Humans DNA is 99% similar to that of chimps?

[rmwilliamsll]

but there are certain events that must have happened or the whole thing is a lie.


this great lumping of things together and making them all essential is not logical at all.

for instance, Adam's historicity has nothing to do with Job's.
David's has nothing logically to do with Jonah's. Why link them all together and make the whole thing so brittle to criticism?

Brittle is a gross mischaracterization, notice I didn't actually tell you what events were vital. Tell me something, apart from the ressurection what events described in the Bible do you think are vital? The miracles of the Exodus, the conquest of Canaan, the shikinah glory of God entering the Tabranacle? I mean seriously, when do we accept a miracle as an actual historical fact?

Answer any way you think is right.

Grace and peace,
Mark

My current research interests are grouped around the American religious scene from about 1880-1930 and concern the rise of the social gospel and the orthodox/progressive split.

One takehome message is that no one has actually been able to list the essential doctrines that are required to be a Christian. Not that there haven't been lots of attempts, just that little success emerges, and no real consensus.

This problem of listing the essential miracles, or necessary historical "facts" is very similiar and i'd expect will have the same outcome, lots of potential lists, very little consensus, and finally a tight grouping around different denominational standards.

But it you look at my reply to your statement, you will see that listing historical events essential to the faith is not my interest, my interest is in avoiding the logical error of composition.

I think brittle is exactly the word i want to use to describe what happens in dozens of online deconversion stories i've read. When you unify Scripture in such a way that requires an all or nothing mentality, either you are for us or against us, either it all is historical or it is false, you make the whole system as brittle as a pane of safety glass. You can't cut safety glass, but you can strike it harder than a regular window pane before it breaks, but when it does break it shatters into many smaller, kind of rounded pieces.

YECism and often fundamentalism with it's tight boundaries is like the safety glass, bears up better than others to blows but shatters at a certain point.

And one of the ideas that leads to this brittleness is the number of composition errors it proposes.
either the Bible is entirely true or Jesus is a liar.
either the Bible is historically true in all it's parts or it is entirely false.
either Gen is literal or it is figurative.
we see these kind of statements all the time here.

the first quote i replied to is in this form:
but there are certain events that must have happened or the whole thing is a lie.


What whole thing? Christianity? Fundamentalism? Credobaptism? the rapture?

outside of Jesus died and resurrected there is very little consensus in the greater church about what events, how to interpret the words "happened" or "historical" and what exactly is "the whole thing".

my interest is not to recapitulate a systematic theology and assign everything to one of two catagories: essential or not essential, but rather to point out that the basic logic of the statement is not clearly true, and that the parts of the statement are far more complex than people think.

 

[mark kennedy]

This is too broad a statement. Aside from the life, death, and resurrection of Christ, can you tell us what events must have occured literally else the entire body of scripture becomes a lie?

I am thinking here of redemptive history which is my primary concern. The Exodus with it's devastating judgments on Eqypt for instance are either history or they are fiction. The Bible does not give us a lot of room for speculation, it is explicit in it's description of God's work in history. Genesis speaks of major historical transitions and they are presented as narratives, not nebulous maxims and pithy generalities. The creation, the tower of Bable, the miracle of Issac's birth, the life of Jacob...etc. These all mark major events in God's work in redemptive history. There are others, Daniel in the Nebucannezer's court, Esther in the Persian court and there are many others.

My investigation of the Bible as history started and ultimatly ends with the Gospels and Acts. I don't think how you view Genesis one is going to make a big difference in how you respond to the promise of God in Christ. My biggest concern is that the focus of the Bible is redemptive history and we do well to look at it in that light.

That is where creationism is coming from and Christians should recognize a kindred spirit when faith in God's revelation takes preferance over secular sources. I don't think the TEs and YECs are that far apart if they can agree on certain central issues. The Bible as history in non-negotiable for me personally, that is not something I am prepared to compromise.

Grace and peace,
Mark

 

[sfs]

You do realize I'm sure most of these indels would do absolutly nothing.

Of course. That's why I continue to be baffled about your insistence that the indels present a problem for evolution, or why you keep bringing up the deleterious effects of some mutations.

When they have an effect is is most often deleterious. The heart of the issue is adaptive evolution expanding the cranial capacity of our ancestors.

If you would stick to making an argument along those lines, we wouldn't be having this (endless) discussion. Instead, you keep bringing up a supposed mismatch between the mutation rate and the amount of divergence between humans and chimps. You swap back and forth between the two arguments as if they were the same thing. Take the following, for example:

I think I have been pretty consistant in my insistance that ape evolving into human beings defies normative genetics. The next time you are at work, or at your desk in your home take a good look around. How many tools do you see? Televisions, computers, pens, paper, phones...etc. Apes do not and cannot use tools except in the most crude way.

For me there is a large distinction between adaptive evolution that we all know happens and the projection of genetic statistics over millions of years.

Your reply makes no sense. We were talking about whether humans could accumulate one indel (that is, one neutral mutation -- you've just pointed out that they're mostly neutral) every two years, and suddenly you switch to talking about the evolution of human tool-making ability, which has nothing at all to do with the accumulation of neutral mutations. Do you see yourself as making a logical argument here? Because to me all you have done is change the subject.

Galileo said once, 'did you ever notice that sometimes things are the opposite of what you would have initially expected' (that's a paraphrase of course). Usually when there is an indel the reading frame gets a stop codon inserted and the reading frame is shut down.

Those are the ones that are deleterious and are eliminated by selection. Since 98% or more of indels aren't in genes, most of them don't have any such malign effect. Which you already know, since that's how you started this post. So what's your point here?

