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Another implication of the finding is that we are more different to our closest living relative, the chimpanzee, than previously assumed from earlier studies. Instead of being 99 per cent similar, we are more likely to be about 96 per cent similar.
I wonder how similar we are to styrofoam?
Scientists have discovered a dramatic variation in the genetic make-up of humans that could lead to a fundamental reappraisal of what causes incurable diseases and could provide a greater understanding of mankind.
The discovery has astonished scientists studying the human genome - the genetic recipe of man. Until now it was believed the variation between people was due largely to differences in the sequences of the individual " letters" of the genome.
It now appears much of the variation is explained instead by people having multiple copies of some key genes that make up the human genome.
Until now it was assumed that the human genome, or "book of life", is largely the same for everyone, save for a few spelling differences in some of the words. Instead, the findings suggest that the book contains entire sentences, paragraphs or even whole pages that are repeated any number of times.
The findings mean that instead of humanity being 99.9 per cent identical, as previously believed, we are at least 10 times more different between one another than once thought - which could explain why some people are prone to serious diseases.
The studies published today have found that instead of having just two copies of each gene - one from each parent - people can carry many copies, but just how many can vary between one person and the next.
Right. I am aware of that. But before it was 99.9% we were related to chimps. Now apparently it must be 96%. What next? 85%?You know, we had a lot of useful discussion on the thread you started on the same issue 2 months ago.Maybe you could go and read up from it and then if you have any questions ask away!
http://www.christianforums.com/t3068160
Apparently we are only 96% similar to chimps now.
I doubt so. The sequencing this time took into account every difference you can think of - indels, single-base substitutions, pericentric inversions, the lot. I don't see any indication that this "heterochromatin" was not sequenced by the group.Right. I am aware of that. But before it was 99.9% we were related to chimps. Now apparently it must be 96%. What next? 85%?
I doubt so. The sequencing this time took into account every difference you can think of - indels, single-base substitutions, pericentric inversions, the lot. I don't see any indication that this "heterochromatin" was not sequenced by the group.
In other words, AFAIK, there's simply nothing left lurking in either genome that could cause the divergence measurable to increase, other than possibly that new copy-number variation thing.
Apart from the information that Mark is talking about, which is over my head, it seems the study suggests errors in the way we read "similarity." A monkey arm may look alot like a human arm, but the evidence of common features at least shows a common origin -- whether it is common creator or common ancestory requires a lot more. To take the most simplistic analogy, the fact that they all use adenine, guanine, etc. does not prove a common hominid ancestor.
Apart from the information that Mark is talking about, which is over my head, it seems the study suggests errors in the way we read "similarity." A monkey arm may look alot like a human arm, but the evidence of common features at least shows a common origin -- whether it is common creator or common ancestory requires a lot more. To take the most simplistic analogy, the fact that they all use adenine, guanine, etc. does not prove a common hominid ancestor.
The study does suggest that reading similarities is over-rated, since slight inversion or repetition of common strings of code make huge differences.
That begs the question about what more we are missing simply in the complexity of how this equation works. Obviously I am prejudiced in my YEC views, but I do question your conclusion about the extent to which the problem has been comprehended.
And if arguing against YEC or TE, does a 6%, 10% or 20% swing really mean much when you can't read the whole code and figure out how we go from amino acid sequences to the ability to see a fast ball or get saved?
However, if one were to find mere similarity persuasive, the TE's would still have the high ground here.
The thing is, if these mutations are happening in the so called 'junk DNA' then they are happening in the genes. For every percentage point you are looking at 3 million base pairs. When you take into account the indels the number of base pairs jumps up 100 million base pairs. It is also know that there are a lot of differences in the brain and liver, way more then could be explained by random mutations.
Darwin admitted that the gradual development of the eye seemed unlikely in the extreme. When it came to the brain he just said the smallest human brain is about the same size of the largest ape brain. We now know that brains are built by highly specific and conserved genes that do not respond well to mutations.
