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According to this article:
Gene mutations can be classified in two major ways:
Hereditary mutations are inherited from a parent and are present throughout a person's life in virtually every cell in the body…
Acquired (or somatic) mutations occur at some time during a person's life and are present only in certain cells, not in every cell in the body. These changes can be caused by environmental factors such as ultraviolet radiation from the sun, or can occur if a mistake is made as DNA copies itself during cell division. Acquired mutations in somatic cells (cells other than sperm and egg cells) cannot be passed on to the next generation.
The "random mutations in genes" appear to be called Somatic mutations. For the context of this question, these are the mutations I am asking about (not the hereditary mutations).
My question: Is it possible for there to be a random un-mutation of genes? Some sort of reverse-somatic mutation. If so, have there been any clinically proven instances of it?
After-thought: Or is it all a Somatic mutation, aka you can experience a mutation that makes you more susceptible to a particular disease, then another mutation that makes you less susceptible to the same disease… so not necessarily a reverse mutation, but a 'forward' mutation that negates the original ill effect of the first mutation.
A large part of the body of your question seems relatively unrelated to the main question which is a little confusing. I will focus on the question
Is it possible for there to be a random un-mutation of genes?
Yes, these are usually called reversed mutation. It is quite common though that a second mutation at a distinct locus may reverse the phenotypic effect of a first mutation. This is called a compensatory mutation.
Is it possible to have a random un-mutation of genes? - Biology
Mutations can be beneficial, neutral, or harmful for the organism, but mutations do not "try" to supply what the organism "needs." Factors in the environment may influence the rate of mutation but are not generally thought to influence the direction of mutation. For example, exposure to harmful chemicals may increase the mutation rate, but will not cause more mutations that make the organism resistant to those chemicals. In this respect, mutations are random whether a particular mutation happens or not is unrelated to how useful that mutation would be.
For example, in the U.S. where people have access to shampoos with chemicals that kill lice, we have a lot of lice that are resistant to those chemicals. There are two possible explanations for this:
|Hypothesis A:||Hypothesis B:|
|Resistant strains of lice were always there and are just more frequent now because all the non-resistant lice died a sudsy death.||Exposure to lice shampoo actually caused mutations for resistance to the shampoo.|
Scientists generally think that the first explanation is the right one and that directed mutations, the second possible explanation relying on non-random mutation, is not correct.
Researchers have performed many experiments in this area. Though results can be interpreted in several ways, none unambiguously support directed mutation. Nevertheless, scientists are still doing research that provides evidence relevant to this issue.
In addition, experiments have made it clear that many mutations are in fact random, and did not occur because the organism was placed in a situation where the mutation would be useful. For example, if you expose bacteria to an antibiotic, you will likely observe an increased prevalence of antibiotic resistance. Esther and Joshua Lederberg determined that many of these mutations for antibiotic resistance existed in the population even before the population was exposed to the antibiotic and that exposure to the antibiotic did not cause those new resistant mutants to appear.
The Lederberg experiment
In 1952, Esther and Joshua Lederberg performed an experiment that helped show that many mutations are random, not directed. In this experiment, they capitalized on the ease with which bacteria can be grown and maintained. Bacteria grow into isolated colonies on plates. These colonies can be reproduced from an original plate to new plates by "stamping" the original plate with a cloth and then stamping empty plates with the same cloth. Bacteria from each colony are picked up on the cloth and then deposited on the new plates by the cloth.
Esther and Joshua hypothesized that antibiotic resistant strains of bacteria surviving an application of antibiotics had the resistance before their exposure to the antibiotics, not as a result of the exposure. Their experimental set-up is summarized below:
When the original plate is washed with penicillin, the same colonies (those in position X and Y) live even though these colonies on the original plate have never encountered penicillin before.
Is it possible to teach evolutionary biology “sensitively”?