Dispite that there are something like 15 gross stuctural differences that were identified by the Chimpanzee Chromosome 22 Consortium. It seems to be assumed that because it's there it must have had somekind of a selective advantage. In my opinion that assumes entirely too much, there has to be a mechanism for changing protein coding genes on that level.

Did any of the 15 structural differences disrupt the reading frame of a gene? If not, why do are you linking these changes to disrupted reading frames? And who assumes that the structural changes had to have had a selective advantage? I certainly don't: my default assumption is that they were neutral.

By the way, I wanted to ask you something that has been on my mind for a while now. Do you think that gene expression could be a better expanation for adaptive evolution then spontaneous mutations?

Not a good distinction. Changes in gene expression are also caused by spontaneous mutations, either mutations in a gene that regulates this gene or mutations in a regulatory region. They're all mutations.

Mutations do get through this selective process and come in the form of cancer and other diseases and disorders.

If a mutation kills you, it hasn't gotten through the selective process; your death is the selective process at work. For a mutation to become fixed in the population, it has to have next to no overall negative effect.

I don't question that there will be a rare benefit from some inversions, SNPs and idels. It just doesn't result in the kind of changes nessacary for humans to evolve from apes.

Your assertion, backed up with evidence, would prompt a stunning revolution in biology. Lacking evidence, your assertion has as much weight as the drunken mumblings of the guy you try to avoid sitting next to on the subway. The evidence is the only thing that matters.

Would you care to suggest what the divergance actually is? This is a casual discussion forum, no one is going to hold it against you if you estimate is a little off or modern science isn't really sure.

0.4% would be the prediction based on the chimp/human results, i.e. 4x the single-base divergence.

You brought up an inversion of ~90,000 nucleotides.

900,000 bases, not 90,000. Factors of ten don't seem to be your strong point this week.

The ones you guys identified were millions of nucleotides long. The identification of an inversion millions of nucleotides between to seperate human populations would be an extra-ordinary discovery especially if it provided an advantage.

In another post I pointed you to an inversion in some modern humans that's almost five million bases long. It's interesting, but not an extraordinary discovery. There are many inversions that are polymorphic in modern humans -- quite possibly hundreds of them. Your conviction that they are extremely unlikely and must have large phenotypic effect is misplaced.

Did part of the various chromosmes rearrange spontaeously or did this happen in sequences of tens of thousands of nucleotides.

I'm not sure what you mean here. An inversion occurs as a single error in recombination, probably because of mirror-image sequences at the two ends of the inversion (i.e. an inverted repeat).

I realize that you have to be very precise in how you describe things. I am mostly concerned with how a polymorphism is actually fixed in a particular population. It first has to have a direct cause and an advantage.

No, completely wrong. The vast majority of polymorphisms that fix are neutral, and have nothing to do with natural selection.

One of the things that stands out in my mind is that humans don't have a real mating season. I'm not trying to be cute here, Our generations with populations as high as they are means that these indels would be happening every day constantly. Yet the divergance rate is still much less then 1%, or at least it would seem so. Most of these indels are not going to be cumulative as far as I can tell or do I have that completly wrong?

Your reponse doesn't seem to have much to do with what I wrote. Did you do what I asked? Think about your copy of the genome picking up 10 new indels, compared to your parent's copy, and your parent's copy picking up ten new ones compared to your grandparent's? Of course these are cumulative, except in the rare case that a later deletion takes out an earlier insertion.

What bugs me about this is I never saw an estimate of the divergance that included indels until fairly recently. Then the estimate jumps from less then 1% to about 4%.

You didn't see the estimate earlier because the estimate didn't exist earlier. That's why we measure things -- because we don't know how big they are.

I don't have a problem with someone insisting that we are very simular to chimpanzees, we do have a lot in common with those comical little guys. It's just that the paper you worked on only looked at 13 thousand genes and some change. There are something like 20-25 thousand genes in human genomes so the jury still out on just how much were really diverge from the chimpanzee.

Probably less than 20,000 genes, in fact. Do you have any reason to think the 7000 we couldn't study will look different than the 13,000 we could?

Yet it can be assumed without reservation that we did indeed have a common ancestor with chimpanzees.

Yes. That's because the hypothesis of common descent explains so much about the data that we do have. You have never dealt with those successes, successes that are not matched by any alternative hypothesis. I gave you a list of some of them once, and you dismissed them out of hand, without a word of explanation.

The directly observed and demonstrated effect of indels on populations. It is most often deleterious and as a result they are eliminated by natural selection.

Go back and read the first line of your own post. The "directly observed and demonstrated effect of indels on populations" is that most of them don't do anything at all. This is a basic fact about biology that you keep ignoring.

 

[sfs]

[on humans speciating]
Sure, if you want to drop back hundreds of thousands of years. In the modern world it is not happening and we occupy every ecological niche in the world.

Exactly. A species with world-wide distribution and large gene flows everywhere is very unlikely to speciate.

The only things that change are a lot of the same thing Mendel observed, size, shape, texture, color...etc. Darwin predicted and concluded the presense of human subspecies, they simply don't exist.

I don't know whether Darwin predicted human subspecies or not, but if he did he was wrong. Not surprising, since his understanding of speciation was quite primitive. It is now understood that speciation (at least in animals) normally requires some kind of isolation between subpopulations, something that no longer happens to humans.

If we are the result of evolution then why do we evolve so little dispite being exposed to evolutionary trigger in creation?

What makes you think we evolve little? We do evolve regional traits where they are beneficial. Look around at the color of people's skin -- the regional variations in that trait evolved in just a few thousand years.

That's the thing, I don't see the need for mutations in any of this. Now, the stronger beaks do provide a small advantage but what do we really have to suggest that this has anything to do with mutations.

