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My argument here is that mutations are not a viable cause.
There is an arctic cod that developed an antifreeze gene, a protein coding gene that was developed at least 4 times.
It's composed of simple repeats and is different in at least four populations of arctic cods and exists in none of the warm water cods. On the other hand Polar Bears and Grizzles can still interbreed, that's a pretty strong indicator they have a close common ancestor.
I'm saying mutations are not an explanation at all. What you are looking for is the molecular mechanism capable of producing these adaptive traits and if you simply assume genetic mutations your going down a blind alley in the dark with a stranger, your going to get mugged.
You are wrong Mark, handful of cherry picked deleterious mutations notwithstanding.
For a really cool example of rapid mutation based (though in this case it's a transposon rather than substitution) gain of function, have a look at DDT resistance in fruit flies, or indeed the genetics of pesticide resistance in general.
If differences in the DNA sequence of species' genomes is not a viable explanation for why there are physical differences between the species, then what in the world causes them to have physical differences?
So other than your disbelief,what is the argument?
What do you mean "was developed" 4 times?
OK, I believe that there would be sufficient genetic data available to at least do a rudimentary analysis on grizzly and polar bear genomes.
I can guide you through the process.
Yes, you keep saying this, and when asked for explanations, you make a new analogy or use a different phrase and say the same thing.
Mutations in the PAH gene cause phenylketonuria. The PAH gene provides instructions for making an enzyme called phenylalanine hydroxylase. This enzyme converts the amino acid phenylalanine to other important compounds in the body. If gene mutations reduce the activity of phenylalanine hydroxylase, phenylalanine from the diet is not processed effectively. As a result, this amino acid can build up to toxic levels in the blood and other tissues. Because nerve cells in the brain are particularly sensitive to phenylalanine levels, excessive amounts of this substance can cause brain damage. (Phenylketonuria, National Library of Medicine)
Very few mutations are significant on an evolutionary scale:
Among the mutations that affect a typical gene, different kinds produce different impacts. A very few are at least momentarily adaptive on an evolutionary scale. Many are deleterious. (Rates of Spontaneous Mutations)
They don't exclusively. There's a mutation that causes a person to require less sleep to be well rested, I mentioned that to you before. It impacts REM sleep in the brain, and has no negative effects, just the positive of gaining an extra hour or two to work with during the day.The point is that mutations in brain related genes cause disease and disorder, not adaptive evolution.
Yup, a metabolic disorder, regardless of what tissue is most heavily impacted.Mutations in the HEXA gene cause Tay-Sachs disease. The HEXA gene provides instructions for making part of an enzyme called beta-hexosaminidase A, which plays a critical role in the brain and spinal cord. This enzyme is located in lysosomes, which are structures in cells that break down toxic substances and act as recycling centers. Within lysosomes, beta-hexosaminidase A helps break down a fatty substance called GM2 ganglioside. (Tay-Sachs disease, National Library of Medicine)
Another metabolism one, what would your point be even if these were good examples of disorders of the brain caused by mutations in brain function/formation genes? Seriously, ever heard of schizophrenia? That one's caused by the brain itself malfunctioning. It doesn't matter how many disorders you name, as it is very easy to demonstrate that mutations on brain pertinent genes are not exclusively detrimental. It wouldn't matter if only 0.0005% of them weren't detrimental, your assertion that they are exclusively so would still be wrong, and that still would leave benign mutations for evolution to be influenced by.Wilson disease is caused by mutations in the ATP7B gene. This gene provides instructions for making a protein called copper-transporting ATPase 2, which plays a role in the transport of copper from the liver to other parts of the body. Copper is necessary for many cellular functions, but it is toxic when present in excessive amounts. The copper-transporting ATPase 2 protein is particularly important for the elimination of excess copper from the body. Mutations in the ATP7B gene prevent the transport protein from functioning properly. With a shortage of functional protein, excess copper is not removed from the body. As a result, copper accumulates to toxic levels that can damage tissues and organs, particularly the liver and brain. (Wilson disease, National Library of Medicine)
Are you dead? Am I dead? No, but we both have mutations on brain related genes that not everyone has.The issue is the adaptive evolution of brain related genes and mutations are the worst cause imaginable. Whether or not they directly effect reproduction is irrelevant to the fact that mutations in brain related genes result in disease, disorder and death.
-_- 60 genes in 12 million years, oh boy, what a problem (sarcasm). With 40-60 new mutations per person born, that's nothing.It matters if you are arguing that the three fold expansion of the human brain from that of apes is the result of mutations. It's also even more significant when you realize there are no less then 60 de novo genes that would have had to be built from the ground up.
That's not how a genetic mutation is defined:
In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair. (Kimbal Biology Pages, Mutations)
Genetic mutation is the reason variation exists. If not for mutation, populations would just continuously have less and less variety until everyone was as genetically similar as siblings, due to the fact that death before reproduction reduces variation within a population.Your problem is you want to equivocate a genetic mutation with any variation whatsoever.