Michael Reiss, a professor of science education at University College London and an Anglican Priest, suggests that “we need to rethink the way we teach evolution” largely because conventional approaches can be unduly confrontational and “force religious children to choose between their faith and evolution” or to result in students who”refuse to engage with a lesson.” He suggests that a better strategy would be akin to those use to teach a range of “sensitive” subjects “such as sex, pornography, ethnicity, religion, death studies, terrorism, and others” and could “help some students to consider evolution as a possibility who would otherwise not do so.” [link to his original essay and a previous post on teaching evolution: Go ahead and teach the controversy].
There is no doubt that an effective teacher attempts to present materials sensitively it is the rare person who will listen to someone who “teaches” ideas in a hostile, alienating, or condescending manner. That said, it can be difficult to avoid the disturbing implications of scientific ideas, implications that can be a barrier to their acceptance. The scientific conclusion that males and females are different but basically the same can upset people on various sides of the theo-political spectrum.
In point of fact an effective teacher, a teacher who encourages students to question their long held, or perhaps better put, familial or community beliefs, can cause serious social push-back – Trouble with a capital T. It is difficult to imagine a more effective teacher than Socrates (
470-399 BCE). Socrates “was found guilty of ‘impiety’ and ‘corrupting the young’, sentenced to death” in part because he was an effective teacher (see Socrates was guilty as charged). In a religious and political context, challenging accepted Truths (again with a capital T) can be a crime. In Socrates’ case”Athenians probably genuinely felt that undesirables in their midst had offended Zeus and his fellow deities,” and that, “Socrates, an unconventional thinker who questioned the legitimacy and authority of many of the accepted gods, fitted that bill.”
So we need to ask of scientists and science instructors, does the presentation of a scientific, that is, a naturalistic and non-supernatural, perspective in and of itself represent an insensitivity to those with a super-natural belief system. Here it is worth noting a point made by the philosopher John Gray, that such systems extend beyond those based on a belief in god(s) they include those who believe, with apocalyptic certainty, in any of a number of Truths, ranging from the triumph of a master race, the forced sterilization of the unfit, the dictatorship of the proletariat, to history’s end in a glorious capitalist and technological utopia. Is a science or science instruction that is “sensitive” to, that is, uncritical of or upsetting to those who hold such beliefs, possible?
My original impression is that one’s answer to this question is likely to be determined by whether one considers science a path to Truth, with a purposeful capital T, or rather that the goal of scientists is to build a working understanding of the world around and within us. Working scientists, and particularly biologists who must daily confront the implications of apparently un-intelligent designed organisms (due to ways evolution works) are well aware that absolute certainty is counterproductive. Nevertheless, the proven explanatory and technological power of the scientific enterprise cannot help but reinforce the strong impression that there is some deep link between scientific ideas and the way the world really works. And while some scientists have advocated unscientific speculations (think multiverses and cosmic consciousness), the truth, with a small t, of scientific thinking is all around us.
Photograph of the Milky Way by Tim Carl photography, used by permission
A science-based appreciation of the unimaginable size and age of the universe, taken together with compelling evidence for the relatively recent appearance of humans (Homo sapiens from their metazoan, vertebrate, tetrapod, mammalian, and primate ancestors) cannot help but impact our thinking as to our significance in the grand scheme of things (assuming that there is such a, possibly ineffable, plan)(1). The demonstrably random processes of mutation and the generally ruthless logic by which organisms survive, reproduce, and evolve, can lead even the most optimistic to question whether existence has any real meaning.
Consider, as an example, the potential implications of the progress being made in terms of computer-based artificial intelligence, together with advances in our understanding of the molecular and cellular connection networks that underlie human consciousness and self-consciousness. It is a small step to conclude, implicitly or explicitly, that humans (and all other organisms with a nervous system) are “just” wet machines that can (and perhaps should) be controlled and manipulated. The premise, the “self-evident truth”, that humans should be valued in and of themselves, and that their rights should be respected (2) is eroded by the ability of machines to perform what were previously thought to be exclusively human behaviors.