Things like beak size are largely determined by genetics, by which alleles an organism has. New alleles arise by mutation. Therefore, variation in things like beak size ultimately comes from mutation.

You did what Darwinians and evolutionists do as a matter of course, you just projected the scenerio over a vast period of time. I'm a creationist so that makes me one of the most radical evolutionists around. I don't have a lot of time to work with so radical and dramatic adaptive evolution has to be a given when you think about it.

All I care about is finding a consistent explanation for observed phenomena. Genetic variation looks exactly like it is the result of random mutations. So until someone comes along with a model that explains that appearance as well, I'm going to adopt the explanation that genetic variation is produced by random mutations.

Ok, 65 nucleotides fixed over 600,000 generation comes to 39 Mbs if it is assumed they are cumulative. However, we are looking at at least 125 Mbs of nucleotide divergance between chimpanzees and humans. Maybe I am not explaining this very well but this is an astronomical number of changes. I am far from convinced that this is accounted for by the current mutation rate.

Since no one but you has suggested that only 65 nucleotides are fixed every generation (I've suggested several hundred as the number), I still don't know where you're coming from here.

You seemed to think I was confused about the difference between a mutation event and the number of nucleotides involved. I'm not, but because of the effects of things like synergistic epistasis and Muller's rachet the larger mutations are potentially more deleterious.

I can't think of any polite way of saying this. Your statement here is just nonsense. Muller's ratchet and synergistic epistatis tell you nothing at all about whether large mutations are more deleterious. It is in fact likely that large mutations are likely to be more deleterious than small deleterious mutations, but that doesn't have anything to do with the fact that the vast majority of large and small mutations don't have any effect at all.

The Human Genome project surely has accomplished more reliable research then the Chimanzee Genome project for obvious reasons. The indels are mentioned explicitly in the Initial Sequence of the Chimpanzee Genome. I understand what you are getting at though, this kind of research takes time, money and the patience of Job. I quess I will have to wait for a better idea of how much human genomes diverge between individule humans.

Sorry, but the Human Genome Project simply did not study human genetic variation. Sequencing the genome was a large enough problem that they didn't need to tackle another one at the same time. The chimpanzee genome project (which was largely done by the same people, by the way) was able to study human/chimpanzee indels because they already had the human genome in hand; when the human genome was done, there was no other genome to compare it to. As far as polymorphic indels are concerned, there is still no global survey of them.

70 mutation events per generation for 600,000 generations. That does not include the ones that were eliminated by natural selection.

Correct. Perhaps one or two per generation are eliminated by natural selection.

There are 6,600,115,810
people in the world as of July 1. are you suggesting that everyone of them have the cumulative genetic divergance you are describing?

Yes, that's what I'm suggesting.

Bottom line, human divergance would be growing with our population numbers being so high.

Correct; human divergence is growing.

Many, if not most of these are cyclical not cumulative or we would either be experiencing enourmous genetic divergance.

Incorrect. They are indeed accumulating, and are not cyclical. They do not imply enormous genetic divergences, however. Let me be concrete. Human genetic diversity is about 0.1% for single-base substitutions, with about another 0.015% of sites differing by an indel (note that I'm counting entire indels, not each base individually). I have two copies of the genome, so let's say they differ in an average number of places, which is 3,450,000 differences. My sons each have 70 (say) new mutations in each of their copies of the genome, so they each have 140 new differences. That means they have 3,450,140 differences instead of 3,450,000. Their children, if they have any, will each have 3,450,280 differences. Not really a big change, is it?

It will take more than 200 generations for human diversity to increase by 1%, that is to go from 0.115% to 0.116%, and 20,000 generations (half a million years) for it to double. The explosion in genetic diversity that you're talking about is fictitious.

 

[robalan]

I'm stuggling with this right now. I've read that human dna is 99% similar to the dna of chimps. How do we as creationists reconcile that to our belief that we are not related to apes?

The fact that our DNA is 99% the same as chimps--according to omniscient scientists--doesn't mean anything. Everything in the universe is made from a small number of elements on the periodic table. So you might as well say that, since humans and rocks are made from the basic elements, we are basically the same thing as rocks--or that we evolved from rocks.

People who make these claims need to learn that, just because two things share similar qualities, it doesn't mean one came from another or that they are both the same.

Next time someone tells you that chimps are 99% the same as humans, ask them, "Can chimps build 99% of a skyscraper in Manhattan? Can chimps write 99% of a classical symphony?"

And you also need to realize that science deals merely with the physical world. Even if it is true that chimps share 99% of our DNA, that still says nothing about their spiritual makeup. When the Bible says that God created mankind in his image, it isn't merely referring to the physical aspect, but the spiritual aspect as well. Doesn't it say that God breathed his spirit into man? It doesn't say this for any of the animals.

When you start using modern science, which excludes spiritual things, it won't be too long before you believe that humans are like rocks.

 

[mark kennedy]

Of course. That's why I continue to be baffled about your insistence that the indels present a problem for evolution, or why you keep bringing up the deleterious effects of some mutations.

Because the indels dwarf the SNPs and deleterious effects are the biggest problem with mutations. The OP is a classic example of how the actual evidence is slanted toward the naturalistic assumptions of secularists. The direct comparison of nucleotide sequences found that there were much more divergance then previously believed.

If you would stick to making an argument along those lines, we wouldn't be having this (endless) discussion. Instead, you keep bringing up a supposed mismatch between the mutation rate and the amount of divergence between humans and chimps. You swap back and forth between the two arguments as if they were the same thing. Take the following, for example:

Well, I don't know why we keep going over it so many times. The mutation rate indicates that in the time frame since the LCA there would be about 65 Mb that diverge. Instead we are just going to ignore the fact that the divergance is actually at least double that. That is not really even an argument, it's an undisputed fact directly from the evdence.

