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Humans DNA is 99% similar to that of chimps?

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gluadys

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Poke said:
But, even 98% represents a massive chasm for Evolution to overcome.

Yet when I point to a 7-year experiment in which two groups of fruit flies both from the same ancestral population, developed a 3% genetic difference, as well as significant differences in physiology and mating choice, creationists say this is not a huge chasm at all. After all both groups are still fruit flies!


Why should we expect chimps to have very different DNA? They're made by the same designer, using the the same biochemical laws, and a there is a lot of physical similarity. The Evolutionist DNA similarity argument really boils down to the illogical "Monkeys sure do look like us."

Chimps are not monkeys, and monkeys do not display 98% genetic similarity to either chimps or humans.

No one here disputes that all species were made by the same designer. But the pattern of similarity and difference indicates that the designer used evolution as his instrument of design.
 
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gluadys said:
Yet when I point to a 7-year experiment in which two groups of fruit flies both from the same ancestral population, developed a 3% genetic difference, as well as significant differences in physiology and mating choice, creationists say this is not a huge chasm at all. After all both groups are still fruit flies!

How about a link to this study? I sure hope you're not comparing millions of years of Natural Selection crafting a genome to garbage created in a lab.

Chimps are not monkeys, and monkeys do not display 98% genetic similarity to either chimps or humans.

1) I really didn't say chimps are monkeys. I used an expression.

2) Chimps are monkeys. (even if chimps are anthropoid apes and monkeys aren't)

3) Even if chimps aren't monkeys, I wouldn't be so petty as to raise an objection to someone else say it, if it weren't relevant.
 
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gluadys

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Poke said:
How about a link to this study?


http://links.jstor.org/sici?sici=0014-3820(198007)34:4<730:AMGIOS>2.0.CO;2-J

It has been discussed here before at

http://www.christianforums.com/t722770&page=5

The relevant post is #45. The poster, lucaspa, is a professional biologist at the New York Medical Centre.

I sure hope you're not comparing millions of years of Natural Selection crafting a genome to garbage created in a lab.

The experiment did not "craft a genome". It did, however, show genetic change with one of the descendant populations showing more than a 3% difference from the genome of its ancestral population.

Most creationists consider this insignificant, since the evolved species is "still a fruit fly", yet at the same time consider the smaller genetic difference between chimps and humans "a massive chasm for Evolution to overcome".

I see a disconnect in this reversal of logic.

1) I really didn't say chimps are monkeys. I used an expression.

2) Chimps are monkeys. (even if chimps are anthropoid apes and monkeys aren't)

3) Even if chimps aren't monkeys, I wouldn't be so petty as to raise an objection to someone else say it, if it weren't relevant.

Good. You have heard of cladistics. On that basis, humans are monkeys too. And anthropoid apes.

When you throw an expression about monkeys into the middle of a discussion about the similarity of chimp and human genomes, it makes it look as if you are confusing chimps and monkeys.

As it happens you do know the difference, but many people don't so I was not certain whether you did or not.
 
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mark kennedy

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shernren said:
Why do I get the feeling that you're only plucking out the numbers which look nice? I'm looking at the "Initial sequence of the chimpanzee genome" paper and I can't find your 83% and 96% numbers, where are your sources? I'm assuming that your 29% identical statistic comes from:

http://hgm2003.hgu.mrc.ac.uk/Abstracts/Publish/Plenaries/Plenary01/hgm01.html

Start there and then we can talk about the specific changes that scientists have found. You can't help but believe that it is readily explainable how apes transposed into humans but it is impossible.



Firstly, don't you think it's strange that when a researcher starts by saying the genomes are extremely similar, and then uses the 29% statistic to back his statements, that you can arrive at the exactly opposite conclusion - that the two genomes are extremely dissimilar?

They have an apriori assumption that is irrelevant to the evidence at hand, pure and simple. It does not matter if the DNA is 96% simular or it is 80%, they need a common ancestor or they have no naturalistic explanation.

Full explanation:

Baloney!

Look what the researchers are saying: that the genomes were so similar that it actually hampered their efforts to study their evolution, presumably because it became difficult to identify the small changes here and there in a sea of conserved genetic material. And note that the median number of substitutions is (to be generous, using the synonymous figure) three. Three substitutions change one or at the most two amino acids. Insulin alone has about 100 amino acids when first transcribed from DNA.

One of the expressed purposes of the chimpanzee genome project is to explain human evolution. They failed miserably but we are supposed to pretend that the difference jumping from 99% to 96% (and I do mean simular not identical) is no big deal. The mutation rate directly observed and demonstrated accounts for the 35 million SNPs and that's just a maybe. There are still around 5 million indels adding up to 90 million nucleotides that are not so easily explained away, in fact, they made no attempt to do so.