Humans and their societies have, after all, been around for only a few tens of thousands of years. During this time, human social organizations have passed from small wandering bands influenced by evolutionary kin and group selection processes to produce various social systems, ranging from more or less functional democracies, pseudo-democracies (including our own growing plutocracy), dictatorships, some religion-based, and totalitarian police states. Whether humans have a long term future (compared to the millions of years that dinosaurs dominated life on Earth) remains to be seen – although we can be reasonably sure that the Earth, and many of its non-human inhabitants, will continue to exist and evolve for millions to billions of years, at least until the Sun explodes.
So how do we teach scientific conclusions and their empirical foundations, which combine to argue that science represents how the world really works, without upsetting the most religiously and politically fanatical among us? Those who most vehemently reject scientific thinking because they are the most threatened by its apparently unavoidable implications. The answer is open to debate, but to my mind it involves teaching students (and encouraging the public) to distinguish empirically-based, and so inherently limited observations and the logical, coherent, and testable scientific models they give rise to from unquestionable TRUTH- and revelation-based belief systems. Perhaps we need to focus explicitly on the value of science rather than its “Truth”. To reinforce what science is ultimately for what justifies society’s support for it, namely to help reduce human suffering and (where it makes sense) to enhance the human experience, goals anchored in the perhaps logically unjustifiable, but nevertheless essential acceptance of the inherent value of each person.
- Apologies to “Good Omens”
- For example, “We hold these truths to be self-evident, that all men are created equal, that they are endowed by their creator with certain unalienable rights, that among these are life, liberty and the pursuit of happiness.”
Can we make and apple that doesn't turn brown?
1. Understand why the apple turns brown in the first place. What causing browning?
Browning is caused by the protein PPO, which is controlled by a gene
2. Why does lemon juice slow browning?
Lemon juice affects the shape of the protein, it doesn't function as well.
3. What would happen if we silenced the PPO gene?
The protein would not be produced, no browning.
4. Is the arctic apple considered transgenic?
No, it does not have new genes added, the PPO gene has been turned off.
Lifestyle Factors May Alter Genetic Traits, Study Finds
A new scientific study appearing in this week's issue of the journal Nature is challenging familiar ideas about genetic inheritance.
We can't change the genes we received from our parents. But our genes are controlled by a kind of instruction manual made up of billions of chemical markers on our DNA, and those instructions can be rewritten by our circumstances -- for instance, by obesity. According to the new research, they can even be passed along to children.
In a way it's saying the metabolic sins of the father can be visited on the daughters, even if the daughters haven't been conceived yet.
Andy Feinberg, professor of medicine and molecular biology, Johns Hopkins School of Medicine
The study was directed by Margaret Morris, an obesity researcher at the University of New South Wales in Sydney. Morris had previously explored the reasons why the children of obese mothers often become overweight themselves. But her attention shifted when a new graduate student from Malaysia arrived in her laboratory.
"She noted, in a clinic, that when a child arrived for weight management, usually both parents were obese, not just the mother," says Morris.
This wasn't too surprising. It makes sense that if a father is genetically predisposed to obesity, his daughter might be, too. But Morris wondered whether she might be seeing more than genes at work.
The Consequences Of Overeating
Morris set up an experiment with lab rats to see if the biological consequences of a father overeating could somehow get passed on to his daughters. "This is a study that I did for love," she says. "I didn't really have much funding for it. I had to crib money from all over to do it."
Morris took a group of genetically identical male rats, and put half of them on a high-fat diet. Predictably, those rats got fat and suffered symptoms of diabetes.
Then all the rats mated with normal females and had children. Morris looked specifically at the daughters. All of them had a similar genetic makeup, but those with overweight fathers had some of the same problems that their dads did. They weren't overweight, but their production of insulin was impaired.