I mention the use of tools because that distinguishes us from ever living creature on earth. It is directly relevant particularly given our cranial capacity being almost 3 times that of apes. So we evolved from apes according to the seemingly universal affirmation of scientists yet the genetic basis for this unprecedented expansion remains unknown. Then when I bring it up I'm told I'm being non-sensical. Here is a prime example of what I am talking about:

Your reply makes no sense. We were talking about whether humans could accumulate one indel (that is, one neutral mutation -- you've just pointed out that they're mostly neutral) every two years, and suddenly you switch to talking about the evolution of human tool-making ability, which has nothing at all to do with the accumulation of neutral mutations. Do you see yourself as making a logical argument here? Because to me all you have done is change the subject.

When I was studing for my current MOS (job designation in the Army) I saw a distinction I found interesting. There is a difference between a logical deletion and a physical one. When you put something in the recycle bin it's not really gone it's just logically seperated. Bear in mind we are talking about evolution which for natural selection to operate there must be an advantage, specifically an adaptive one. When a certain gene is turned off or on by a prion or genes are recombined a certain way it can provide a adaption. You simply don't need to physically alter genes for diversity in living systems to be accounted for, at least most of the time.

Those are the ones that are deleterious and are eliminated by selection. Since 98% or more of indels aren't in genes, most of them don't have any such malign effect. Which you already know, since that's how you started this post. So what's your point here?

The point is that there are gross structural differences between chimpanzees and humans. Indels in a reading frame usually gets it shut down and only in the rarest of instances provide even a slight selective advantage. So the question of how they got there in the first place goes unanswered.

Did any of the 15 structural differences disrupt the reading frame of a gene?

In all but one case the reading frame is still open.

If not, why do are you linking these changes to disrupted reading frames?

Because that is what happens when in indel is introduced to an open reading frame. A stop codon is inserted because the protein would be too garbled to be of any use.

And who assumes that the structural changes had to have had a selective advantage? I certainly don't: my default assumption is that they were neutral.

At some point there has to be an effect, neutral changes don't evolve a species into an altogether different kind. Let me ask you this, has there ever been in indel that has a beneficial effect on the human brian?

"Sakaki said their analysis found about 68,000 insertions or deletions. "That is almost one insertion/deletion every 470 bases," he said. In addition, a small proportion of genes showed a relatively higher rate of evolution than most other genes. "We haven't known what proportion of the genes shows adaptive evolution. This study shows it to be about 2 to 3%," he said."

Why would this be a problem? I am amazed that not one scientist has openly admitted this does create a problem even though every publication I've read on the subject does.

Under conservative assumptions, we estimate that an average of 4.2 amino-acid-altering mutations per diploid per generation have occurred in the human lineage since humans separated from chimpanzees. Of these mutations, we estimate that at least 38% have been eliminated by natural selection, indicating that there have been more than 1.6 new deleterious mutations per diploid genome per generation.

‘High genomic deleterious mutation rates in hominids’ (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9950425&dopt=Abstract )

Not a good distinction. Changes in gene expression are also caused by spontaneous mutations, either mutations in a gene that regulates this gene or mutations in a regulatory region. They're all mutations.

I know but I like to make a distinction between the different kinds of changes. For instance, the Nylon Bug is a common example of a benefical effect from an indel. When I looked into this I found that this was not really a new reading frame. Some how another reading frame was inserted, it is this kind of an evolutionary mechanism I am interested in.

If a mutation kills you, it hasn't gotten through the selective process; your death is the selective process at work. For a mutation to become fixed in the population, it has to have next to no overall negative effect.

That sounds like classic creationism to me, I would be comfortable saying the exact same thing as an argument against a common ancestor for chimps and humans. The indels are differences that existed at creation, they are not the result of genetic mutations. That is exactly why a large indel in an open reading frame raises red flags.

Your assertion, backed up with evidence, would prompt a stunning revolution in biology. Lacking evidence, your assertion has as much weight as the drunken mumblings of the guy you try to avoid sitting next to on the subway. The evidence is the only thing that matters.

Nothing in biology would change, eliminate Darwinism and the presumption of a single common ancestor and you have biology limited to observed living systems. Here is an example of a difference between a human and chimpanzee AA (amino acid) difference. C21 orf81 is 145 amino acids long with 13 of them being different. There are 140.6 syn sites and 294 nonsyn sites. I don't know what this gene actually does but genes don't respond well to changes on this level.

Let's look at some specific genes known to be involved in human brain development.

"ASPM encodes a protein involved in spindle formation, so it is tempting to think that changes in its sequence might result in an increased rate of cell division and hence brain size. But, cautions Walsh, “we really have no idea yet how or even if ASPM is involved in brain evolution...

...Walsh has recently reported that deletion of a gene called Nde1 produces mice with very small brains. “Our experiments indicate that the loss of Nde1 causes neurons to mature prematurely. This stops them dividing so the mice end up with small brains”, explains Walsh, who is now investigating whether human NDE1 variants have been positively selected during human evolution."

The effect of changes to these two gene are known to result in reduced fittness. A defective spindle and a prematurly develped neuron does not strike me as an efficient evolutionary mechansim. These researchers are clear that there would have to be tremendous costs and an elaborate reorganization:

"A bigger, more complex brain may have advantages over a small brain in terms of computing power, but brain expansion has costs. For one thing, a big brain is a metabolic drain on our bodies. Indeed, some people argue that, because the brain is one of the most metabolically expensive tissues in our body...The end result is that the human brain is not just a scaled-up version of a mammal brain or even of an ape brain."