Dispite their dramatic arguements to the contrary they don't have a clue how it could have happened.
Firstly, mark's argument thus far has been from mere dissimilarity. Mark has three major lines of argument:
"Indels make divergence jump, therefore evolutionary researchers are hiding something";
"Human-chimp speciation needs changes in brain and liver genes and they can't happen because I don't believe they can";
"Fossil humans are all human or all ape".
out of which the first one is the most discussed at the moment and is the one he draws the most flak for due to repeated arguments over units
If you look properly his first argument is an argument from mere dissimilarity - and if I point out how similar the genomes actually are, that argument goes away.
In terms of the portion that actually codes for proteins (coding genes), chimp and human sequences are 99.4% identical. That's a lot of similarity that supposedly can't be explained by random mutation + natural selection. Furthermore, what are shared between the species are not just "design features" but also genetic features which are neutral or even deleterious. For example, in both chimps and humans, the GULOP gene is broken in the same way, causing both chimps and humans (as well as other primates, all with the same genetic defect) not to be able to synthesize vitamin C enzymatically. If a shared design feature indicates a common designer, does a shared design flaw indicate a common Un-designer?
Please back your assertions. In particular, why do you keep acting like the indels are a big deal, or too much for evolution to handle, or more than scientists predicted?
Scientists see indels contribute 4-5 times, and even more, nucleotide variation than single-base substitutions routinely, across the phylogenetic tree. There is nothing amazing about seeing indels "dwarf" single-base substitutions by 4-5 times. It happens with other organisms and yet you never raise any complaints about those:
It was recently shown that indels are responsible for more than twice as many unmatched nucleotides as are base substitutions between samples of chimpanzee and human DNA. A larger sample has now been examined and the result is similar. The number of indels ishttp://www.pnas.org/cgi/content/full...urcetype=HWCIT1/12th of the number of base substitutions and the average length of the indels is 36 nt, including indels up to 10 kb. The ratio (Ru) of unpaired nucleotides attributable to indels to those attributable to substitutions is 3.0 for this 2 million-nt chimp DNA sample compared with human. There is similar evidence of a large value of Ru for sea urchins from the polymorphism of a sample of Strongylocentrotus purpuratus DNA (Ru = 3-4). Other work indicates that similarly, per nucleotide affected, large differences are seen for indels in the DNA polymorphism of the plant Arabidopsis thaliana (Ru = 51). For the insect Drosophila melanogaster a high value of Ru (4.5) has been determined. For the nematode Caenorhabditis elegans the polymorphism data are incomplete but high values of Ru are likely. Comparison of two strains of Escherichia coli O157:H7 shows a preponderance of indels. Because these six examples are from very distant systematic groups the implication is that in general, for alignments of closely related DNA, indels are responsible for many more unmatched nucleotides than are base substitutions. Human genetic evidence suggests that indels are a major source of gene defects, indicating that indels are a significant source of evolutionary change.
I'd expect a quotemine like this from a less experienced creationist but from you? Are you grasping at straws now?
This only shows that he was a good rhetoricist and understood well both the emotional power and the logical vacuity of the argument from incredulity.
Firstly, mark's argument thus far has been from mere dissimilarity. Mark has three major lines of argument:
"Indels make divergence jump, therefore evolutionary researchers are hiding something";
"Human-chimp speciation needs changes in brain and liver genes and they can't happen because I don't believe they can";
"Fossil humans are all human or all ape".
out of which the first one is the most discussed at the moment and is the one he draws the most flak for due to repeated arguments over units
If you look properly his first argument is an argument from mere dissimilarity - and if I point out how similar the genomes actually are, that argument goes away.
In terms of the portion that actually codes for proteins (coding genes), chimp and human sequences are 99.4% identical. That's a lot of similarity that supposedly can't be explained by random mutation + natural selection. Furthermore, what are shared between the species are not just "design features" but also genetic features which are neutral or even deleterious. For example, in both chimps and humans, the GULOP gene is broken in the same way, causing both chimps and humans (as well as other primates, all with the same genetic defect) not to be able to synthesize vitamin C enzymatically. If a shared design feature indicates a common designer, does a shared design flaw indicate a common Un-designer?