One or two amino acids out of at least a hundred differ in each protein. Is that a substantial difference? You have failed to show how it is. And I am getting quite annoyed at what seems to be a consistent bias towards misinterpreting data - first the chromosome 22 study and now the 29% figure.

A single nucleotide being changed can cause cancer, tumors, mental retardation or maybe something like this:

"The research of Alzheimer's disease (AD) genetics has been extremely prolific over the past decade, and currently more than 10 genes are reported to show either positive or negative evidence for disease association per month. Here, we review all 90 studies from 2003 reporting a total of 127 association findings between candidate genes and AD. While most positive results were largely contradictory, we identified three loci&#8212;on chromosomes 6p21, 10q24, 11q23&#8212;that yielded positive results in three or more independent studies, in addition to the well-established AD association with the gene encoding apolipoprotein E (APOE). Based on these data, we suggest that it may be prudent for investigators to pay closer attention to issues such as power, replicability and haplotype structure prior to initial publication. This should serve to greatly decrease the likelihood of false positive and false negative findings reported in future years."​

http://hmg.oxfordjournals.org/cgi/content/full/13/suppl_1/R135

The question that is never raised (because of the obvious implications) is how this was avoided and the brain tripled in size and complexity? You don't have an answer but I would be very interested in your attempt at a substantive response.
 
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Robert the Pilegrim

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mark kennedy said:
26%... 96%... 80% ... similar not identical...
Gene pair 1:

abcabcabca
abcabcabcx

Gene pair 2:

xyzxyzxyzx
xyzxyzxyzm

Gene pair 3:

mnomnomnom
mnomnomnoa

Gene pair 4:

rstrstrstr
rstrstrstr

25% of the above "genes" are identical.

100% are similar.

They are also 92.5% identical.
 
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gluadys

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Poke said:
A link to an abstract doesn't do much good. But, it doesn't matter.

Sorry, that is the extent of the access I have. But it is enough to show that the study exists and that you can see the full paper if you fulfill the conditions for gaining access. Your choice.


You're choosing to ignore the qualitative difference between chimps and humans vs. between two fruitfly populations.

You are choosing to ignore that the measured difference in expressed genes (not the whole genome) between the two fruitfly populations is greater than the measured difference between chimps and humans. Why is the latter qualitative and the first not?

That's my point.

Could you explain what you think this point is? I don't see anything to be gained in criticising a research project for not doing what it did not set out to do.
 
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shernren

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One of the expressed purposes of the chimpanzee genome project is to explain human evolution. They failed miserably but we are supposed to pretend that the difference jumping from 99% to 96% (and I do mean simular not identical) is no big deal. The mutation rate directly observed and demonstrated accounts for the 35 million SNPs and that's just a maybe. There are still around 5 million indels adding up to 90 million nucleotides that are not so easily explained away, in fact, they made no attempt to do so.

Do you have any good reason to believe that the indel rate is far higher than expected? Do you have literature showing what actual measured indel occurrence rates are? Or is this purely an argument from personal incredulity?

A single nucleotide being changed can cause cancer, tumors, mental retardation or maybe something like this

What are you arguing against now? The magnitude of genotypic changes, or phenotypic changes?

If phenotypic, then the proper unit of measurement is the darwin, and a brain expansion by triple in 5 million years is roughly 0.25 darwins, whereas experiments have observed rates on the order of thousands of darwins. Thus there is no difficulty in evolution accounting for the phenotypically observed rates of change.

In terms of the energetic costs involved in evolution, I don't have firsthand experience so you would have to ask someone like sfs to confirm my conjecture. But my conjecture is that the human genome is an attractor in the genomic phase space, and that the energetic costs of mutating into it are far lower than the energetic costs of mutating out of it. Your argument is akin to saying that since a car cannot roll uphill without human intervention, therefore it cannot roll downhill without human intervention either: just because evolution away from the fixed human norm has high energetic costs, does not automatically prove that evolution into the fixed human norm has high energetic costs.

In terms of genotypic divergence, the very fact that a small genotypic change can cause a large phenotypic change in fact lends credence to the idea that humans may have evolved from earlier anthropoids. For if even a single nucleotide's worth of difference can cause cancer, Down's Syndrome, or Alzheimer's Disease, is it really that incredulous to believe that 1.5% divergence in a genome (quoting the earlier 98.5% figure), or 48 million base pairs (out of 3.2 billion over the total human genome), cannot adequately explain the difference between chimps and humans?


Are you referring to this?

If we consider only highly-similar regions between chimp and human then we are on the order of 97-98% similar. However, if we take into account larger insertions and deletions, then the similarity drops to 94-95%. At the gene level, we have found all of the known human chromosome 21 genes in the equivalent finished regions of chimpanzee chromosome 22. In most cases they appear to be identical, but in the cases where they are not we have taken a closer look and have confirmed our sequence was correct by additional experiments in multiple chimps and humans.