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Of Fish And Flies: The Evolutionary Role Of Genes
This finding is fascinating, says Andy Feinberg, at the Johns Hopkins School of Medicine in Baltimore. "In a way it's saying the metabolic sins of the father can be visited on the daughters, even if the daughters haven't been conceived yet," he says.
The Grammar Of DNA
Feinberg thinks he knows how this may be happening. It's an example of an "epigenetic" effect, which is his specialty.
This field -- epigenetics -- is getting a lot of attention these days. It refers to things in and around our DNA, such as billions of chemical markers that attach to it. Those markers are signals that turn genes on and off. They tell the genes of a liver cell to behave differently from genes in a blood cell, for instance.
The sequence of our DNA -- the human genome -- has been called the book of life. Feinberg has his own metaphor for the billions of added signals that he studies. If the genetic sequence is the words of the book, the epigenome is the grammar, he says. "It helps to tell what the genes are actually supposed to do, and puts them in context."
Our genes don't change, or if they do, it's a rare and random event. But the grammar of the epigenome is changing all the time. It can also be disrupted by chemicals we eat or breathe.
Apparently it can also be disrupted by obesity, because Feinberg thinks those fat dad rats in Australia created sperm cells with a different pattern of epigenetic marks on their DNA that's how the effect showed up in their children.
Michael Skinner at Washington State University in Pullman says epigenetic effects are swinging the pendulum of scientific attention from the genetic code back toward the impact of environment.
"I think that we're eventually going to have sort of a merger of this," he says. "I think that we're going to have an appreciation of the fact that there is an environmental influence on biology that probably through more epigenetic mechanisms. There's also a baseline genetic element of biology. And the two combined will actually give us more information about how things work."
Much of epigenetics is still a mystery. Scientists would like to know, for instance, how often epigenetic signals are passed on from parent to child, or even grandchild. So Morris, in Australia, is hoping to repeat her experiment and see if the effect persists over multiple generations.
Is it possible that COVID-19 could mutate to become non-functional?
Sorry if this has been asked before or if it's a stupid question. But I remember either hearing or reading somewhere that viruses can mutate to become non-functional. Could this ever happen with the Sars-Cov-2 virus? If so, would that mean that it couldn't infect people anymore & the pandemic would just be over?
Also, is there anything that determines whether or not a virus will mutate to become non-functional, or does it happen randomly? Thanks in advance, looking forward to hearing the responses :)
Of course, this happens to individual viruses. But evolution is at play. Nonfunctional viruses will not survive and pass on their genes for obvious reasons, so functional viruses survive and dominate.
This actually happens all the time with fast mutating viruses. They (the ones with loss of function mutations) die out because they have no chance of spreading their nonfunctional genes.
Most mutations are not beneficial for the virus.
But any beneficial mutation that will increase the survival chances or infectiveness, will cause the viruses with that mutation to multiply in larger numbers, globally speaking, as strains without that mutation.
So all disadvantageous mutations lead to a decrease in the population with that mutation, while all advantageous mutations lead to an increase.
A negative mutation in one individual therefor cannot extinct the entire species.
Non-advantageous and even disadvantageous mutations can often spread faster than advantageous ones for external reasons. For example, if a mutated strain of a virus that decreases how effectively it can transmit between or infect hosts is picked up by someone who interacts closely with lots of people all over the world and many of those people also do the same, then that harmful (to the virus) mutation might quickly become more common than other variants that make the virus better at transmitting or infecting, but didn't happen to get into this super-spreader network.
This is called genetic drift and it can be a much stronger force of evolution that natural selection, especially in rapidly expanding populations like a virus during an outbreak. So mutations that are quite detrimental to the organism can become fixed while more beneficial mutations are completely lost. It's all just up to chance events, though.
This is the fundamental underlying principle of natural selection:
Mutations don’t affect everything in a species. They affect individuals. Mutations that cause something to reproduce better result in individuals with that mutation reproducing more and the mutation becoming widespread. Mutations that causing something to be worse at reproducing result in individuals with the mutation reproducing less and so the mutation dies out.