Please back your assertions. In particular, why do you keep acting like the indels are a big deal, or too much for evolution to handle, or more than scientists predicted?
Scientists see indels contribute 4-5 times, and even more, nucleotide variation than single-base substitutions routinely, across the phylogenetic tree. There is nothing amazing about seeing indels "dwarf" single-base substitutions by 4-5 times. It happens with other organisms and yet you never raise any complaints about those:
It was recently shown that indels are responsible for more than twice as many unmatched nucleotides as are base substitutions between samples of chimpanzee and human DNA. A larger sample has now been examined and the result is similar. The number of indels ishttp://www.pnas.org/cgi/content/full...urcetype=HWCIT1/12th of the number of base substitutions and the average length of the indels is 36 nt, including indels up to 10 kb. The ratio (Ru) of unpaired nucleotides attributable to indels to those attributable to substitutions is 3.0 for this 2 million-nt chimp DNA sample compared with human. There is similar evidence of a large value of Ru for sea urchins from the polymorphism of a sample of Strongylocentrotus purpuratus DNA (Ru = 3-4). Other work indicates that similarly, per nucleotide affected, large differences are seen for indels in the DNA polymorphism of the plant Arabidopsis thaliana (Ru = 51). For the insect Drosophila melanogaster a high value of Ru (4.5) has been determined. For the nematode Caenorhabditis elegans the polymorphism data are incomplete but high values of Ru are likely. Comparison of two strains of Escherichia coli O157:H7 shows a preponderance of indels. Because these six examples are from very distant systematic groups the implication is that in general, for alignments of closely related DNA, indels are responsible for many more unmatched nucleotides than are base substitutions. Human genetic evidence suggests that indels are a major source of gene defects, indicating that indels are a significant source of evolutionary change.
I'd expect a quotemine like this from a less experienced creationist but from you? Are you grasping at straws now?
This only shows that he was a good rhetoricist and understood well both the emotional power and the logical vacuity of the argument from incredulity.
I guess my question for Mark is why don't you accept the sort of "hyperevolution" of the human brain?
It are so annoying that the media world swallow every word they say, if they would be smart they would take to notice to how many times they ahve changed there mind .... I mean if you keep on changing your mind what trustworthiness will you end up with ...Apparently we are only 96% similar to chimps now.
What "commonly known effect"? If it's common, I must be out of the loop.Mostly due to the commonly known affect of mutations on the human brain.
No "random mutations"? Are you suggesting God-directed mutations instead?I dare say that most of the changes surronding adaptation do not incude random mutations.
With only two individuals of each "kind" surviving the Flood, I don't see how your gene pool could be considered large at all.That major adaptive radiation probably was the result of a much larger gene pool and far fewer psuedo genes that now are disfunctional because of random mutations.
Right. I am aware of that. But before it was 99.9% we were related to chimps. Now apparently it must be 96%. What next? 85%?
That's not even an argument, it's a glaring fact. The indels laid undiscovered for a half a century while we were told or DNA was virtually identical to apes. Then the indels are discovered and they represent 3x more diversity. It's as simple as that.
My contention is that it doesn't happen and this whole myth of random mutations plus natural selection is highly presumptive. The genetic mechanism for the human accelerated regions remains a mystery despite extensive research in the field. Nevertheless it is tauted as an indisputable fact which begs the question of proof.
This is 100% consistent with the Creationist position that the fossils are either ape or human. No one is suggesting that neither the apes nor humans have not or do not evolve, their alleles do change over time. It just seems odd that every fossil dug up in Africa is immediately identified as one of our ancestors. Some look more like chimpanzee and gorilla ancestors but that possibility is never explored apart from being a common ancestor. It's an a priori assumption that is distorting our understanding of the fossil record.
