates and vertebrates 2) horizontal genetic transferences and the importance of viruses in host adaptation and evolution 3) the role of non-coding DNA and non-transcriptional genes 4) homeotic evolution and the limitations of gradual evolution and 5) excessive emphasis on extrinsic barriers to animal speciation.

This paper reviews each of these topics in an effort to contribute to a better comprehension of organic evolution. Molecular findings suggest the need for a new evolutionary synthesis.

Key terms: Evolution, non-transcriptional genes, viruses, homeosis, epigénesis, imprinting, neo-Lamarckism, sympatric speciation.

The synthetic theory of evolution is considered the most unifying theory of life science. This theory is mainly based on neo-Darwinism, particularly on Mendelism, population genetics, mutations, natural selection, gradualism, and the central dogma of molecular biology. These are key topics to explain genome changes, speciation phenomena, and biodiversity.

Neo-Darwinism roots are found in August Weissmann's theory of continuity of the germplasm. Weismann established that organisms have two sets of cells: somatoplasm and germplasm. In the latter, there are particles or biospheres associated with chromosomes responsible for the transmission of inherited characters. Thus, Weismann laid the foundations of chromosome theory of inheritance. He rejected Lamarck's theory of acquired characteristics, and challenged all these ideas of the natural selection theory of Charles Darwin. Thus, Neo-Darwinism emerged, by adding Weismann's theory of the continuity of germplasm (East, 1929 Darlington, 1937).

The rediscovery of the principles of Mendel by Hugo de Vries, Carl Correns and Erich Von Tschermak strengthened Neo-Darwinism, and with the contributions of Fisher, Wright, Haldane, Dobzhasky, Mayr, Simpson, Stebbins and Huxley, "Population Genetics" and "The Synthetic Theory of Evolution" emerged. Since its origins, this theory has dominated the minds and thoughts of scientists in explaining the mechanisms involved in the phenomenon of speciation. However, important omissions have prevented a full understanding of the processes involved in organic evolution. Especially, there is little consideration regarding: 1) the lack of a bridge between somatic and germinal eukaryote cells, 2) lateral genetic transferences performed by plasmids and viruses in the genome of eukaryotes, 3) the lack of a holistic concept of the gene, determinism, and genetic reductionism, 4) non-coding DNA, 5) epigénesis, 6) homeotic mutations and the genetics of development, and 7) sympatric speciation.

The goal of this article is to discuss these topics to contribute to a better understanding of the mechanisms involved in organic evolution.

The absence of a bridge between somatic and germinal cells in some phylum of invertebrates and the heredity of somato clonal variation

One of the assumptions of population genetics is that genes are vertically transmitted to the progeny according to the laws of Mendelian inheritance. In this context, and based on Weissmann's barriers between somatic and germinal cells, only genetic changes that take place within gametes are inherited by the next generation. Nevertheless, in many invertebrate organisms there are no barriers between somatic and germinal cells. For example, in the phylum porifera (sea sponges) and coelenterata (medusa) there are no differentiated germinal lines. Sexual sponge cells originate from a cellular group denominated choanocytes and archaeocyte amoeboids that have several functions, such as obtaining, digesting, and transporting food, besides sexual and asexual reproduction. In the phylum Echinoderms, there is a germ line with late differentiation during embryonic development (Storer and Usinger 1966 Ruppert and Barnes 1996). Thus, changes in the genetic material of somatic cells could be inherited in the next generation under a neo-Lamarckian model of heredity by natural somatoclonal variation. Somatoclonal selection frequently occurs naturally in angiosperms through rhizomes, tubers, and stems (Hoffmann, 1998). Although we know a great deal about natural cloning, there is still much to learn about vegetative propagation and its evolutionary implications. Due to great advances in genetic engineering and biotechnology, the meaning of genetic changes has been verified with somatoclonal cells and somatic embryogenesis through plant improvement (Ahuja, 1988 Mohan et al., 1988). In addition, this occurs in many primitive phylum of invertebrates, such as porifera, coelenterata, platyhelminthes, nemertinea, and bryozoa, by alternating sexual and asexual reproduction either by cell dispersion, transversal excision, or budding.

New organisms may arise through all these processes (Storer and Usinger, 1966, Ruppert and Barnes, 1996). There is a great regenerative power existing in some of these species, for example the planarian (Turbellarian) any piece of a body may develop into a new entire being (Legner et al., 1976).

In a chapter entitled The Heredity of Acquired Characters of his book The Scientific Basis of Evolution (1943), Thomas H. Morgan stated: "It is not known if the new work in the field of genetics is a mortal blow to the old doctrine of the inheritance of acquired characteristics. The old doctrine held that a modification of the body's cells, produced during development or in adult stages by external agents, is inherited. In other words: a change in the character of the somatic cell determines a change in the germ cells." Morgan then gave arguments to prove the fallacy of the inheritance of acquired characteristics, using stable heritable traits in Drosophila. Undoubtedly, many such arguments are solid and indisputable, but genomic sequencing shows that the genome of many eukaryotic organisms have retrovirus genes that have firstly parasitized somatic cells. According to Steele et al., (1998) the barrier between somatic and germ cells can be sorted through retrovirus and could be responsible for paternal transmission of acquired immunological tolerance.