New strains of COVID that are better at infecting people will infect more people and will spread far and wide. Strains of COVID that are bad at infecting people won’t infect anyone and will quickly die out. In either case, the appearance of a new strain has no effect on any other existing strain except possibly by getting to new hosts first.
In order for a mutation that makes COVID less infectious to end the pandemic, it would have to spread and take the place of all other strains, which by definition of being bad at spreading, it will not do.
Best case scenario would be a more infectious but less dangerous strain appearing that still confers resistance and have that spread through the population and outcompete deadlier variants.
But you’re not going to see all of the viruses suddenly and spontaneously stop working at once. That’s not how mutations works
There are individual viruses that almost certainly have mutations that make them in effective. However because of that they are out competed by stronger viruses. It’s technically not impossible for a strain to develop that is both ineffective and also more contagious but it still wouldn’t really out compete other viruses anyway. You would just have both strains present
As others have said, the vast, vast majority of mutations will make the individual virus less effective. But we never hear of those because they just die out, while the unmutated versions persist. It is only the very few cases in which a random mutation makes the virus better at spreading that this new strain starts spreading faster than other strains. That seems to be what is happening with the new UK and South African strains.
That doesn't necessarily mean that such strains are worse for us - viruses do not benefit from rendering their hosts immobile or dead. That means there is a general trend for viruses to evolve towards lower lethality. We haven't seen that yet with Covid - the new strains seem to be just as lethal as previous ones, but it could happen. The viruses that cause the common cold, for example cause such mild infections, that most people barely notice. They don't die, they don't stay in bed, they don't keep distance from others - allowing the virus keeps spreading
Ironically, the lower severity of the latest West-African Ebola strain meant that it infected many more people than previous strains and ultimately killed more people than any previous outbreak, but Covid-19 is so much less lethal than Ebola that this isn't likely to happen.
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One of my friends has blond hair and blue eyes despite being mixed (mother, white blond hair and blue eyes father African-American, black hair brown eyes). My biology teacher says this is impossible, since both of those traits are recessive however his sister also has blue eyes (but not blonde hair). Can you explain the genetics that would cause this?
— A high school student from LA
February 12, 2020
Your biology teacher is most certainly right that blonde hair and blue eyes are indeed recessive traits!
There’s a few possible ways in which your friend ended up with blonde hair and blue eyes.
- Caucasian relatives sometime in the father’s past
- A new mutation in the eye color and hair genes
Albinism can be ruled out if your friend is not light-skinned. Albinism is an inherited genetic condition that results in loss of melanin pigment in the eyes, hair and skin. People with albinism have severe vision problems, often becoming “legally blind.”
Since poor vision is part of the diagnosis for albinism, if your friend does not have poor vision, they are not albino. So we’re left with two possibilities.
Image from Wikimedia
New eye and hair mutations
Blue eyes actually originally came about because of mutations! Thousands of years ago, someone had a random change in the genes that affect eye color. Over time, this genetic difference spread and became more common.
But the chance of anyone having a new random mutation that does this is pretty low.
Remember, our bodies have “proofreading” repair machinery that fix these mutations. So even if a mutation occurs, these enzymes swoop in and try to correct them! Usually our cells catch these mistakes and fix them.
But occasionally, some mutations get missed and eventually inherited. Scientists have studied how good these repair enzymes are, and how often they make mistakes. Based off these estimates, one would expect to find one mutation at a specific spot in a specific gene per one million people. 1
The odds of a new mutation causing blue eyes is very unlikely, especially if two siblings in the family have blue eyes. Literally a 1 in a million chance!
The most likely genetic explanation for your friend is that her father is a carrier for blue eyes and blonde hair. Let’s unpack what it means to be a genetic carrier.
Everyone has two copies of each gene, one from their mom and one from their dad. Each gene can come in slightly different versions, called alleles. So for example, a gene that affects eye color could come in two versions: a blue eye allele, and a brown eye allele.