Most of which are bogus, you guys are trying to make the indels go away and it isn't going to happen. The mutations would still have to accumulate at either a constant rate or show marks of punctuated equilibrium and you have yet to do either. The debate has been over mutation rates and you missed the obvious fact that they don't have one for indels. I saw no reason to point that out while you ran in circles trying to refute something that did not exist.
I was not making an argument, I was offering quotes and links because I couldn't make heads or tails of the one in the OP. Then you bust in here trying to be confrontational which is an exercise in futility since all I did was present commonly understood facts.
First of all we were told and are currently being told that the DNA of Chimpanzees and Humans is 99% the same. This was found to be false and the protein coding genes may or may not be 99%, I would have to compare specific genes since I really don't trust evolutionists and their jacked up homology arguments. The GULOP gene is a psuedo gene that would produce vitamin C if it were functioning properly. Since it doesn't have any discernible selective pressure preserving it it is subject to random mutations. The mutations are not identical they are random and sometimes you find the same ones in the same place but not always. Check it out in a gene browser and you will see what I mean.
They have to determine the rate at which they occur in human populations, currently estimated to be close to the point mutation rate. This will happen in time but until then the indels are of considerable length and are not easily dismissed the way you are trying to do.
You missed the bottom line:
"Human genetic evidence suggests that indels are a major source of gene defects, indicating that indels are a significant source of evolutionary change."
They are a major source for the evolution of disease and disorder not the accumulation of adaptive traits. This is precisely why it is vital to understand that genes involved in neural development do not respond well to random mutations. You can dance around this fact as much as you like but adaptive evolution is the prize.
I responded to an OP with a link I thought I could improve on, so I offered a couple of sources. Then someone mentioned that it was a little complicated so I tried to boil it down to basic genetics. Those were general information posts only, not the elaborate arguments I aim at evolutionist zealots.
To suppose that the eye, with all its inimitable contrivances for adjusting the focus to different distances, for admitting different amounts of light, and for the correction of spherical and chromatic aberration, could have been formed by natural selection, seems, I freely confess, absurd in the highest possible degree. Yet reason tells me, that if numerous gradations from a perfect and complex eye to one very imperfect and simple, each grade being useful to its possessor, can be shown to exist; if further, the eye does vary ever so slightly, and the variations be inherited, which is certainly the case; and if any variation or modification in the organ be ever useful to an animal under changing conditions of life, then the difficulty of believing that a perfect and complex eye could be formed by natural selection, though insuperable by our imagination, can hardly be considered real. How a nerve comes to be sensitive to light, hardly concerns us more than how life itself first originated; but I may remark that several facts make me suspect that any sensitive nerve may be rendered sensitive to light, and likewise to those coarser vibrations of the air which produce sound.http://www.literature.org/authors/darwin-charles/the-origin-of-species/chapter-06.html
Notice that Ole Flycatcher was openly admitting that natural selection was not much of an explanation for the neural system. He was at least honest about that and didn't consider natural selection to be how life originated. The Creationist knows how life was originated and the Naturalist has not explanation other then some nebulous random accumulation of beneficial traits.
Is an argument from credulity any better, Sir Francis Bacon would seem to have thought otherwise:
Lastly, there are idols which have immigrated into men's minds from the various dogmas of philosophies, and also from wrong laws of demonstration. These I call Idols of the Theater; because in my judgment all the received systems are but so many stage-plays, representing worlds of their own creation after an unreal and scenic fashion. Nor is it only of the systems now in vogue, or only of the ancient sects and philosophies, that I speak: for many more plays of the same kind may yet be composed and in like artificial manner set forth; seeing that errors the most widely different have nevertheless causes for the most part alike. Neither again do I mean this only of entire systems, but also of many principles and axioms in science, which by tradition, credulity, and negligence have come to be received.FRANCIS BACON, "The Idols of the Mind" From Novum Organum
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