Horizontal genetic transferences and the importance of viruses in the host's adaptation and organic evolution

In the classic models of population genetics and heredity, small effect mutations are the most important cause of evolutionary novelty by which natural selection acts. With McClintock's discovery of transposable elements in maize, the mechanism of variability became more horizontal. Mobile elements regulate genetic action (Mc Clintock, 1950, 1951) and could also have evolutionary implications through the induction of hybrid dysgenesis and sympatric speciation (Syvanen, 1984). Salvador Luria in 1959 postulated that temperate bacterial viruses might play a role in the evolution of the host (Villarreal, 1999). Stebbins and Ayala (1986) provided new data and a modern reinterpretation in order to expand the Synthetic Theory of Evolution. In that publication these author said: "When new genes arise by duplication, both the original and the duplicated genes have the tendency to be transmitted coupled to the offspring of the organism where the duplication was produced. However, a variant of this process has been discovered that constitutes one of the ways, apparently countless of the evolution at the genetic level. Occasionally, the gene is found in a species and the duplicated gene is present in a distant phylogenetic species. This phenomenon is called horizontal transfer of DNA as it passes from one species to another and co-existing with it. This horizontal genetic transmission is opposed to vertical transmission from parents to children through gametes. The real mechanisms for horizontal gene transfer are unknown. Probably, the vector could be small ring-shaped chains of DNA called plasmid, capable of transporting hereditary material from one cell to another." With the advent of genetic engineering, we now know that plasmids and viruses are vectors in the framework of recombinant DNA technology. The impact of these lateral transferences between bacteria and primitive eukaryotes on organic evolution has been detected in the new tree of life described by Carl R. Woese (1998). According to this new tree, there are three domains: bacteria, archaea, and eukarya. Unique vertical transfer of genes among these domains is not consistent. It was expected that eukarya, with the exception of mitochondria and chloroplast genes, should have only genes from archaea. However, this is not the case, because eukaryotes often have genes from bacterial origin that are not related uniquely to respiration and photosynthesis (Doolittle, 2004).

Horizontal gene transfer has been described in detail in cases of bacterial transformation mediated by viruses (restricted and generalized transduction). Bacteria have obtained a significant proportion of their genetic diversity through the acquisition of sequences from distantly related organisms. These lateral transfers have effectively changed the ecological and pathogenic character of bacterial species (Ochman, et al, 2000, Bardarov, 2002).

The human genome shows evidence that genes were laterally transferred into the genome from prokaryotic organisms. About 40 to 113 genes have been found to be exclusively shared by humans and bacteria and are examples of a direct horizontal transfer from bacteria to the human genome (Salzberg et al., 2001, Villarreal 2001). In addition, many transposable elements in the human genome, such as LINES, SINES (long and short interspersed sequences), are clearly related to endogenous retroviruses (ERV) embedded in the host genome. As well, some DNA polymerases from eukaryotes have a viral origin (Villarreal, 2000, Villarreal 2001). Human chromosome 21 carries 225 protein-encoding genes, but also carries 2000 ERV elements. About 5% of the human genome contains retroviral and related sequences, similar to proportions exhibited by other species (Prak and Kazazian, 2000 Tristem, 2000), while a lower proportion of human, genome (about 2%) contain structural genes.

As part of the host genetic heritage, ERV are transmissible to the next generation in a Mendelian model. Their abundance in animal genomes and their expression in primarily germ cells, embryonic tissue and cancer cell lines raised the question of their biological significance (Prudhomme et al., 2005). The presence of ERV in humans and in the placenta of other mammals has been known for the past 25 years, but the significance of this observation is still not fully understood. It is probably that ancient trophoblastic ERVs had a role in the evolution and divergence of all placental mammals (Harris, 1998).

All mammalian genomes have specific and distinct sets of ERVs and much greater numbers of defective retroviral derivatives, suggesting that mammalian genomes were colonized by specific lineages of ERV soon after placental species radiated from one another. The human genome project indicates that there are thousands of human ERVs that seem to comprise 24 families. Humans have both ancient and newly acquired versions of ERVs, which distinguishes humans from close primate relatives. Mammals are phylogenetically congruent with their ERVs, whereas birds are not. Most mammals express their corresponding ERVs in placental and embryonic tissues. This expression is needed, possibly for immune suppression and other vital developmental processes. ERV forms part of the placental immunosuppressive barrier between mother and fetus, and their expression prevents the rejection of the fetus by the maternal immune system. This has solved a major problem of live birth (viviparous) placental mammals. It could also play a role in the origin of adaptive immune systems in animals (Venable et. al, 1995, Villarreal, 1997, 1999, 2001, 2003 Prudhomme, et al. 2005). Therefore, these ERV viruses have a symbiotic relationship with the host.

A similar example of ERV has been described in DNA viruses of parasitic wasps. Mutualistic relationships with polydnavirus have been described in the families Braconidae and Ichneuminidae. The DNA virus is integrated into the parasitoid wasp host genome and seems to be the first documented example of an integrated, nonretroviral DNA virus in insects, and vertically transmitted as a provirus (Fleming, 1991). These viruses are formed only in calyx cells in the ovary of the wasp (Wyler and Lanzrein, 2003). When female wasps implant their eggs into host caterpillar larvae, the viruses are released into the body cavity of a lepidoptera host, suppressing the immune system. This allows the survival of the wasp eggs and larvae to develop into new adults. In this way, polydnavirus in wasps plays a role as a nurse cell by surrounding the eggs and larvae and blocking the caterpillar host's anti-parasite defense response (Villareal, 2001).

