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Chimps and humans: How similar are we really?

tas8831

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My argument here is that mutations are not a viable cause.

So other than your disbelief,what is the argument?
There is an arctic cod that developed an antifreeze gene, a protein coding gene that was developed at least 4 times.

What do you mean "was developed" 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.

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.

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.

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.
 
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mark kennedy

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You are wrong Mark, handful of cherry picked deleterious mutations notwithstanding.

You would find mutations in brain related genes result in deleterious effects, with no exceptions that I'm aware of.

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.

Ever heard of the CRISPR gene?

CRISPR is actually an ancient bacterial defense system. It's like an immune system for bacteria, which is surprising because for a long time, scientists didn't think bacteria had adaptive immune systems. But in 1987, some Japanese scientists were looking for something in DNA, and they saw this weird group of nucleotides, pieces of DNA. They had no idea what they were doing and what they meant and what their function was. And in a piece they published in The Journal of Bacteriology, the last sentence literally was, and we saw this weird, crazy group of nucleotides, and we have no idea what they're doing there. And that was that. And that was not for a very long time. (New Gene-Editing Techniques Hold the Promise Of Altering The Fundamentals Of Life, NPR)
Those are not the result of random mutations, there are molecular mechanisms that adapt the immune system. There are also DNA repair mechanisms:

230px-DNA_Repair.jpg
DNA ligase, repairing a Chromosome (DNA Repair)

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.

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?

The genetic differences in brain related genes is a long list, these are just the most dramatic:
  • HAR1F: Vital regulatory gene involved in brain development, 300 million years it has only 2 subsitutions, then 2 million years ago it allows 18, no explanation how.
  • SRGAP2: One single amino-acid change between human and mouse and no changes among nonhuman primates. accumulated as many as seven amino-acid replacements compared to one synonymous change. 6 known alleles, all resulting in sever neural disorder.
  • 60 de novo (brand new) brain related genes with no known molecular mechanism to produce them.
 
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mark kennedy

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So other than your disbelief,what is the argument?

It's not what I believe or what I don't believe, it's what the researchers are telling us.

What do you mean "was developed" 4 times?

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.
OK, I believe that there would be sufficient genetic data available to at least do a rudimentary analysis on grizzly and polar bear genomes.

Of course there are:

F1.medium.gif

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)​

I can guide you through the process.

Always happy to learn something.

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.

Because the arguments don't need a lot of update or revision.
 
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PsychoSarah

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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)​
Thanks for making a quote that demonstrates my point that PKU isn't caused by a mutation in a brain formation or function gene.


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)​

-_- 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.
The point is that mutations in brain related genes cause disease and disorder, not adaptive evolution.
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.


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)
Yup, a metabolic disorder, regardless of what tissue is most heavily impacted.​



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)
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.​



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.
Are you dead? Am I dead? No, but we both have mutations on brain related genes that not everyone has.


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.
-_- 60 genes in 12 million years, oh boy, what a problem (sarcasm). With 40-60 new mutations per person born, that's nothing.


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)​

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.​



Your problem is you want to equivocate a genetic mutation with any variation whatsoever.
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.

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.
-_- how would it make the gene pools larger without mutation to increase the variety of genes?

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.
Define "adaptive evolution" and how you think it works without the influence of mutation.

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.
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.


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.
-_- do you think the default human state is "genius" and that any other level of intelligence is the result of mutation?
 
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PsychoSarah

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You would find mutations in brain related genes result in deleterious effects, with no exceptions that I'm aware of.
I've told you about the gene that reduces time needed to sleep multiple times. Why are you ignoring that?


 
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mark kennedy

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Thanks for making a quote that demonstrates my point that PKU isn't caused by a mutation in a brain formation or function gene.

I said it was brain related:

Phenylketonuria (PKU) can be defined as a rare metabolic disorder caused by a deficiency in the production of the hepatic (liver) enzyme phenylalanine hydroxylase (PAH). PKU is the most serious form of a class of diseases referred to as "hyperphenylalaninemia," all of which involve above normal (elevated) levels of phenylalanine in the blood. The primary symptom of untreated PKU, mental retardation, (phenylketonuria, TFD Medical Dictionary)
-_- 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.