In some 1.5 million years the brain triples in size and complexity and we are not modified apes. The average human brain weight is 1,300 grams and an ape is between 300 and 400 grams. It is actually natural selection that prevents apes from evolving the size of their brains over time because of the deleterious effects of mutations.

http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=1065704

0.4% would be the prediction based on the chimp/human results, i.e. 4x the single-base divergence.


900,000 bases, not 90,000. Factors of ten don't seem to be your strong point this week.

Ok, you got me on that one.

In another post I pointed you to an inversion in some modern humans that's almost five million bases long. It's interesting, but not an extraordinary discovery. There are many inversions that are polymorphic in modern humans -- quite possibly hundreds of them. Your conviction that they are extremely unlikely and must have large phenotypic effect is misplaced.

Actually, I was under the impression that there were millions of them.

"Scientists believe SNP maps will help them identify the multiple genes associated with such complex diseases as cancer, diabetes, vascular disease, and some forms of mental illness. These associations are difficult to establish with conventional gene-hunting methods because a single altered gene may make only a small contribution to the disease.

Several groups worked to find SNPs and ultimately create SNP maps of the human genome. Among these groups were the U.S. Human Genome Project (HGP) and a large group of pharmaceutical companies called the SNP Consortium or TSC project. The likelihood of duplication among the groups was small because of the estimated 3 million SNPs, and the potential payoff was high."

http://www.ornl.gov/sci/techresources/Human_Genome/faq/snps.shtml


I'm running out of time, I'll have to skip some of this...sorry about that.

Yes. That's because the hypothesis of common descent explains so much about the data that we do have. You have never dealt with those successes, successes that are not matched by any alternative hypothesis. I gave you a list of some of them once, and you dismissed them out of hand, without a word of explanation.

The simple statement in the paper said that the predictions of Huxley and Darwin have been confirmed. I've read both of them and what they predicted has not been confirmed by anything I'm seeing. Darwin specifically claims that there are existing sub-species in human population and there are not, not even one. By the way, even though I didn't respond to your list of articles doesn't mean I didn't read them. You called Creationism 'scientifically bankrupt' when I asked you what would lead you to conclude seperate lineage.

I have tried to follow as much of the fossil and genetic evidence as closely as I can. I would have abandoned this kind of debate years ago if not for the evidence being so strong. The tripling of the size of a primate brian in such a short space of time would be one of the biggest evolutionary leaps in natural history. At every major transition you see this and yet TOE is never challenged by it.

Go back and read the first line of your own post. The "directly observed and demonstrated effect of indels on populations" is that most of them don't do anything at all. This is a basic fact about biology that you keep ignoring.

Ignoring it? That is the basic fact that is at the heart of this whole arguement. Indels either do nothing or they are deleterious except in the rarest of instances. Then you look at a comparision of the two genomes and there are lengthy differnces in vital regions.

There are vast differences between humans and chimpanzees. The key to this whole issue is determining the historicity of an event. In order for an ape brain to expand in size and complexity at some point the genes have to be altered dramatically. Researchers admit freely that the genetic basis for this remains elusive. No demonstrated mechanism then you don't have a valid evidential proof for a common ancestor.

http://ircamera.as.arizona.edu/NatSci102/NatSci102/images/allman1a.jpg

Look at the image, see the difference Steve? Am I suppose to think that this creates no problem for us having a single common ancestor with the chimpanzee? You might still come to the conclusion of a single common ancestor but one thing is crystal clear, Darwinian gradualism is no explanation at all.

Grace and peace,
Mark

 

[mark kennedy]

Exactly. A species with world-wide distribution and large gene flows everywhere is very unlikely to speciate.

That is the exact opposite of what I am getting, Koalas have a uniform distribution from northern to southern Australia. Gorrillas have two species, Eastern and Western Gorrillas. Troglodyte and Pygmy chimps can still even interbreed but there are enough differences that they are still seperate species. I could muster a long list, the only exception would seem to be human populations.

I don't know whether Darwin predicted human subspecies or not, but if he did he was wrong. Not surprising, since his understanding of speciation was quite primitive. It is now understood that speciation (at least in animals) normally requires some kind of isolation between subpopulations, something that no longer happens to humans.

Pardon the shock and awe but that is as basic as Darwinism gets or at least Charles Darwin:

"I could show fight on natural selection having done and doing more for the progress of civilization than you seem inclined to admit. Remember what risk the nations of Europe ran, not so many centuries ago of being overwhelmed by the Turks, and how ridiculous such an idea now is! The more civilised so-called Caucasian races have beaten the Turkish hollow in the struggle for existence. Looking to the world at no very distant date, what an endless number of the lower races will have been eliminated by the higher civilized races throughout the world." (Letter to W. Graham July 3rd, 1881)

"At some future period, not very distant as measured by centuries, the civilised races of man will almost certainly exterminate, and replace, the savage races throughout the world. At the same time the anthropomorphous apes, as Professor Schaaffhausen has remarked, will no doubt be exterminated. The break between man and his nearest allies will then be wider, for it will intervene between man in a more civilised state, as we may hope, even than the Caucasian, and some ape as low as a baboon, instead of as now between the negro or Australian and the gorilla." (The Descent of Man 1882 p.156)

See what I mean, this is nothing more then undiluted racism that has been totally disproven by modern genetics. In all fairness he did make some pretty brilliant insights into speciation based on hybrids. Man has allways raised livestock and selectivly interbreeded them. Darwin called this artifical selection which is where he got that term natural selection. He pointed out something I found particularly insightfull, he called infertility the bane of horticulture.

What makes you think we evolve little? We do evolve regional traits where they are beneficial. Look around at the color of people's skin -- the regional variations in that trait evolved in just a few thousand years.