These examples in humans and wasps show that not all viral infections are pathogenic. Many viruses can infect their host persistently throughout the host's lifetime without disease. Such viruses can bring the viral seeds of genetic creation into their host (Villareal, 2001, 2003).

Nucleotide sequencing of DNA polyadenvirus has revealed a complex organization, resembling a eukaryote genomic region more than a viral genome. Although endocellular symbiont genomes have undergone a dramatic loss of genes, evolution of symbiotic viruses appears to be characterized by extensive duplication of virulence genes coding for truncated versions of cellular proteins (Espagne et al, 2004).

The importance of heterochromatin, epigenesist, non-coding DNA, and non-transcriptional genes

In the framework of the VIII International Congress of Genetic, in 1949, Richard Goldschmidt finished his oral presentation about " heterochromatic heredity" with the next question: "Should hetrochromatic mutation be considered a major factor in macroevolution?". However, in the synthetic theory of evolution framework, these ideas were not accepted. Evolutionists at that time focused their attention on euchromatic regions where protein coding genes are located. Years later, with the advent of the central dogma of molecular biology, structural genes became even more important in evolutionary genetics. In this conceptual space, the gene was strictly considered as a sequence of nucleotides that resulted from a protein. The rest of the genome was considered "useless genetic material" or "genetic junk".

Heterochromatin, where DNA satellite repeats are located, mediates many diverse functions within the cell nucleus, including centromere functions, gene silencing, and nuclear organization. Recent studies identified methylation of the histone H3 tail as a post-translational marker that affects acetylation and phosphorylation of histone tail residues, and also acts as a recognition signal for binding of heterochromatin protein 1 (HP1) (Dillon and Festnstein, 2002). These persistent non-genetic alterations in chromatin have been named epigenetic changes (Dang et al. 2009). The post-translational modification of histone tails generate a " histone code" that defines local and global chromatin states the resultant regulation of gene function is thought to govern cell fate, proliferation and differentiation (Stral and Allis, 2000). Other epigenetic methylation markers in the histone 3 (H3) in eukaryote X chromosomes have been correlated to active gene expression and also to gene silencing (Lachner et al., 2001, Nakayama et al., 2001). Regulation of X inactivation in mammals is another classic example of epigenetics. The original choice of which X chromosome will be inactivated occurs early during embryogenesis. Inactivation is random in those cells that form the proper embryo, whereas the paternal X chromosome is always chosen for inactivation in those cells that will form extraembryonic tissues (Park and Kuroda, 2001). This last epigenetic mechanism is an example of a genomic imprinting, similar to those described in sex determination of Coccids (Insecta) (Brown, 1964, 1966).

In recent years, DNA sequencing has revealed that the human genome comprises 3 billion base pairs, but only approximately 2% correspond to protein coding genes or structural genes. There are other functional genes in this area, such as ribosomal RNA and transfer RNA. The remaining 98% are non-coding DNA located in heterochromatic areas and repeated DNA. Studies of molecular genetics have shown that these non-coding DNA are useful for the organism and have been called, in a holistic concept, "non-transcriptional genes" (Frías, 2004). Thus, in a broad concept of genes, they correspond to coding or non-coding sequences of DNA that have a role in the body. Therefore, telomeric genes, centromeric genes and origin of replication genes are located in these repeated DNA areas (Frías, 2007a). Recently, non-coding RNA essential in genetic regulation has been discovered and in Pearson's opinion (2006) they could be called "genes". At present we know that many non-coding RNA (small RNA and interference RNA) are important in genetic expression. Many of these double-helix RNA have a viral origin (Lau and Bartel. 2003).

Prokaryotes and virus have only structural genes that are also present in all eukaryotes. Therefore, these genes can be considered as "precursor genes" or "lower genes" (plesiomophies) of evolutionary processes. Non-transcriptional genes, present only in eukaryotes, are more advanced or higher genes (apomorphies) (Frías, 2007a).

In recent years, studies of speciation have principally focused their attention to DNA sequencing in order to find molecular diagnostic characters at the species level. Molecular phylogenies do not always coincide with morphological phylogenies (Bitsch et al., 2004, Rubinoff and Holland, 2005). Species description is still based on morphology, but molecular tools applied to phylogenetic analysis can be a good complementary approach to infer evolutionary relationships.

The homeotic mutation and the limitation of gradual evolution

Classically, mutations with small effects have been very important to explain gradualism in organic evolution and biodiversity. Homeotic mutations that regulate the development of eukaryotes were not considered initially in the synthetic theory of evolution. Homeosis is a term coined by William Bateson in 1894 in his book Materials for the Study of Variation. Homeotic mutation explains the replacement of a segmental structure by another during development, for example: eye-stalks and antennae (Goldschmidt 1945a). In 1915, Calvin Bridge found the mutation Bithorax in Drosophila. Years later, Goldschmidt described several homeotic mutations in D. melanogaster, particularly those in podoptera, antenna-pedia mutation, tetraltera mutation (transformation of wings into halteres), and tretaptera (transformation of halteres in wings) (Goldschmidt 1945b, 1945c). In his book, The material basis of evolution Goldschmidt proposed a new theory of organic evolution based on these homeotic mutations and introducing the concepts of macroevolution and microevolution (Goldschmidt 1943). Goldschimidt thought that these macromutations explain speciation (macroevolution) by changes in the development of organisms. But this view was not considered by contemporary evolutionists (Dobzhansky, 1940). The cornerstones of the synthetic theory of evolution are microevolution and gradualism, based on mutations with small effects (poligenes). The microevolutionary mechanisms are the same as those that operate at different levels of species and explain the existence of higher taxonomic categories (macroevolution) such as genera, families, orders, class, phylum etc.