Yet mutations result in disease and disorder in the human brain, certainly mental retardation is a deleterious effect.
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.

We are talking about those mutations that do have an effect and they are always deleterious.

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.

There you go again, attributing genetic variation to mutations.

That's not a viable cause for the nearly three fold expansion of the human brain, it's not even anecdotal.

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.​

It's caused by genetic mutations:

The study was the largest ever of its kind and is currently published in the online journal Neuron. To investigate, the team of researchers compared the genetic data of 11,355 patients with schizophrenia against a control group of 16,416 people without the condition.

In comparing the DNA of the two groups, the researchers found that the schizophrenia patients had CNVs that were not present in the individuals without the condition. According to the press release, CNVs are mutations in which large stretches of DNA are either deleted or duplicated. In the schizophrenic patients, the mutations tended to disrupt genes involved in specific aspects of brain function. A healthy brain works thanks to a precise chemical balance between signals which both excite and inhibit nerve cell activity. The combination of mutations found in the schizophrenia patients disrupted this natural balance. (Schizophrenia's Causes Revealed With 'Strongest Evidence Yet' Of Chemistry-Altering Mutations, Medical Daily)​

Are you dead? Am I dead? No, but we both have mutations on brain related genes that not everyone has.

But we are not a part of adaptive evolution because of it, we are just lucky there are no deleterious effects. They simply have no effect.

-_- 60 genes in 12 million years, oh boy, what a problem (sarcasm). With 40-60 new mutations per person born, that's nothing.

They wouldn't have existed until 2 million years ago when the meteoric rise of the human brain began. You don't have twelve million years to play with, you have a brief window 2 million years ago for them to be built from the ground up and fixed. They exist in none of our taxonomic cousins including the Chimpanzees, you have 5 mya at best.

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.​

We are talking about the effect of mutations on brain related genes.

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.

That variation, those CVNs related to Schizophrenia, are the core evidence against mutations being a driving force of the evolution of the human brain from apes as the result of mutations.

-_- how would it make the gene pools larger without mutation to increase the variety of genes?

Gene editing molecular mechanisms like CRISPR.
Define "adaptive evolution" and how you think it works without the influence of mutation.

It's not related to mutations, that's the point.

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.

Brain related genes permanently fixed in the human genome. That's why we all have the same ones.

-_- do you think the default human state is "genius" and that any other level of intelligence is the result of mutation?
Of course not.
 
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Tanj

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You would find mutations in brain related genes result in deleterious effects, with no exceptions that I'm aware of.

That you are aware of being the key phrase. Now I guess I could hunt down a list of brain specific transcripts, then map them to dbSNP, and provide you will a list that probably runs to the millions of mutations with no deleterious effects, but that's a lot of work. The fact you are not aware of their existence doens't mean they are not there.

Ever heard of the CRISPR gene?

Heard of it, worked with it.

Those are not the result of random mutations, there are molecular mechanisms that adapt the immune system.

They are, however random insertions. The fact they are site specific makes them no less random.

As for DNA repair, if the break occurs across a heterozygous SNP, then the homologous repair will result in homozygosity. And in case that's too technical, what I am saying is that the DNA repair system is one way that mutations can enter the genome.

There are a lot more housekeeping and repair mechanisms then those responsible for adaptive traits.

So what? that is irrelevant to the discussion.

One thing is sure, mutations are not the explanation for the giant leap in brain development since the split.

Constantly repeating your unevidenced assertion doesn't make it any more true Mark. And by the way, all of the evidence you posted at the bottom of your post which I haven't quoted, are only true if evolution is true. All of that work involved multi species comparative genomics which has evolution=true as an assumption.

You disbelieve in evolution and then provide evidence that requires evolution to be true.
 
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Tanj

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pshun2404

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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, it was once something other which later became this. Thus "mutation" as used in this sense is a weasel word. There is no evidence it was or is mutated unless one defaults to an "ancestor of the gaps" argument. Nothing evidences that the additional base pairs once were not there, and now are in these respective creatures.

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). 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).

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)
 
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Tanj

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The truth is that this gene is found in almost all mammals.

You forgot chickens.

The difference between chimps and any other mammal except humans boils down to only 1 or 2 base pairs

Right.