For most pigmentation genes, the allele for darker colors is stronger, or dominant. You only need to inherit one brown eye allele to see the color.
The allele for lighter colors (like blue eyes!) is weaker, or recessive. You won’t see these light colors unless you inherit two copies of the allele.
So someone with one brown allele and one blue allele would have brown eyes. Even though they have the DNA for blue, it’s hidden. Someone like this is called a carrier, because they invisibly carry the DNA for blue eyes.
A recessive gene can hide in a family, and take a few generations to reappear. But if two carriers for blue eyes have a child, they can have a blue eyed child!
And the chances of a blue eyed child are even higher if one of the parents has that recessive trait.
Some traits are inextricably tied to your ancestry. Certain ethnicities share some traits more frequently than other groups.
Traits like blonde hair and blue eyes occur most often in European countries -- especially Northern Europe 2,3 . Traits like straight black hair occur most often in Indigenous American and East Asian people 4 . Lactose tolerance is commonly associated with Europeans, Central Asians, and some African groups 5 .
That means knowing your ancestry can reveal information about your genetics.
The likelihood of your friend’s father being a carrier for blonde hair and blue eyes from Caucasian ancestry is actually quite high.
In fact, many African Americans have European ancestry, on average between 20 and 25%. 6
For many people, learning their ancestry may come as a shock. Learning information that calls into question your identity can feel overwhelming and disorienting. Our genes don’t just tell us about ourselves now, but also give us a window into the past.
Sometimes that past is a painful history--a memento of slavery, bondage by another nation. With the stupendous rise of at-home genetic testing, many people around the nation are now facing their identities in a very new way, in light of our “hidden” genetic information.
- for infants and children that are diagnosed with the condition. Evidence suggests that children with 47 XXX syndrome are very responsive to early intervention services and treatment. These services may include speech, occupational, physical or developmental therapy, starting in the early months of life or as soon as needs are identified.
- Periodic screenings throughout childhood: Specific recommendations include developmental assessment by 4 months of age to evaluate muscle tone and strength language and speech assessment by 12 months of age pre-reading assessment during preschool years and an assessment of additional learning disabilities as well as social and emotional problems.
- Educational assistance. Receiving educational help to learn techniques and strategies to be successful in school and daily life.
- Supportive environment and counseling. Girls with triple X syndrome may be more prone to anxiety, as well as behavior and emotional problems. It is important to have a supportive environment and psychological counseling which may help teaching the family how to demonstrate love and encouragement, and discourage behaviors that might negatively impact learning and social functioning.
- Assistance and support in daily functioning. If there is developmental delays, this assistance and support may include help with activities of daily living, social opportunities and employment.
Related diseases are conditions that have similar signs and symptoms. A health care provider may consider these conditions in the table below when making a diagnosis. Please note that the table may not include all the possible conditions related to this disease.
There is no available objective laboratory test for VACTERL association. The diagnosis is based on having at least three of the following features (which make up the acronym VACTERL):  
(V) Vertebral defects, commonly accompanied by rib anomalies
(R) Renal (kidney) anomalies including renal agenesis, horseshoe kidney, and cystic and/or dysplastic kidneys
Because these malformations were observed to occur together more often than would be expected by chance alone (but for which no specific cause has been determined), the condition was termed an association. The diagnosis is a diagnosis of exclusion, which means that other conditions need to be ruled out before making a diagnosis of VACTERL. 
Evidence of New Genetic Information?
Can duplication and mutations cause new information to “arise” in the genome? Dr. Georgia Purdom accepts this challenge posted to creationists.