But, for Goldschmidt, microevolutionary mechanisms do not explain the formation of species, they only generate polymorphism in populations that are frequently reversible. Homeotic and systemic mutation are fundamental factors on the origin of new species and on other higher taxonomic categories. Many homeotic mutations are not adaptive while others could be. For instance, the mutation of ophthalmoptera described by Morgan in D. melanogaster, which appears as large inflated expansions, usually originating in the eyes, is not an adaptive mutation in Drosophila. Nevertheless, in several species of the genus Phytalmia (Haplostomata, Phytalmiidae) the male is adorned with expanded outgrowths from its eyes, bearing a remarkable resemblance to the more extreme types of ophthalmoptera found in Drosophila. Thus, these homeotic mutations, which are monstrosities in Drosophila, appear as a normal taxonomic feature of the other fly (Goldschmidt and Lederman-Klein, 1959). Many other exaggerated structures have been described in insects, generally seen in males, that are useful for sexual selection (Whittington, 2006 Emlen and Nijhout, 2000).

Currently the works of Garcia-Bellido (1977) and Lewis (1978) on Drosophila homeotic mutations have become fundamental to explain the genetic basis of development and evolution in eukaryote organisms (Carroll, 1995). Homeotic genes are highly conservative and have an important role in the regulation and expression of the gene during the development of eukaryotes. These genes are found in the most primitive invertebrates, vertebrates and plants (Busch et al., 1999 Shenk et at., 1993) and also in the human genome. Major genes are Hox and Pax genes that produce disturbances in early development. The human Hox genes show homology with homeotic box genes of Drosophila. Pax genes contain a nucleotide sequence called paired box, originally described in a segmentation gene in Drosophila (Solari, 1999).

In most taxa, genotypic changes are morphologically manifested to cause evident phenotypic discontinuities in different populations. Based on these discontinuities and fossil evidence, the paleontologists Eldredge and Gould (1972) postulated the theory of punctuated equilibria an alternative to phyletic gradualism. However, sometimes, morphological changes are minimal, resulting in cryptic species complexes. In these cases, the greatest differences are found in the behavior of individuals. The evolutionary leap is not morphological, but rather behavioral and ecological and the new mechanism of reproductive isolation is pre-mating.

Another aspect that has not received sufficient attention in neo-Darwinism is changes in morphology due to heterochrony and epigénesis during development. Conrad H. Waddington and Richard Goldschmidt warned about this exclusion in a timely manner, but their claims were not considered by other contemporary scientists (Reig, 1991). A few years later, Gould (1977) proposed a model primarily based on development acceleration (hypermorphy) or retardation (neoteny). Both processes cause morphological discontinuities and could give rise to new species (Frías 2009).

Excessive importance to extrinsic barriers in animal speciation

The mode of speciation in natural populations is a central problem in the synthetic theory of evolution. In The Origin of Species Darwin considered speciation as synonymous to evolution and that one species proceeds pre-existing species. Romanes (1897) called speciation the transformation of a species over time and its multiplication in the space (Mayr, 1949). There is consensus that new species arise when new reproductive mechanisms, post-copulatory or pre-copulatory, appear and suspend the gene flow among populations. However, there is no consensus if these new isolating mechanisms arise in sympatry, allopatry or parapatry. Thus, a problem in speciation is understanding the origin of intrinsic isolating barriers that prevent the gene flow in sympatry. Another task is understanding which evolutionary forces produced these barriers (Coyne and Orr, 2004). The allopatric model is the most widely accepted model of speciation in the framework of the synthetic theory of evolution. Ernest Mayr was the architect this model, in which interest has focused on geographic speciation ( Mayr, 1949, Mayr , 1968). This model is designed as a process of change in a biological system due to external forces. The existence of an extrinsic barrier is a prerequisite to the emergence of new reproductive isolation mechanisms and new species (Mayr, 1949). Therefore, this is a mechanistic model in which animal behavior does not have a role without a prior interruption of gene flow among populations by an extrinsic barrier (Reig, 1991). Considering that several million species have been described and many others have not yet been described, there are not enough geographical barriers to explain the origin of new intrinsic isolation mechanisms and speciation in allopatric conditions. Apparently the allopatric model is not the most parsimonious model to explain speciation. Intrinsic mechanisms of species, such as homeosis, chromosomal rearrangements, development genetics, epigénesis, and behavioral imprinting could be the most common to explain the origin of new isolation mechanisms and speciation in sympatry or in semi-geographic conditions.