-_- how would it make the gene pools larger without mutation to increase the variety of genes?When a population begins to dwindle in numbers because they are hunted to near extinction a bottle neck happens and the gene pool shrinks. When there is a large gene pool there is more possibilities for adaptive traits. Assuming accelerated adaptive evolution following the Flood it only makes sense that there would be much larger gene pools.
Define "adaptive evolution" and how you think it works without the influence of mutation.Over time as adaptive evolution takes hold the gene pools shrinks to maintain adaptive traits. The GULO gene is supposed to produce vitamin C but our GULO gene is broken so we have to get vitamin C from our food.
I don't understand this "fixed" assertion you have. Also, detrimental genes can influence adaptation as well. Do you honestly think male peacocks benefit from having such large tails when it comes to survival? Nope, but the peahens sure love 'em.In order for a brain related gene to adapt on an evolutionary scale it must be changed with beneficial effect and be inheritable, then fixed.
-_- do you think the default human state is "genius" and that any other level of intelligence is the result of mutation?The only brain related gene variation you will find resulting in an effect strong enough for selection to act will be disease, disorder and death. That's not a formula for adaptive evolution, it's a formula for extinction.
I've told you about the gene that reduces time needed to sleep multiple times. Why are you ignoring that?You would find mutations in brain related genes result in deleterious effects, with no exceptions that I'm aware of.
Thanks for making a quote that demonstrates my point that PKU isn't caused by a mutation in a brain formation or function gene.
-_- why would deleterious genes not be of evolutionary significance? They can eliminate entire lineages, of course they matter. The ones that don't significantly impact survival and reproduction chance are the ones that are irrelevant to evolution.
Additionally, it wouldn't matter even if only 1% of genes impacted function for better or worse; the shear number of mutations and generations of organisms would still allow evolution to occur.
They don't exclusively. There's a mutation that causes a person to require less sleep to be well rested, I mentioned that to you before. It impacts REM sleep in the brain, and has no negative effects, just the positive of gaining an extra hour or two to work with during the day.
Most of the variation in human intelligence is attributable to genetic variety. You cannot ignore that no two minds are alike, yet less than 30% of the human population exhibits any brain related disorders.
Yup, a metabolic disorder, regardless of what tissue is most heavily impacted.
Another metabolism one, what would your point be even if these were good examples of disorders of the brain caused by mutations in brain function/formation genes? Seriously, ever heard of schizophrenia? That one's caused by the brain itself malfunctioning. It doesn't matter how many disorders you name, as it is very easy to demonstrate that mutations on brain pertinent genes are not exclusively detrimental. It wouldn't matter if only 0.0005% of them weren't detrimental, your assertion that they are exclusively so would still be wrong, and that still would leave benign mutations for evolution to be influenced by.
Are you dead? Am I dead? No, but we both have mutations on brain related genes that not everyone has.
-_- 60 genes in 12 million years, oh boy, what a problem (sarcasm). With 40-60 new mutations per person born, that's nothing.
I never said mutations weren't the result of mistakes in DNA repair. Why would them being mistakes make them any less responsible for the variation in intelligence between people? Roughly 5% of mutations are benign. About 30% are detrimental, and the rest are neutral. With every person having at least 40 mutations from the day they are born, that means each person born has around 2 benign mutations, 12 detrimental mutations, and 26 neutral mutations. Anyone that manages to survive to reproduce doesn't have bad enough detrimental mutations to weed them out of the population, and they have the chance to pass down their 2 benign ones.
I think your problem is, you see that the number of detrimental mutations outnumbers benign mutations, and think "oh gosh, how could anything work with such a buildup of bad compared to the good"? -_- you forgot about recessive and dominant genes. Pretty much everyone is a carrier for 3-4 detrimental mutations that would result in death... if they had 2 copies of them. Hence, the risk of having children with people related to you; they're more likely to share some of those mutations and then you end up with sick kids.
The redundancy of genes helps ease the burden of detrimental genes as well. Who cares if one copy of an important protein producing gene is rendered useless when your DNA contains 5 more functioning copies of it?
By the way, with about 7 billion people on this planet, just with the people alive today, there are at least 14 billion benign mutations within our current population.
Genetic mutation is the reason variation exists. If not for mutation, populations would just continuously have less and less variety until everyone was as genetically similar as siblings, due to the fact that death before reproduction reduces variation within a population.
-_- how would it make the gene pools larger without mutation to increase the variety of genes?
Define "adaptive evolution" and how you think it works without the influence of mutation.
I don't understand this "fixed" assertion you have. Also, detrimental genes can influence adaptation as well. Do you honestly think male peacocks benefit from having such large tails when it comes to survival? Nope, but the peahens sure love 'em.