(which they attribute to mutation.

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.

but actually cannot show, nor have ever show

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.

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).

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.

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).

Once again, biological scientist here, 30 years experience, 100 published papers.

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)

Of course it's significant. The fact you think we claim the opposite speaks volumes to your knowledge.
 
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tas8831

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It's not what I believe or what I don't believe, it's what the researchers are telling us.

Which researchers are telling us that the 3-fold increase in brain volume cannot be due to mutation?
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.

Just wante to double-check. Of note, you ellipsed out:

"...it is not surprising that these genes have apparently arisen by straightforward duplication and divergence..."

Of course there are:

F1.medium.gif

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.
Then it should be an easy task to find homologous regions in a few species and do a simple identity analysis.

I suggest downloading the free program package "Bioedit".

Genome information here:

https://www.ncbi.nlm.nih.gov/genome/browse/?report=5

Because the arguments don't need a lot of update or revision.

So say you.
 
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tas8831

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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.

Not sure what the relevance of those tidbits of information are. Who said that bears do NOT share a recent 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.

Yes, you are saying this. So what?

Other than paraphrasing some interesting (though irrelevant) soundbites and asserting "it ain't mutations!!!", what evidence is there to support your position? If it is not mutations, what is it?

Of note, Bruce Lahn, whom you have cited many times, no longer even does research on HAR genes. Guess it wasn't quite the profound evolution-busting stuff it was made out to be.
 
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tas8831

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We are talking about those mutations that do have an effect and they are always deleterious.

Mental retardation is an 'observable', detrimental' phenotype. This makes it worthy of investigation, and numerous causes of the same general outcome are known, from, sure, mutations, to nutritional status of the mother, etc.

There is a process for locating genes associated with detrimental phenotypes. But who is looking for beneficial phenotypes, and how would they know when to look?

IOW, we can "see" mental retardation and then look for its cause, but what do we "see" when the effect is beneficial?

So your quoted statement is, in essence, a no-brainer. we "see" the detrimental phenotype, and if its cause can be traced, when it is genetic, it is obviously due to detrimental mutations (of some sort).

Extrapolating this to more general population genetics - it is "easier" to select against a less fit individual than it is to select for a more fit individual (granting that there are exceptions).

But as your position appears to be 'all mutations are bad', please tell us which labs are looking for beneficial mutations, and what they would look for.*


*I actually know, but lets play the game...
 
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tas8831

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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).

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!
 
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pshun2404

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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.


(which they attribute to mutation.)

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.

The “they” refers, in general, to the group on forum’s like these that attribute these differences to mutations who are incapable of conceiving the possibility they just may be the consistent and unchanging structure which makes one creature what it is and another what it is (as opposed to one earlier creature transforming into another). They have no demonstrable proof these are all in fact mutations.


but actually cannot show, nor have ever shown

I am not going to address your lack of understanding of phylogenetic and genetic inference on a board like this. Suffice to say, you are completely and utterly wrong.

Sadly you, mistake my disagreement with some interpretations and explanations of these things with a lack of understanding. Just because I do not agree with everything someone or a whole crowd claims is inferred (even if there is no alternative explanations allowed) does not equal my not understanding what that inference or explanation is. So no...I am not “completely and utterly wrong.”

What they cannot show nor have ever shown is that these differences ARE mutations from some un-mutated earlier versions. And yes this may not be the appropriate place or time to explore this but feel free to open a thread (or perhaps I should) where we can discuss some of these opinions.



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).

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.



I have read articles that describe this area in different creatures but while we HAVE seen that “the protein-coding potential of the HAR1A RNA is poor or absent, but that it forms a stable RNA structure” (Pollard, K. S., Salama, S. R., Lambert, N., Lambot, M.-A., Coppens, S., Pedersen, J. S., Katzman, S., King, B., Onodera, C., Siepel, A., Kern, A. D., Dehay, C., Igel, H., Ares, M., Jr., Vanderhaeghen, P., Haussler, D. An RNA gene expressed during cortical development evolved rapidly in humans. Nature 443: 167-172, 2006. [PubMed: 16915236)), we cannot at this time say it has no “function” (though everyone is entitled to their OPINION). Function is not only coding for proteins they may serve to support that function in other surrounding genes. For example we know it has something to do with our having larger brains, and expresses rapidly at this early embryonic stage, but as the consortium of Encode biological scientists might define “function”, sometimes what once appeared (or appears) to be non-functional may have hitherto unseen relationships to why or how another gene DOES function (as one example).