You still have populations of humans that can interbreed with virtually any other world-wide. You are describing size, shape, color...etc but the Darwinian sub-species does not exist in human populations. That is dispite the fact that we have faced every ecological challenge the world has to offer.

Things like beak size are largely determined by genetics, by which alleles an organism has. New alleles arise by mutation. Therefore, variation in things like beak size ultimately comes from mutation.

Mendel managed to reduce this to a ratio and the elementum (his word for genes) simply recombine. The future apart genes are the more often the recombine. I can see how something like an inversion can bring about new alleles. What I don't think is nessacary is that the nucleotide sequence has to be altered at random.

All I care about is finding a consistent explanation for observed phenomena. Genetic variation looks exactly like it is the result of random mutations. So until someone comes along with a model that explains that appearance as well, I'm going to adopt the explanation that genetic variation is produced by random mutations.

I'm not saying that random (at least seemingly random) mutations are not a source of variety. I'm pretty hard headed but I'm not that dense. Genes recombine at random without the genes being mutated and that is a source and a lot of variety as well.

Since no one but you has suggested that only 65 nucleotides are fixed every generation (I've suggested several hundred as the number), I still don't know where you're coming from here.

I've seen a lot of different estimates so I assume it all depends. The way I have understood it was that mutations usually result from a transcript error. There are several checkpoint that screen for transcript errors. To be honest I don't like the term 'mutation' because it's too much of a catch all phrase. It seems to me that there is some kind of a dynamic at work that can reorganize certain parts of the genome. There has to be a distinction between a natural mechaninism bringing about variety and a random transcript error.

I can't think of any polite way of saying this. Your statement here is just nonsense. Muller's ratchet and synergistic epistatis tell you nothing at all about whether large mutations are more deleterious. It is in fact likely that large mutations are likely to be more deleterious than small deleterious mutations, but that doesn't have anything to do with the fact that the vast majority of large and small mutations don't have any effect at all.

It seems to me that a larger mutation is clearly going to be more deleterious. A single letter misplaced in a post can make it harder to read but not really not incomprehensible. Getting a garbled paragraph turns the whole thing into gibberish which is how I see the difference between an SNP and an indel.

Sorry, but the Human Genome Project simply did not study human genetic variation. Sequencing the genome was a large enough problem that they didn't need to tackle another one at the same time. The chimpanzee genome project (which was largely done by the same people, by the way) was able to study human/chimpanzee indels because they already had the human genome in hand; when the human genome was done, there was no other genome to compare it to. As far as polymorphic indels are concerned, there is still no global survey of them.

There will be further comparisons of genomes over time and I'm pretty comfortable with the .1% variation. They have found millions of SNPs and the main reason they are interested is because of the role of these mutations in created disease and disorder. Every chromosome has a list of diseases as long as your are and it is impossible to assign a simular list of beneficial varieties. Mutations may well be the 'ultimate' source of variety but they are clearly a source of disease, disorder and death. Mutations are resulting in less fittness not greater, that's where I'm coming from.

Correct. Perhaps one or two per generation are eliminated by natural selection.


Yes, that's what I'm suggesting.


Correct; human divergence is growing.

It's nice to get something right once in a while.

Incorrect. They are indeed accumulating, and are not cyclical. They do not imply enormous genetic divergences, however. Let me be concrete. Human genetic diversity is about 0.1% for single-base substitutions, with about another 0.015% of sites differing by an indel (note that I'm counting entire indels, not each base individually). I have two copies of the genome, so let's say they differ in an average number of places, which is 3,450,000 differences. My sons each have 70 (say) new mutations in each of their copies of the genome, so they each have 140 new differences. That means they have 3,450,140 differences instead of 3,450,000. Their children, if they have any, will each have 3,450,280 differences. Not really a big change, is it?

That all seems perfectly reasonable except human population is in the billions. The amount of diversity should be well into the billions if every individule has 70 mutations plus the ones they are inheriting from their parents. You have to understand that we have a very different view of history. I see the ancient world as being much more lush and people being a lot more robust. Over time I don't think we are evolving, if anything the human condition is devolving, for lack of a better word.

It will take more than 200 generations for human diversity to increase by 1%, that is to go from 0.115% to 0.116%, and 20,000 generations (half a million years) for it to double. The explosion in genetic diversity that you're talking about is fictitious.

That is assuming a linear progression and a 20 year generation. The reality is that with our populations in the billions the amount of genetic diversity should be growing exponentially. Babies are being born every second and you are telling me that everyone of the has cumulative germline mutations.

Prions turning genes on and off I get, genes recombining makes sense to be. Random mutations on the other hand does not strike me as any explanation at all except for things like cancer, tumors and mental retardation.

Where are the evolutionary mechanisms that triple the size of a primate brain? To be completly honest if the choice is between random mutations and special creation it's a no brainer.

Grace and peace,
Mark

 

[sfs]

Well, I don't know why we keep going over it so many times. The mutation rate indicates that in the time frame since the LCA there would be about 65 Mb that diverge.

We keep going over this so many times because you keep writing things like this. It's wrong. It's been wrong every time you've written it. I've corrected you repeatedly, and yet you just keep on writing it. So I'll have to say it once again: there is no measured mutation rate that indicates that there should be about 65 Mb of divergence between humans and chimpanzees. I don't know where you got that number.

Instead we are just going to ignore the fact that the divergance is actually at least double that. That is not really even an argument, it's an undisputed fact directly from the evdence.

No one is ignoring the size of the divergence. What we're ignoring (except for me) is the disagreement between the observed divergence and a number you made up.