New information can arise in genomes by duplication and mutation. The myosins, the opsin family and the voltage-gated K+ channel family come to mind as examples. The globin gene clusters are great examples. The beta globin gene resembles those of other globins, suggesting that they are derived from the beta gene. Phylogenies do a good job of telling us when and how the genes evolved. There are pseudogenes found in these clusters that closely resemble the functional genes, suggesting that duplication events occurred. Misalignment during recombination, causing gene duplication, followed by point mutations explains this. Usefulness is the key. This is conceivable assuming the species can afford the selective cost. I could not find anything on your site that could adequately explain why new information can’t spontaneously arise. A thorough mathematical treatment akin to Gibbs free energy equations is needed, but does one exist? Is this another creationist bluff? I’ll call. En Garde!
—D. S., US
As has been said many times on this site, duplications (see “Yeast Fails to Rise to Evolutionists’ Expectations” [PDF]) and mutations do not add new information to the genome. Duplications are the result of duplicating existing genetic information, and mutations alter existing genetic information (whether original or duplicated). Neither of them adds new information.
Think about it this way: if I give someone a copy of a book they already own, then they don’t have any new information, just a copy of information they already had. If I subsequently take a marker and mark out some of the letters or words in the copy of the book I gave them, they still don’t have any new information—just a messed up copy of one of the books.
Rejoicing in Heaven
I wanted to write and thank you so much for the ministry of AIG. My husband was not a Christian, and I prayed for his salvation for over 8 years. He decided one day he would prove me wrong and was going to read the Bible to show me there was no way it could be true. He found your book The Answers Book, and it changed his life. He admitted the Bible was true, became a Christian, and was baptised two years later. But the story doesn’t end there. His sister was visiting once and asked him a few questions, so out came your book she took it home with her, and she too was saved and was baptised last summer. I thank God for your ministry! Thank you !!
Preaching the Word
On Jan. 15th, 2008, I went to Cole Harbour High School. Over 120 teens came at lunch to here me preach a creation message! Most of whom were dead set against God. I’m a youth pastor who started a Christian group in the school with some of my youth that go there. We approached the leadership of the school to make our proposal, and to our surprise, they gave permission: “We need all the help we can get,” they said (Why Won’t They Listen? by Ken Ham describes it well here). After my presentation, I was not even challenged they then just attacked God ’s character, which I was able to defend flawlessly—thanks to AIG! I was also able to share the gospel, too—all in one lunch! It was awesome! 40 of them came back after school to ask more questions because they were cut to the heart! I go every Tuesday to this school of 1100. We are doing 2 more local high schools soon. Thanks for all your hard work that makes this possible.
Have Something to Add?
That is not to say that sometimes mutations can’t have beneficial outcomes, such as antibiotic resistance in bacteria, but this is not an example of new information being added. Mutations alter a current functional system (i.e., nutrient transport) in the bacteria that is the target of the antibiotic such that the bacteria are no longer affected by the antibiotic. It has come at the cost of that functional system performing its original function inefficiently or not at all. To get from bacteria to man, there must be a mechanism to add genetic information such as genes to make arms, legs, and brains. Thus, in reality “tweaking” the genome of a bacterium through duplication and mutation will not result in a human genome.
It must be assumed that duplications and mutations lead to new information/genes in order to state that the beta globin gene cluster is the evidence of multiple duplication events followed by mutations resulting in the different globin genes. It cannot be evidence for evolution if evolution must be assumed prior to examining the evidence. This is an example of circular reasoning.
The human beta globin gene cluster consists of five genes including beta, delta, gamma (G and A), and epsilon. All of the globin proteins have similar—but different—functions and are expressed differentially throughout embryonic development to adulthood. Their spatial arrangement on human chromosome 11 is essential to their proper expression. If the genes are rearranged, they are not expressed at the proper times. How would an organism have survived embryonic development while waiting for the proper duplication and mutation events to occur? Instead the human beta globin cluster is highly organized and well designed.
Again, phylogenies invoke a form of circular reasoning. Phylogenies cannot be used as evidence for evolution when evolution must be assumed in order to design the phylogeny. It is not surprising that many organisms from insects to worms to fish to humans carry similar globin genes. The globin proteins are necessary for carrying and transporting oxygen, which is needed by almost all eukaryotic life for making energy (also using similar processes).