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)

Of course it's significant. The fact you think we claim the opposite speaks volumes to your knowledge.

Of course any biological scientist, like yourself, would agree this constitutes a difference! The point of the OP was not to say you individually claim this or that difference is not different between these two creatures but that we (Joe Public and students) should not be fooled into think the similarities are the final word! This thread was to point out and discuss the DIFFERENCES which are WAY MORE than a mere 1.8%. That statistic only represents interpretive opinion regarding a very small selected area of the genome (which many a biological scientist say is more likely 4 or 5%).

For example when we see the effect a change in one or two base pairs can have in a given gene (such as in sickle cell or cystic fibrosis), and in this case we are talking about 120 million base pair differences (about 4%), to not make this equally important for Joe Public and students to consider is a travesty. IMO it is a lack of full honest disclosure in the study hall and popular media.

To over emphasize the statistically selected (so to support the hypothesis that was already accepted long before being demonstrated...see Huff’s How to lie with Statistics) and not at least equally emphasize the vast amount of differences (again for Joe Public and our students) is the use of persuasive rhetoric. Pardon me if I think it is done with intention but I do (and I am not saying individuals like yourself have such motive).

And I do not believe I am incorrect in this assessment of the popularized rhetoric:

"Honest critics of the evolutionary way of thinking who have emphasized problems with biologists' dogma and their undefinable terms are often dismissed as if they were Christian fundamentalist zealots or racial bigots. But the part of this book's thesis that insists such terminology interferes with real science requires an open and thoughtful debate about the reality of the claims made by zoocentric evolutionists." (Lynn Margulis and Dorion Sagan, Acquiring Genomes: A Theory of the Origins of the Species, (Basic Books, 2003)

"It is dangerous to raise attention to the fact that there is no satisfying explanation for macroevolution. One easily becomes a target of orthodox evolutionary biology and a false friend of proponents of non-scientific concepts. According to the former we already know all the relevant principles that explain the complexity and diversity of life on earth; for the latter science and research will never be able to provide a conclusive explanation, simply because complex life does not have a natural origin." (Günter Theiben, "The proper place of hopeful monsters in evolutionary biology," Theory in Biosciences, 124: 349-369 (2006)

"We've been told by more than one of our colleagues that, even if Darwin was substantially wrong to claim that natural selection is the mechanism of evolution, nonetheless we shouldn't say so. Not, anyhow, in public.

Neo-Darwinism is taken as axiomatic; it goes literally unquestioned. A view that looks to contradict it, either directly or by implication is ipso facto rejected, however plausible it may otherwise seem. Entire departments, journals and research centers now work on this principle." (Jerry Fodor and Massimo Piattelli-Palmarini, What Darwin Got Wrong (Farrar, Straus and Giroux, 2010)

And everyone of these people believe in ToE just not everything some evolutionists say these things mean. There are so many "biological scientists" that do not agree with every premise of the popularized ToE (some disagreeing or seeing alternate possibilities here or there) they cannot even be all mentioned in this forum (for example consider the work and reasoning of some of the Third Way evolutionists)
 
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pshun2404

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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!

No! Include and emphasize both...a 15% difference in sequence of an organized section can have any number of of effects (many possibly unknown)...and I am not saying they all are bad (I am not in that camp). Also even 85% similarity does not indicate one is mutation of the other and scientists know this so they conclude with an ancestor of the gaps argument that the mutation responsible for producing these two distinct outcomes occurred in a common ancestor (which the brainwashed automatically accept) but no one has been able to produce one example upon which to base this conclusion. Anyone can pick a proverbial rabbit out of the hat and choose a creature that does not have this variation from an earlier time and say this eventually BECAME these others but that is a blind leap of foundationaless faith in the preconceived conclusion.

To demonstrate such a mutation occurred one must show a before and after in the same line of organisms (the same problem exists for many alleged indels...no demonstrative cases if insertion or deletion just assumption to explain their distinct presence).
 
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