The point is that there are gross structural differences between chimpanzees and humans. Indels in a reading frame usually gets it shut down and only in the rarest of instances provide even a slight selective advantage. So the question of how they got there in the first place goes unanswered.

So why are you talking about 65 Mb of difference between humans and chimps, when almost none of that consists of indels within reading frames? There are very few indels in reading frames.

In all but one case the reading frame is still open.

So we're not talking about disrupted reading frames . . .

Because that is what happens when in indel is introduced to an open reading frame. A stop codon is inserted because the protein would be too garbled to be of any use.

Or maybe we are. . . Except you were talking about gross structural changes, which is not the same thing as an indel inserted into a reading frame. And no, indels do not always disrupt a reading frame. If the indel is three nucleotides long (or a multiple of three), it adds or removes an amino acid, but does not usually produce a stop codon.

I'm trying very hard to find a coherent argument here, but all I'm seeing is random, disconnected ideas.

At some point there has to be an effect, neutral changes don't evolve a species into an altogether different kind. Let me ask you this, has there ever been in indel that has a beneficial effect on the human brian?

I haven't any idea. The question is irrelevant to the issue we're talking about, which is whether the mutation rate can explain the number of (purely neutral) indels in humans and chimps. It's quite possible that indels have had no effect on the development of any human trait, and that every indel with any functional effect was weeded out by natural selection long ago. So what are we talking about?

"Sakaki said their analysis found about 68,000 insertions or deletions. "That is almost one insertion/deletion every 470 bases," he said. In addition, a small proportion of genes showed a relatively higher rate of evolution than most other genes. "We haven't known what proportion of the genes shows adaptive evolution. This study shows it to be about 2 to 3%," he said."

Why would this be a problem? I am amazed that not one scientist has openly admitted this does create a problem even though every publication I've read on the subject does.

Here's a clue: if you think something is a big problem and every single scientist in the field says it isn't, you're wrong. It's a simple rule of thumb, but it's highly reliable. I'm a scientist in the field, and after hours of exchanges with you, I still cannot figure out what you think the problem is. Too many substitutions between humans and chimps to be explained by neutral evolution? Too many indels? Too many mutation? Too few? Too many deleterious mutations? Dealing with you is like playing whack-a-mole: every time I explain why one thing isn't a problem, another issue pops up and you drop the first -- until the next time it pops up and I repeat the same explanation again. It's driving me absolutely nuts.

Could you state in one sentence what problem 80 Mb of indels cause for evolution?

Under conservative assumptions, we estimate that an average of 4.2 amino-acid-altering mutations per diploid per generation have occurred in the human lineage since humans separated from chimpanzees. Of these mutations, we estimate that at least 38% have been eliminated by natural selection, indicating that there have been more than 1.6 new deleterious mutations per diploid genome per generation.

‘High genomic deleterious mutation rates in hominids’ (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9950425&dopt=Abstract [)

Like the above, for instance. We've been talking about neutral indels, and suddenly deleterious single-base subsitutions are the problem.

Actually, I was under the impression that there were millions of them.

There are millions of SNPs, not millions of inversions.

"Scientists believe SNP maps will help them identify the multiple genes associated with such complex diseases as cancer, diabetes, vascular disease, and some forms of mental illness. These associations are difficult to establish with conventional gene-hunting methods because a single altered gene may make only a small contribution to the disease.

Several groups worked to find SNPs and ultimately create SNP maps of the human genome. Among these groups were the U.S. Human Genome Project (HGP) and a large group of pharmaceutical companies called the SNP Consortium or TSC project. The likelihood of duplication among the groups was small because of the estimated 3 million SNPs, and the potential payoff was high."

http://www.ornl.gov/sci/techresources/Human_Genome/faq/snps.shtml

Close, but not quite an accurate history. One set of SNPs was found by the TSC project, and another was found by mining overlapping clones from the Human Genome Project, but the HGP itself didn't do the mining. That was all done as part of the TSC paper, which was the companion paper that I mentioned earlier. We came up with some bland name for the combined operation, but I forget what it was. (I did almost all of the analysis of diversity for that paper, by the way.) It was never part of the HGP organization.

Ignoring it? That is the basic fact that is at the heart of this whole arguement. Indels either do nothing or they are deleterious except in the rarest of instances. Then you look at a comparision of the two genomes and there are lengthy differnces in vital regions.

Which differences in vital regions? You keep talking about the hundred million bp difference between the two species, but very little of that is in genes. So which differences are you talking about?

 

[sfs]

That is the exact opposite of what I am getting, Koalas have a uniform distribution from northern to southern Australia. Gorrillas have two species, Eastern and Western Gorrillas. Troglodyte and Pygmy chimps can still even interbreed but there are enough differences that they are still seperate species. I could muster a long list, the only exception would seem to be human populations.

No, there are lots of species that don't have subspecies (including bonobos, I note). Subspecies typically have major geographical divisions supporting the genetic divisions. That's certainly the case for chimpanzees.

See what I mean, this is nothing more then undiluted racism that has been totally disproven by modern genetics. In all fairness he did make some pretty brilliant insights into speciation based on hybrids. Man has allways raised livestock and selectivly interbreeded them. Darwin called this artifical selection which is where he got that term natural selection. He pointed out something I found particularly insightfull, he called infertility the bane of horticulture.

I have very little interest in Darwin. It's the science I'm interested in.

You still have populations of humans that can interbreed with virtually any other world-wide. You are describing size, shape, color...etc but the Darwinian sub-species does not exist in human populations. That is dispite the fact that we have faced every ecological challenge the world has to offer.

We faced all of those ecological challenges in a very short time, genetically speaking, and continued to exchange genes with other populations while we did it. Under those conditions, speciation is highly unlikely. In other words, you're pointing out a successful prediction of evolutionary theory.