It is a form of prejudicial conjecture to say that an insect or fish is more “primitive” and therefore their globin proteins are more primitive than the human globin proteins (while it may be a conclusion drawn from an evolutionary worldview, there is no concrete evidence to support it). That is equivalent to saying that a bicycle is an inferior form of transportation and a car is a superior form of transportation. It really depends on the situation as to whether the bicycle or car is a better choice for getting around. When I traveled in China, the streets were so crowded that bicycles were clearly the superior form of transportation! The globin proteins were designed specifically for each organism to carry out the demand for oxygen.
Again it is a form of prejudicial conjecture to suggest that pseudogenes are non-functional leftovers from past duplication events. The function/non-function of pseudogenes has been hotly debated for years. Several studies have shown that some pseudogenes are, in fact, functional. The ENCODE Project has revealed that much of the human “junk” DNA (pseudogenes fall into this category) may have a function, especially in the area of regulation. Regulation of gene expression is especially important to prevent cancer and other diseases. The psi beta pseudogene in the human beta globin gene cluster has been suggested to play a regulatory role in the expression of the other globin genes in that cluster. Another possibility is that some pseudogenes are the result of genes originally designed by God to have a function but as a result of mutation after the Fall are no longer performing this function.
I agree that usefulness would be key to selecting for duplication/mutation events however, most mutations do not produce useful outcomes, and duplications/mutations have never been observed to add new information. Natural selection merely selects from existing genetic information.
I also agree that the species must be able to afford the selective cost unfortunately, most species cannot. Bacterial populations reproduce much faster and produce more offspring than humans. This rapid generation time and large population size mean that bacteria can afford the “cost” of selection. When a bacterial population faces adverse environmental conditions, 99.999% of the cells may fail to adapt (through mutation or other genetic alterations) and subsequently die. However, the small percentage that do survive are sufficient for the population to survive. It can rapidly replenish the population back to the original population size.
Humans have much longer generation times and much fewer offspring than bacteria. The “cost” of selection becomes more than the population can pay. Fish-to-fishermen evolution becomes impossible, as the selective cost is too high for most organisms.
Throughout this feedback I have referenced numerous articles available on our website and others relating to this issue. I would also recommend Genetic Entropy and The Mystery of the Genome by Dr. John Sanford, In the Beginning Was Information by Dr. Werner Gitt and The Biotic Message by Walter ReMine for more in-depth information (including mathematical treatments) on this topic. I would like to call the evolutionists’ bluff and ask for an adequate explanation—with evidence—as to how new information can spontaneously arise. En garde!
Ultimately the burden of proof lies with those who believe that duplications and mutations can lead from fish to fishermen, not with those who don’t (even though we have spent and continue to spend considerable research showing that this is not possible). However, it’s important to remember that we are both looking at the same evidence. The central issue is what our starting point is when looking at the evidence belief in the constantly changing ideas of man or belief in the unchanging Word of God .
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These resources provide more information about this condition or associated symptoms. The in-depth resources contain medical and scientific language that may be hard to understand. You may want to review these resources with a medical professional.
Where to Start
- Genetics Home Reference (GHR) contains information on Tetrasomy X. This website is maintained by the National Library of Medicine.
- Unique is a source of information and support to families and individuals affected by rare chromosome disorders. Click on the link to view information about tetrasomy X.
- The Monarch Initiative brings together data about this condition from humans and other species to help physicians and biomedical researchers. Monarch’s tools are designed to make it easier to compare the signs and symptoms (phenotypes) of different diseases and discover common features. This initiative is a collaboration between several academic institutions across the world and is funded by the National Institutes of Health. Visit the website to explore the biology of this condition.
- Orphanet is a European reference portal for information on rare diseases and orphan drugs. Access to this database is free of charge.
- PubMed is a searchable database of medical literature and lists journal articles that discuss Tetrasomy X. Click on the link to view a sample search on this topic.