As an alternative to allopatric speciation, Benjamin Walsh (1864) offered a theory in which a host race of phytophagous insects evolves in sympatry. In The Origin of Species, Darwin emphasized Walsh's idea of the origin of new varieties and species of phytopagous insects in sympatry. Maynard Smith (1966) proposed a theoretical model for sympatric speciation through disruptive selection in a two niche situations. Guy Bush, studying host-race formation in Rhagoletis pomonella (Walsh), has been the main defender of sympatric speciation. It has been shown that the choice of a new host plant can separate populations just as a mountain, an ocean or a river can (Gibbons, 1996 Wu, 1996 Via, 2001, Frías, 2005, Frías, 2007b). Precopulatory reproductive isolation in sympatry has been extensively demonstrated in phytophagous insects, especially in the family Tephritidae of Díptera (Bush, 1969, 1994, Feder et al, 1994, Frías 1989, 2001, 2005). Males and females show host fidelity and their entire life cycle take place on host plants. Host fidelity is mainly due to two classes of odorant: a) characteristic odor released by plants (Christenson and Foote, 1960) and, b) pheromones released by males and females on their host plants (Katsoyannos, 1975 Prokopy, 1976). The olfactory system of insects consists of three classes of proteins: 1) odorant binding protein (OBPs) 2) olfactory receptors (ORs) and 3) odorant degrading enzymes (ODEs). OBPs constitute multi-gene families and consist of two groups: 1) binding proteins of general odorant and 2) pheromone binding proteins (Sanchez-Gracia, 2005). Changes in chemicals of plants and in proteins of odorant receptors in flies may explain host changes under sympatry.

Most paradigms of sympatric speciation involve colonization by a phytophagous insect of an introduced cultivated host plant (Bushl969, Frías 2007b). Recently however, a model of sympatric speciation has been postulated through the co-evolution between species of the genus Trupanea (Tephritidae) and their host plants of the genus Haplopappus (Asteraceae), based on the hybridization of host plants (Frías, 2005). Compared to other models of sympatric speciation, this is the most parsimonious model of speciation because the hybrid plant is only distributed to places where both parental plants coexist, corresponding to a primary state of the evolution of polyploid complexes in plants, as has been postulated by Stebbins. The new species Trupanea simpatrica is associated with hybrid plants and derived sympatrically from a T. foliosis population, which is associated with one of the parental plants (Frías, 2005). Since frequent natural hybridization takes place simpatrically among angiosperm species (Grant, 1981), the model of sympatric speciation in phytophagous insects, involving colonization of newly established hybrid plant species, could be very common in insects associated with Asteraceae ( Frías, 2005).

Recent studies of molecular biology in the nervous system of Drosophila provide a basis for understanding how learned behavior of the larvae could be inherited by the adult. It has been found that some nerve cells of the cephalic ganglion of Drosophila larvae contribute to forming the nervous system of adults. (Gerber and Stocker, 2007). Studies of the parasitoid wasp Aphidium ervi have demonstrated that odor learning during immature stages is transferred to adults, suggesting that the acquisition of an olfactory memory during the larval stage persists through metamorphosis (Gutierrez-Ibañez et al. 2007). These findings indicate that host fidelity could also be determined by behavioral imprinting in the framework of a neo-Lamarckian model.

Although sympatric speciation by hybridization and allopolyploidy in plants is widely accepted, Gallardo et al. (1999) discovered polyploidy in a mammal. This finding gave a window to sympatric speciation in animals in the absence of geographic barriers.

Another model of speciation without geographic barriers, in semi-geographic conditions or parapatric speciation, occurs through intrinsic barriers caused by chromosomal rearrangements and negative heterosis of hybrids (White , 1974White, 1978 Frías and Atria 1998 Gravilets, 2000). To refer to these karyotypes changes, Goldschmidt introduced the concept of "systemic mutation" based on the transformation of intra-chromosomal pattern. A new spatially different rearrangement of intrachromosomal constitution originates from inversion, translocations, or heterochromatic modifications. And thus a new, stable system emerges that leads to speciation (Goldschmidt 1943 Bush, 1982). Stegnii (1996) extends the concept of systemic mutation incorporating those changes that lead to new rearrangements of the chromocentric apparatus, as well as changes related to the chromosome-membrane connection system.

Goldchmidt's ideas contributed significantly to understanding the role of chromosomal rearrangements in the speciation of certain groups of organisms, especially in Drosophila species (Dobzhansky, 1973 Brncic, 1957). However, the roles of heterochromatic changes and chromocentric apparatus have not been extensively studied. It has been argued that macroevolution has a relationship to centromeric and telomeric heterochromatin changes and also to changes in the chromocentric apparatus for species belonging to two different phyletic groups, Díptera (Tephritidae) and Mepraia (Reduviidae). All these chomosomic rearrangements, especially those in Mepraia spp, explain how postcopulatory reproductive isolation mechanisms, without an extrinsic barrier, originated (Frías and Atria, 1998 Frías, 2009).

It is clear that the genetic code is found in structural genes, lower genes or ancestral genes, which are shared with viruses and prokaryotes. Apparently however, much of the genetic program that makes differentiation and development of a multicellular organisms possible is in non-coding DNA, where non-transcriptional genes, transposable elements and endogenous viruses are located. These genes are linked to the advent of new and vital roles in eukaryotes, such as chromosome origin, mitosis, meiosis, cell differentiation and development. However, the genetic program is not only located in the DNA, but also in higher levels of genomic organization. It has been argued that DNA methylation is a stable epigenetic modification and gene imprinting that evolved independently in angiosperm plants and mammals. (Hsieh et al., 2009 Gehring et al., 2009). Due to genomic imprinting, epigenetic changes are inherited in a different manner from Mendel's principles.

The genetic code is universal, here we find the basic elements of the genetic program responsible for developing a new organism and new life forms. This program is expressed or terminated due to genetic and epigenetic information and external environmental conditions. Speciation always involves genotypic, epigenotypic and phenotypic leaps. Small leaps originate species, large leaps originate genera, other larger leaps originate families, and thus progressively larger leaps could even explain the emergence of higher systematic categories.