I have already discussed chromosome 22 data here: http://www.christianforums.com/showpost.php?p=24830925&postcount=56 ... is there any reason you believe my analysis to be wrong? Other than personal incredulity?
 
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mark kennedy

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shernren said:
Do you have any good reason to believe that the indel rate is far higher than expected? Do you have literature showing what actual measured indel occurrence rates are? Or is this purely an argument from personal incredulity?

Just apply the mutation rate to the current level of divergance. The SNPs don't seem all that difficult but the indels dwarf them by a considerable amount. One of the biggest problems is that there is not indel rate because they don't happen anywhere near as frequently as they would have had to. You also have no basis for the much needed beneficial affect, particularly on the brain and liver.



What are you arguing against now? The magnitude of genotypic changes, or phenotypic changes?

Neither really, just the level of divergance and how is could be accounted for, because it cant'. Do the math; 35,000,000 + 90,000,000 + 20,000,000 / 7,000,000. Then you take that ratio and apply it to the existing mutation rate for higher primates like apes and humans.

If phenotypic, then the proper unit of measurement is the darwin, and a brain expansion by triple in 5 million years is roughly 0.25 darwins, whereas experiments have observed rates on the order of thousands of darwins. Thus there is no difficulty in evolution accounting for the phenotypically observed rates of change.

I don't know where you are getting this but it is a little silly for a serious question. For one thing its 5-7 million and if it makes it easier you can stretch it out to 10 million years. You have the mutation rate or at least a rough idea of what it should be, just go from there.

In terms of the energetic costs involved in evolution, I don't have firsthand experience so you would have to ask someone like sfs to confirm my conjecture. But my conjecture is that the human genome is an attractor in the genomic phase space, and that the energetic costs of mutating into it are far lower than the energetic costs of mutating out of it. Your argument is akin to saying that since a car cannot roll uphill without human intervention, therefore it cannot roll downhill without human intervention either: just because evolution away from the fixed human norm has high energetic costs, does not automatically prove that evolution into the fixed human norm has high energetic costs.

No, the energetic costs would be if you needed a new part or adaptation in order for the car to go up the hill. If you needed an engine that was three times the size you would need three times the energy...

Sorry...out of time again.
 
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shernren

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Just apply the mutation rate to the current level of divergance. The SNPs don't seem all that difficult but the indels dwarf them by a considerable amount. One of the biggest problems is that there is not indel rate because they don't happen anywhere near as frequently as they would have had to.

Neither really, just the level of divergance and how is could be accounted for, because it cant'. Do the math; 35,000,000 + 90,000,000 + 20,000,000 / 7,000,000. Then you take that ratio and apply it to the existing mutation rate for higher primates like apes and humans.

I don't know where you are getting this but it is a little silly for a serious question. For one thing its 5-7 million and if it makes it easier you can stretch it out to 10 million years. You have the mutation rate or at least a rough idea of what it should be, just go from there.

I've explained what darwins are and why I feel justified to use them. Given that the initial characteristic of a population has a quantitative measure x1, and its final characteristic after a time t of divergence (in millions of years) is measurable on the same scale as x2, the divergence in darwins is

ln (x2/x1) / t = [ln (x2) - ln (x1)] / t

This is a useful unit in cases where phenotypic divergence is being measured, where the direct genes responsible for the divergence still have not been identified causing an inability to directly apply predictions concerning genetic mutation.

I'll let TO talk to you: http://www.talkorigins.org/faqs/comdesc/section5.html#morphological_rates

No, the energetic costs would be if you needed a new part or adaptation in order for the car to go up the hill. If you needed an engine that was three times the size you would need three times the energy...

But I'm not comparing a car to a person. I think I'm doing a crappy job explaining my idea of the phase space, I keep forgetting that people don't think in math like me :p

Okay. Imagine a flat sheet of rubber with a lined grid and the x-axis representing a particular configuration of brain genes and the y-axis representing a particular configuration of liver genes. Imagine a little ball which I can place on the rubber sheet: its current position represents the particular state of those genes in the human genome at any given time. If the ball is at (2,1), this corresponds to a particular set of genes, and if mutation occurs the ball shifts from (2,1) to say (2,2).

Now, let's say humankind's current genome is represented by (0,0) the origin, and the chimp's genome is represented by (1,1). The spot (0,0) corresponds to the brain and liver genes we see in humans today. What you are saying is that a change as small as from (0,0) to say (0,0.1) is hugely deleterious to humans. If humanity can't even make such a small step, how can I say that they could get all the way from some point between (1,1) and (0,0) to (0,0) without getting exterminated along the way?