Of course not.-_- do you think the default human state is "genius" and that any other level of intelligence is the result of mutation?
Close enough to fool the educated; far enough that the faithful know better.Chimps and humans: How similar are we really?
You would find mutations in brain related genes result in deleterious effects, with no exceptions that I'm aware of.
Ever heard of the CRISPR gene?
Those are not the result of random mutations, there are molecular mechanisms that adapt the immune system.
There are a lot more housekeeping and repair mechanisms then those responsible for adaptive traits.
One thing is sure, mutations are not the explanation for the giant leap in brain development since the split.
For the record, here's a list of the 829 non deleterious mutations in HAR1A
har1A[Gene Name] - SNP - NCBI
Most of those occur around the gene, but 16 of them are inside it (and it's only 118bp long)
https://genome-asia.ucsc.edu/cgi-bin/hgTracks?db=hg38&lastVirtModeType=default&lastVirtModeExtraState=&virtModeType=default&virtMode=0&nonVirtPosition=&position=chr20:63102142-63102259&hgsid=471889634_umNSpGQfMtpZBCmXQM7M355fEiGU
The truth is that this gene is found in almost all mammals.
The difference between chimps and any other mammal except humans boils down to only 1 or 2 base pairs
(which they attribute to mutation.
but actually cannot show, nor have ever show
Now in truth, the human HAR1 demonstrates a difference with Chimps of 18 base pairs (and this is a gene so this makes it very different in form and function).
because the Chimps have one form of the gene and Humans have another they count this as a similarity when doing their tallying (to persuade you).
But in reality (not hypothesis driven) this 18 base pair difference is quite significant! (but shhh! you're not supposed to think about the actual data)
It's not what I believe or what I don't believe, it's what the researchers are telling us.
Different AFPs likely arose as relatively recent adaptations to cooling during freezing of the Antarctic or Arctic Oceans. There are now known at least four types of fish AFPs, all apparently unrelated to each other (AFPs types I, II, III, and AFGPs; refs. 5 and 6). If each type arose only once, one would expect each to be characteristic of a single monophyletic group of fish. This has clearly turned out not to be the case for AFPs type II, as they have been found in three phylogenetically disparate fish species, Atlantic herring (Order Clupeiformes), smelt (Order Salmoniformes), and sea raven (Order Scorpaenoformes): the genes have evolved at least three times...
...AFGPs could also have evolved more than once, since they are found in both Antarctic notothenioids (Order Perciformes) and Arctic cod (Order Gadiformes). (Origin of antifreeze protein genes: A cool tale in molecular evolution. PNAS)
That's at least 4 times by my count.
Then it should be an easy task to find homologous regions in a few species and do a simple identity analysis.Of course there are:
![]()
Fig. 1. The number of alleles unique to and shared by three bear species—polar, brown, and American black bear—in all SNP loci (A), and high-quality polymorphic variants resulting in an SAP (B). (Polar and brown bear genomes reveal ancient admixture and demographic footprints of past climate change. PNAS)
Always happy to learn something.
Because the arguments don't need a lot of update or revision.
My argument here is that mutations are not a viable cause. There is an arctic cod that developed an antifreeze gene, a protein coding gene that was developed at least 4 times. It's composed of simple repeats and is different in at least four populations of arctic cods and exists in none of the warm water cods. On the other hand Polar Bears and Grizzles can still interbreed, that's a pretty strong indicator they have a close common ancestor.
I'm saying mutations are not an explanation at all. What you are looking for is the molecular mechanism capable of producing these adaptive traits and if you simply assume genetic mutations your going down a blind alley in the dark with a stranger, your going to get mugged.
We are talking about those mutations that do have an effect and they are always deleterious.
YET...because the Chimps have one form of the gene and Humans have another they count this as a similarity when doing their tallying (to persuade you).
You forgot chickens.
Right.
Who is this "they" to whom you refer? It should be clear by now that I am a biological scientist. Please do me the decency of referring directly to me.
I am not going to address you lack of understanding of phylogenetic and genetic inference on a board like this. Suffice to say, you are completely and utterly wrong.
Really? Have you had an actual look at the folds this ncRNA takes? Have you compared them in different species? Can you even tell me what it's function is in any creature?
Yeah, didn't think so.
Once again, biological scientist here, 30 years experience, 100 published papers.
Of course it's significant. The fact you think we claim the opposite speaks volumes to your knowledge.
The region is 118 bps long. Which means that human/chimp are IDENTICAL in 100 bps, or are 85% identical. Nothing to see here! Ignore the 85% similarity, focus SOLELY on the 15% difference!
'Doing their tally to try to convince you' - ah, I guess you mean when performing phylogenetic analyses? The analyses that you have, due to you unfamiliarity with how they actually work, dismissed?
Shhhh!! Don't even mention the positive, ONLY point out the negative, no matter its relevance!