The great extinction of the Jurassic and the great species explosion in the Cambrian and the Cretaceous demonstrate the existence of leaps in the history of organic evolution. These facts indicate that speciation is not gradual. Natural selection does not have a creative effect on species, but rather barriers that the organism must avoid. Intrinsic epigenetic and genetic factors are responsible for inducing the formation of new species in new ecological environments. Neither has atmospheric pressure led to the creation of birds or butterflies, and as Monod and Jacob said, "It is just by chance and necessity." New genomic and epigenomic combinations randomly emerged, and if environments are suitable for these new genotypes, the species are adapted to the environments. Metaphorically speaking, atmospheric pressure did not create the airplane it is the mechanic who adjusts the vehicle to make it fly.

Moreover, the role of viruses in the evolution and adaptation of prokaryotes and eukaryotes has not been evaluated in the framework of the synthetic theory. There is no bridge between virology and evolutionary theory. This is probably because viruses have long been considered to have originated from the genome of eukaryotes. They would have been fragments of RNA or DNA cells that escaped a long time ago from eukaryotic chromosomes, evolving afterwards by capturing additional genes from the genomes of their hosts. Nevertheless, this view has now been challenged by the discovery of ribozymes and by the surprising homology between viruses with very distantly related hosts, and by phylogenetic analyses suggesting that genes might have flowed from viruses to eukaryotic chromosomes (Fileé et al., 2003).

If RNA viruses were the first living manifestation, then they could be molecular fossils of this primitive RNA world (Chela-Flores, 1994). In this pool, RNA viruses would have evolved first, followed by retro-elements and DNA viruses. The virus world concept and these models of major transitions in the evolution of cells provide complementary pieces of an emerging coherent picture of the history of life (Koonin et al, 2006).

The large amount of retroviruses DNA in the human genome and other eukaryotes, apparently contradicts the debugging role of natural selection. However, the increase in repeated DNA with the complexity of higher organisms shows an adaptive value (Lau and Bartel, 2003). Thus, the paradox of C-value would not be a paradox (Frías, 2007a). A large amount of redundant genetic material in eukaryotes has a viral origin, in particular small RNA, RNA interference, introns and mobile genetic elements. All these genetics elements were horizontally acquired, but once incorporated into the host genome and passing the Weissman barrier, they were vertically transmitted according a Mendelian model of heredity. Thus, Steele's assumption is probably correct and his model could be expanded to explain the heredity of the large amount of DNA retrovirus in eukaryotes. It has been have been found that DNA virus (polydnvirus) in parasitic wasps could be embedded in the genome of the host. Both DNA viruses and retroviruses have a symbiotic relationship with the host.

Findings in the human genome, such as genes from bacteria, viruses acquired by horizontal transmission and homologous regions of human genes with other organisms, such as Drosophila (Katoh and Katoh, 2003), indicate that the eukaryotic genome is unstable over a long time-scale. However, it may be a mosaic flow of information from different sources in a symbiotic co-evolutionary process. The study of the human genome evolution has concentrated on humans and their hominid ancestors, without much attention to other organisms and viruses that also evolved from the same environments (Van Blerkom, 2003).

With respect to genes of endogenous viruses embedded in the host genome, there is doubt whether these genes should be considered foreign or from the host, as occurs with mitochondrial and chloroplast genes. It is necessary to establish bridges between viruses and eukaryotic genome organization to better understanding the role of lateral genetic transferences in macro-evolutionary processes. In particular, it is necessary to carry out functional genomics studies.

Through the contributions of Lynn Margulis (1988), it is currently accepted that mitochondria and chloroplast are endosymbionts of bacterial origin. Many biologists also accept the ecological Gaia hypothesis of Lovelock and Margulis (1974), where living organism are integrated with other physical components in our planet in order to maintain a dynamic balance or homeostasis in the system that counteracts the second law of thermodynamics. It is likely that viruses have participated for millions of years as "workers", remodeling the eukaryotic genome and producing evolutionary novelties together with other classical mechanisms, such as homeotic and systemic mutations and chromosomic rearrangements, joined to other factors like epigénesis and heterochrony during development. All these new molecular aspects uncovered by the synthetic theory of evolution suggest the need to make a new evolutionary synthesis.

This is a posthumous tribute to Dr. Gustavo Hoecker Salas

Thank to an anonymous reviewer for his suggestions that helped me improve the manuscript. This research has been supported by Project FIBAS 06/ 08 DIUMCE.

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Corresponding author: Daniel Frías L, Instituto de Entomología, Universidad Metropolitana de Ciencias de la Educación Avenida José Pedro Alessandrí, 774, Postal code: 7760197, Santiago, Chile, Telephone: 56-2-2412457, Cellular phone: 093331688, Fax number: 56-2-2412728, Email: [email protected]

Received: January 19, 2010. In revised form: June 24, 2010. Accepted: July 6, 2010.

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Conclusions

Here, we have described existing hypotheses from the literature and set forth additional hypotheses and proposals for further consideration, with respect to the causes and consequences of PGC specification mechanisms in metazoans (SI Appendix, Table S1). Together, the data to date suggest that the transition to germ plasm in metazoans occurred convergently via different genetic and developmental mechanisms, which may have involved adaptive processes, or, alternatively, may have arisen as a spandrel effect. Furthermore, PGC specification may be connected to life history parameters such as oviparity and viviparity. We argue that, because PGC specification mode is indispensable for germ-line formation, it is apt to affect the germ-line genomic mutation rate, which is one of the most crucial parameters in evolutionary biology. Expanding research in this area will thus be essential to gaining an understanding of the nature of that relationship.