It seems to me that a larger mutation is clearly going to be more deleterious. A single letter misplaced in a post can make it harder to read but not really not incomprehensible. Getting a garbled paragraph turns the whole thing into gibberish which is how I see the difference between an SNP and an indel.

That's quite true -- provided you're talking about the part of the genome that has a function. Most of the genome is already incomprehensible gibberish, however, and garbling a paragraph of gibberish has very little effect. I'm talking about the 95% of the genome where the particular sequence doesn't seem to matter at all. That's where almost all of these indels are.

There will be further comparisons of genomes over time and I'm pretty comfortable with the .1% variation. They have found millions of SNPs and the main reason they are interested is because of the role of these mutations in created disease and disorder. Every chromosome has a list of diseases as long as your are and it is impossible to assign a simular list of beneficial varieties.

It's possible to come up with a list of beneficial varieties, but it's a much shorter one. This is also as expected by evolution. There are two reasons. First, there are more deleterious mutations than beneficial ones, and second, the beneficial ones are promoted by natural selection, and quickly fix (if they stick around at all), so you'll seldom see them. Deleterious ones tend to hang around at low levels, mostly because new ones keep appearing. (It's called mutation-selection balance, and is a standard part of population genetics.)

Mutations may well be the 'ultimate' source of variety but they are clearly a source of disease, disorder and death. Mutations are resulting in less fittness not greater, that's where I'm coming from.

And yet mutations very clearly enable bacteria to evade antibiotics, and insects to evade pesticides, and malaria to evade chloroquine (and the human immune system), so perhaps your sweeping generalization needs some work.

That all seems perfectly reasonable except human population is in the billions. The amount of diversity should be well into the billions if every individule has 70 mutations plus the ones they are inheriting from their parents.

The total amount of diversity, by which you seem to mean the total number of variants out there in the population, is in the billions. That's not what the 0.1% measures, however. That's the average difference between a pair of chromosomes, and that is much smaller, and is growing as I described. Each of us has only a small fraction of the total variety present in the human population.

That is assuming a linear progression and a 20 year generation.

That's because it is a linear progression and because a generation is about 20 years. Ok, so it's more like thirty years in the developed world now -- so diversity will actually increase a little slower than I said.

Prions turning genes on and off I get, genes recombining makes sense to be. Random mutations on the other hand does not strike me as any explanation at all except for things like cancer, tumors and mental retardation.

Then I suggest you take pyrimethamine if you ever get malaria, and penicillin if you get a multi-drug resistent staph infection. Pathogens don't care about what strikes you as a good explanation -- they just keep using random mutations to defeat our best drugs.

 

[mark kennedy]

Steve,

Obviously we are getting no where with this and all I really wanted to do was to discuss the paper. I’m a Creationist mainly due to my religious beliefs and strong convictions regarding the historicity of the Bible, particularly in the New Testament. The issue of common ancestry can take a lot of tangents and in this discussion it does at every turn. With my training schedule being what it is it is difficult to follow just how the scientific community has drawn the conclusions they have. A couple of things have been clear to me regarding human beings, first of all human beings are unique. The explanation for me as a fundamentalist is that we were created in the image of the Living God and we have a spiritual nature that is way beyond the ability of natural science to measure. Similarly, history is not a science


I have a suggestion and feel free to respond any way you think is right. I learned the Bible for the most part from expositional studies and open forum discussions. One of the biggest deterrents of an open forum discussion is when conflicts over doctrine and semantics distract from the actual message of the text. Maybe we could try working through the text and focus on what it actually says, catch the highlights and clear up a little of the confusion.

From the Abstract:

“Through comparison with the human genome, we have generated a largely complete catalogue of the genetic differences that have accumulated since the human and chimpanzee species diverged from our common ancestor, constituting approximately thirty-five million single-nucleotide changes, five million insertion/deletion events, and various chromosomal rearrangements.”

That is the 5 million mutation events known collectively as indels (insertions/deletions) and the 35 million SNPs (single nucleotide polymorphisms). The stated purpose of the paper was it explores the magnitude and regional variation of mutational forces shaping these two genomes particularly with regards to the genes. Maybe you could give a general discussion of the various ‘mutational forces’, what they are and how they actually work.

I have taken some notes and I am just going to list them so that we can be clear on exactly what some of the main points are. They are in no particular order really since they are just a digest of the points of interest for me personally:

There are 35 million SNPs, totaling 1.23% of differences (14-22% are polymorphisms)
Observable insertions are in two classes:

1) Completely covered insertions within continuous sequences in both species.

2) Incompletely covered insertions, occurring within sequence containing one or more gapes in the chimpanzee but revealed by a clear discrepancy between the species in sequence length.

Chimpanzee-specific sequence indels total 35 Mb (megabases) and human specific sequence indels total 32Mb in 5 million indel events. They range from 1 base to 15 Kb.

Humans and Chimpanzee genomes have 40-45 Mb in their respective genomes which comes to 90 Mb representing 3% of the divergence due to indels.

I’m just interested in discussing these ‘mutational forces’ and how you guys quantified and qualified the divergence. The most important differences would be in the exons of known genes in ’34 regions’ according to the paper. You and apparently every scientist in the world are convinced that the need for a special creation is altogether unnecessary. If the problem here is indeed just the ignorance of creationists like myself this is a prime opportunity to go over the demonstrated mechanisms considered sufficient to explain the level of divergence.

I have been looking at the one to one gene comparisons and trying to track them on Gene Bank. It’s difficult at best so maybe backing up and looking at some of the general principles will prove informative. We can just work our way down the paper I can at least find out how you guys figure common ancestry is a scientific fact.


Grace and peace,
Mark