But to me, your evidence is not conclusive because there is a plausible evolutionary interpretation of the data. In my view, natural selection is pulling the rubber sheet down so there is a hole at (0,0). If I drop a ball anywhere near (0,0), it naturally tends to roll down into (0,0). Of course, a ball can't roll out of (0,0) to even (0,0.1) without large energetic costs, and that is precisely what you are observing. In fact, this proves my point - many disease alleles in genetic disease are actually wild-type alleles in chimps, and if mutating from a current human allele to a chimp wild-type allele causes great deleterious effects, wouldn't it be a corollary that a mutation from a chimp wild-type allele into the current human allele would cause great beneficial effects?
 
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shernren

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Sorry, this is really a spillover of a thread that mark and I left unfinished weeks earlier. What's basically happening is that he's saying that:

Human and chimp genomes are actually very different
and evolutionary observed rates of mutation don't account for this difference
therefore humans must have been separately created from chimps.

while I'm saying that he hasn't really shown that mutations occur too slowly to explain the change.

I hope you don't mind :p we'll move it to a new thread if you want.

To your OP:

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?

I'd ask what's wrong with God creating this way? If God wanted 99% of our genes to be shared with chimps as well, does that prove that it wasn't Him who created us?
 
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Robert the Pilegrim

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Alpine said:
Hey, since this is my thread, could you guys...like...speak in layman's terms?

Cause I am not understanding half of what you're saying at this point
Can't be done ;)
DNA = primary genetic building plan.

amino acids = type of chemical (among other things found in proteins and meteorites from outer space)

nucleotides = building blocks of DNA each nucleotide has an amino acid in it

base pairs = two nucleotides that form a rung in the twisted ladder/double helix that is DNA.


SNP = single nucleotide polymorphism, a change consisting of different nucleotide being substituted

indels = changes to the DNA consisting insertions or deletions of nucleotides

Ah from a glossary[/url at the national institutes of health... you should probably go there and read the definitions for exon, intron, codon

From the [url=http://www.ornl.gov/sci/techresources/Human_Genome/publicat/primer/prim1.html]the human genome projects primer:

The human genome is estimated to comprise more than 30,000 genes.

Human genes vary widely in length, often extending over thousands of bases, but only about 10% of the genome is known to include the protein- coding sequences (exons) of genes. Interspersed within many genes are intron sequences, which have no coding function. The balance of the genome is thought to consist of other noncoding regions (such as control sequences and intergenic regions), whose functions are obscure.​


http://www.indiana.edu/~cheminfo/09-16.html
http://www.isogg.org/tree/ISOGG_Glossary.html
http://www.dorak.info/genetics/glosgen.html
 
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vossler

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Hey if anyone is bored and wants to hear some very educated evolutionists argue for 30 pages about whether man evolved from an ape or a monkey, here you go:

http://www.christianforums.com/t3007475-did-you-say-evolution-doesnt-teach-man-evolved-from-ape.html

I have to admit I read the entire thing and found it quite entertaining, way over my head, but entertaining nonetheless. Some of you however will probably see it as a form of enlightenment which would fit right into your worldview. Therefore it should appeal to all! :D
 
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Robert the Pilegrim

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mark kennedy said:
One of the biggest problems is that there is not indel rate because they don't happen anywhere near as frequently as they would have had to.
The underlined portion seems to include typos or something, I can't understand it.
 
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Interesting2me

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Alpine said:
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?
:scratch: "All flesh is not the same flesh... " [I Cor.15:37-49]! "Whose report will you believe ... "? I will believe the report of The Lord [II Chron.20:20c,d ]!:thumbsup:

Whatever happenned to the cloned "Dolly The Sheep"? Read Gen.1:14-18, 19-(*24)25, 26-*28; *THE BOTTOM LINE!:amen:
 
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Alpine

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Interesting2me said:
:scratch: "All flesh is not the same flesh... " [I Cor.15:37-49]! "Whose report will you believe ... "? I will believe the report of The Lord [II Chron.20:20c,d ]!:thumbsup:

Whatever happenned to the cloned "Dolly The Sheep"? Read Gen.1:14-18, 19-(*24)25, 26-*28; *THE BOTTOM LINE!:amen:

ok, what do those scriptures tell you?
 
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mark kennedy

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Robert the Pilegrim said:
The underlined portion seems to include typos or something, I can't understand it.

I was in a hurry, what I was trying to say is that there is no rate for the occurance of indels. The mutation rate for humans is something like 10^-8, which pretty much could account for the SNPS. There are, as I have been saying, 5 million indels totaling 90 million nucleotides. The directly observed and demonstrated mutation rate does not in any way shape or form account for this level of divergance.
 
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