Independent Domestication Events of the SYNCYTINs in Different Lineages in Eutherians

As mentioned in Section “Introduction,” SYNCYTIN was first discovered in humans (Blond et al., 2000 Mi et al., 2000). Although there are many Env-related DNA sequences in the human genome, only two exhibit fusogenic activity in cell fusion assays and now these are called SYNCYTIN1 and 2 (Blaise et al., 2003). They are derived from different human-specific ERVs, HERV-W, and HERV-FRD, and became integrated into a primate lineage 25 and 㹀 MYA, respectively (Figure 3). Recent studies demonstrated that similar genes exist in an order- or family-specific manner in several mammalian lineages, i.e., producing syncytiotrophoblast cells by cell fusion in the placenta. Mice also have two Syncytin genes, SyncytinA and B, derived from Muridae family-specific integrations of HERV-F/H-related ERV(s) approximately 20 MYA (Dupressoir et al., 2005 Figure 3), and rabbits (Oryctolagus cuniculus) have another SYNCYTIN-Ory1 from Leporidae family-specific integration of a different type-D retrovirus 12� MYA (Heidmann et al., 2009). Therefore, at least three independent domestication events have been confirmed in the eutherians, indicating that domestication from ERVs which were actively functioning during the time of mammalian radiation.

SyncytinA knockout mice exhibit mid-fetal lethality because of the structural abnormality of the placenta (Dupressoir et al., 2009), and double knockout of both SyncytinA and B causes an even more severe phenotype, early embryonic lethality (Dupressoir et al., 2011). Among the eutherians, placental morphology and functions are quite substantially diverged. Therefore, it is very interesting that the SYNCYTINs from the ERVs appear to have important roles in the placenta that they play in an order- or family-specific manner, while PEG10 and PEG11/RTL1 from the LTR retrotransposons are conserved in the therians and eutherians, respectively, and presumably have contributed to the establishment of the basic structure of viviparous reproductive systems in the current eutherian species.


Kerala Plus Two Zoology Notes Chapter 5 Evolution

Origin Of Life
In the solar system, earth was originated 4.5 billion years back. There was no atmosphere on early earth.

Water vapour, methane, carbondioxide and ammonia are found on the surface

The UV rays from the sun broke up water into Hydrogen and Oxygen. Oxygen combined with ammonia and methane to form water, CO2 and others.

Life originated four billion years. Earlier it was believed that life originated from non living things. This is the theory of spontaneous generation.

Later Louis Pasteur demonstrated that life comes only from pre-existing life. He showed that in presterilised flasks, life did not come from killed yeast while in another flask open to air, new living organisms arose from ‘killed yeast’.

Oparin and Haldane proposed that the first form of life that arose from pre-existing non-living organic molecules (e.g. RNA, protein, etc.) and it is followed by chemical evolution.

In 1953, S.L. Miller, an American scientist created similar conditions in a laboratory He created electric discharge in a closed flask containing CH4, H2, NH3 and water vapaur at 800°C. He observed the formation of amino acids.

The first non-cellular forms of life could have originated 3 billion years back i.e RNA, Protein, Polysaccharides, etc…

Later the first cellular forms (single-celled) were originated. These were occurred in water environment only.
Diagrammatic Representation of Miller’s Experiment:

Evolution Of Life Forms – A Theory
Charles Darwin has conducted a voyage ship called H.M.S. Beagle round the world and reach the conclusion that existing living forms share similarities not only among themselves but also with life forms that existed millions of years ago. There has been gradual evolution of life forms.

According to the concept of reproductive fitness, those who are better fit in an environment, produce more progeny than others and survived more. He called it as natural selection an important mechanism of evolution.

In the same time Alfred Wallace naturalist of Malay Archepelago had the same conclusion as Darvin, that all the existing life forms share similarities and share common ancestors.

What Are The Evidences For Evolution?
Evidence of evolution of life comes from fossils that found in sedimentary rocks. Different-aged rock sediments contain fossils of different life-forms. They represent extinct organisms (e.g., Dinosaurs).This type of evidence is called paleontological evidence.

Analysing the comparative anatomy and morphology, shows similarities and differences among organisms of today and those that existed years ago.

Example of homologous organs in (a) Plants and (b) Animals:

For example whales, bats, Cheetah and human share similarities in the pattern of bones of forelimbs (similar anatomical structure).

It contains the bones like humerus, radius, ulna, carpals, metacarpals and phalanges. The same structure developed along different directions due to adaptions to different needs. So they have different functions.

These structures are homologous. This type of evolution is called divergent evolution. Other examples are vertebrate hearts or brains and the thorn and tendrils of Bougainvillea.

Wings of butterfly and of birds anatomically dissimilar but they perform similar functions. These are analogous structures arise due to convergent evolution.

Other examples are the eye of the octopus and of mammals or the flippers of Penguins and Dolphins: Sweet potato (root modification) and potato (stem modification) etc.

Another evidence supporting evolution by natural selection comes from England. Before industrialisation there are more white-winged moths on trees than dark-winged.

This is due to white-coloured lichen covered the trees – in that background the white winged moth survived But after industrialisation, there were more dark-winged moths in the same area because the tree trunks became dark due to industrial smoke and soots.

Under this condition the white-winged moth did not survive due to predators, dark-winged or melanised moth survived.

Lichen are pollution indicators they cannot grow in areas that are polluted. Hence, moths that were able to camouflage themselves.

What Is Adaptive Radiation?
In this, the small black birds -Darwin’s Finches are examples. Darwin found that there were many varieties of finches in the same island.

Their original seed-eating features are changed and become insectivorous and Variety of beaks of finches that Darwin found in Galapagos Island vegetarian finches.

Here the evolution starting from a point and radiating to other areas of geography (habitats) is called adaptive radiation.

Another example is Australian marsupials. A number of different marsupials evolved from an ancestral stock within the Australian island.

Placental mammals in Australia also exhibit adaptive radiation i.e they evolved into varieties (e.g., Placental wolf and Tasmanian wolf marsupial).

Variety of beaks of finches that Darwin found in Galapagos Island:

Biological Evolution
The importance of Darwinian theory of evolution lies in natural selection.

A colony of bacteria (say A) growing on a given medium show variation in terms of feed component. A change in the medium composition results the population (say B) that can survive under the new conditions.

Here the fitness of B is better than that of A under the new conditions. Nature selects for fitness. Adaptive ability is inherited. It has a genetic basis. Fitness is the ability to adapt and get selected by nature.

Branching descent and natural selection are the two key concepts of Darwinian Theory of Evolution Before Darwin, Lamarck had conducted experiments and proposed the use and disuse of organs.

He gave the examples of Giraffes who in an attempt to forage leaves on tall trees had to adapt by elongation of their necks. As they passed on this acquired character of elongated neck to succeeding generations.

The work of Thomas Malthus on populations was influenced Darwin For example, natural resources are limited, populations are stable in size except for seasonal fluctuation.

The population size grow exponentially if reproduced maximally. Darwin was pointed that variations which are heritable, when the resource utilisation better for few, they reproduce more progeny. Hence for a period of time survivors leave more progeny and there would be a change in population characteristics.

Mechanism Of Evolution
Mendel had studied only inheritable ‘factors’ influencing phenotype, But Hugo deVries conducted experiments on evening primrose and proposed the idea of mutation. Mutations are random and directionless while Darwinian variations are small and directional.

Mutation leads to speciation called as saltation (single step large mutation).

Hardy-Weinberg Principle
Diagrammatic representation of the operation of natural selection on different traits:

(a) Stabilising
(b) Directional and
(c) Disruptive

According to Hardy-Weinberg principle allele frequencies in a population are stable and is constant from generation to generation. This is called genetic equilibrium. Sum total of all the allelic frequencies is 1.

For example, p and q represent the frequency of allele A and allele a. The frequency of AA individuals in a population is simply p2. The frequency of p appear on both the chromosomes of a diploid individual, Similarly of aa is q2, and of Aa is 2pq.

Hence, p2 + 2pq + q2 = 1. This is a binomial expansion of (p+q)2.

Disturbance in genetic equilibrium, or Hardy – Weinberg equilibrium, i.e., change of frequency of alleles in a population affected by five factors.

These are gene migration or gene flow, genetic drift, mutation, genetic recombination and natural selection.

When migration of population occurs, gene frequencies change in the original as well as in the new population. If the same change occurs by chance, it is called genetic drift.

Sometimes the change in allele frequency is different in the new sample of population that they become a different species. The original drifted population becomes founders and the effect is called founder effect.

The variation due to mutation or variation due to recombination during gametogenesis, or due to gene flow or genetic drift results in changed frequency of genes and alleles in future generation.

Natural selection lead to the stabilisation (more individuals acquire mean character value)
directional more individuals acquire value other than the mean character value)
disruptive More individuals acquire peripheral character value at both ends of the distribution curve

A Brief Account Of Evolution
About 2000 million years ago (mya) the first cellular forms of life appeared on earth. From this the cells with membranous envelop evolved and developed Some of these cells had the ability to release O2. Slowly single-celled organisms became multi-cellular life forms.

In 500 mya, invertebrates were formed
Jawless fish evolved around 350 mya.
Sea weeds and few plants evolved around 320 mya.
In 350 mya Fish with stout and strong fins evolved

In 1938, a fish caught in South Africa happened to be a Coelacanth which was thought to be extinct. These animals called lobefins evolved into the first amphibians that lived on both land and water.

The amphibians evolved into reptiles. They lay thick shelled eggs. Their modern descendents are the turtles, tortoises and crocodiles.

In the next 200 millions years reptiles of different shapes and sizes dominated on earth.In this period Giant ferns (pteridophytes) were present.

Land reptiles dinosaurs (biggest i.e., Tyrannosaurus rex) went back into water to evolve into fish like reptiles 200 mya (e.g. Ichthyosaurs). About 65 mya, the dinosaurs suddenly disappeared from the earth.

After the reptiles, mammals evolved on this earth. The first mammals were like shrews. Their fossils are small sized. Mammals were viviparous and protected their unborn young inside the mother’s body.

There were in South America mammals resembling horse, hippopotamus, bear, rabbit, etc. Due to continental drift, when South America joined North America, these animals were overridden by North American fauna.

Due to the same continental drift pouched mammals of Australia survived because of lack of competition. Some mammals live wholly in water are Whales, dolphins, seals and sea cows.

Origin And Evolution Of Man

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Watch the video: Animals Reproduce contain three Parous, Oviparous, Viviparous, Oviparous (August 2022).