Creation & EvolutionForum for the discussion of this important topic. This forum is open to non-believers. There is a Christians-only forum in the Christians-only section too.
Np. From the number of times I've been called a "he" here, most people don't look at the little pink icon. It shouldn't really matter anyway. Science is science, and arguments are arguments, and the value of neither depends on a person's karyotype.
Nice try but I know the difference between a substitution in a nucleotide sequence and a triplet coden interrupted by a change in an amino acid sequence in a protein coding gene resulting in a truncated protein.
Which is all well, except it's not the difference we were talking about. We are talking about the difference between a substitution and a frame shift. Substitutions don't normally cause frame shifts, yet IIRC you said a truncated protein (i.e., a premature stop) due to a frame shift is their most common outcome.
They don't impress me, as a matter of fact they are wrong so often that I am amazed that an actual scientist would consider them credible.
Well, I dimly recall one argument in one of the short posts that I thought was dodgy, but by and large, what they say agrees with what I know if I know something about the subject, and I don't remember any glaring errors of reasoning apart from that one bit I once noted (and I should go back to check if it really is dodgy). And, again, the FAQs/essays tend to cite tons of primary sources where you can check the evidence.
That might make sense to you but it entirely too general after the detailed specifics I offered you.
Which "detailed specifics" are you talking about? I was referring to your odd substitution/frame shift confusion, nothing else.
A conclusion made before there was such a thing as genetics, molecular biology or modern paleontology.
And strangely enough, most geneticists, molecular biologists and palaeontologists think their field strengthens it.
Yea I can tell since you have less and less interest in it.
And what does that remark even mean?
No it's easy, you quote what they said, make the correction, cite the source and move on. What other people say is only important when you are depending on a mob psychology to affirm your position.
And again, you are making an argument from the number of times a point is made rather than the merits of the point. Being popular doesn't make an argument right, but it equally doesn't make it wrong.
Gosh, are we really arguing about my entirely subjective decisions to reiterate or not reiterate a point?
You have gotten to the point where you are ignoring every substantive and scientific point and talking in vague generalities.
What substantive scientific point is there in this?
Originally Posted by Mark Kennedy, post 77
That's not the case and the rationalization you are using as a characterature is more of a performance then a valid criticism. This is how it works, responding to the OP is generally a string of ad hominem attacks undermining any visage of credibility on the part of the creationist. This is usually followed by a series of pedantic and circular questions chosen for the dramatic effect rather then their substantive content. Then enters the scientific type who will cherry pick a few points and if pressed will even make a few substantive points. This individual will be limited to the point made previously by the evolutionists who make the initial contact which is Naraoia's primary difficulty except he is probably not aware of it.
This is the paragraph I responded to. Once again, there is not a single concrete example, and not a single trace of scientific information here, so I don't know why responding with a general and non-scientific opinion means that I'm ignoring all of your substantive, scientific points.
Trust me and the real world comparisons that 98% is just plain wrong.
I'm perfectly happy to trust you after you've cited trustworthy sources and made it clear what kind of similarity you're talking about. As I said, I don't have any particular attachment to that number.
It compares the nucleotide sequence of humans and chimpanzees. Now, when it comes to whole genomes being compared it did not happen until the Chimpanzee Consortium finally released it's initial sequence but even then it was about 95%.
Fine with me.
See I have correctly bolded the parts that account for the indels (gaps)
the overall sequence difference was estimated to be approximately 5% by taking regions of insertions or deletions (indels) into account.
Yup, I saw that. But the 98% estimate didn't include indels, at least not the 98% estimate mentioned in that paper. 1.23%-2% divergence was estimated for substitutions in aligned sequences by earlier studies, and for the same measure of divergence, these authors came up with 1.44%. No, this is not the overall divergence, all mutations included.
I think we can agree on that and move on now.
Which are, gross structural changes affecting gene products are far more common than previously, an estimated 20.3% of the PTR22 proteins
Far more common than previously thought, you mean? Yes, but what is the significance of that? If our small amount of sequence divergence translates to relatively big differences in the products, it only becomes easier to reconcile the levels of genetic and phenotypic difference between humans and chimps.
we compared the gene expression profiles of HSA21q genes between humans and chimpanzees in two tissues: 202 genes in brain (cingulate cortex, HG U95Av2, B, C, D and E) and 96 genes in liver (HG U95Av2). We detected 60 genes expressed in brain (this study) and 40 in liver41 in at least one species. Of these, 9 in the brain and 12 in the liver showed a significant change in expression level between humans and chimpanzees in the range of a 1.5–10-fold difference
Where does gene expression come into this? I thought we were talking about sequence divergence??
Furthermore, what are you trying to argue with these expression data? (I don't know if you addressed the mouse Huntington's expression data in another post, so don't respond if you already did.)
That know divergence has grown to include the many genes that have been gained and lost. Now the statistics make it more like 96% and you have completely missed that point or ignored it.
I didn't miss it (remember, that's where I went with the "mob" and pointed out that gene gain/loss differences can't be compared with nucleotide-level differences). I thought the discussion has drifted away from the duplication/loss study long ago, but if you really want to return to it, go ahead.
Congratulations! You have managed to side step every single peer reviewed article on the subject except for one.
I'm not sure what you're referring to. Care to elaborate?
This seems a common communication problem with you. I say something about data you use or an argument you make, and then you reply with something that doesn't directly address what I wrote and doesn't make it clear what (if anything) it does address. Maybe it's just me, or maybe it's you having problems conveying your point.
__________________ "There is much we do not understand about the history of life, and the same will be true of our grandchildren. But, then, if we knew all there was to know, scientific interest would cease. Textbooks may portray science as a codification of facts, but it is really a disciplined way of asking about the unknown." - A.H. Knoll, Life on a Young Planet
"Come on, put your bloody thinking caps on!" - Dr Tony Prave, geology lecture
Np. From the number of times I've been called a "he" here, most people don't look at the little pink icon. It shouldn't really matter anyway. Science is science, and arguments are arguments, and the value of neither depends on a person's karyotype.
Which is all well, except it's not the difference we were talking about. We are talking about the difference between a substitution and a frame shift. Substitutions don't normally cause frame shifts, yet IIRC you said a truncated protein (i.e., a premature stop) due to a frame shift is their most common outcome.
Well, I dimly recall one argument in one of the short posts that I thought was dodgy, but by and large, what they say agrees with what I know if I know something about the subject, and I don't remember any glaring errors of reasoning apart from that one bit I once noted (and I should go back to check if it really is dodgy). And, again, the FAQs/essays tend to cite tons of primary sources where you can check the evidence.
Which "detailed specifics" are you talking about? I was referring to your odd substitution/frame shift confusion, nothing else.
And strangely enough, most geneticists, molecular biologists and palaeontologists think their field strengthens it.
And what does that remark even mean?
And again, you are making an argument from the number of times a point is made rather than the merits of the point. Being popular doesn't make an argument right, but it equally doesn't make it wrong.
Gosh, are we really arguing about my entirely subjective decisions to reiterate or not reiterate a point?
What substantive scientific point is there in this?This is the paragraph I responded to. Once again, there is not a single concrete example, and not a single trace of scientific information here, so I don't know why responding with a general and non-scientific opinion means that I'm ignoring all of your substantive, scientific points.
I'm perfectly happy to trust you after you've cited trustworthy sources and made it clear what kind of similarity you're talking about. As I said, I don't have any particular attachment to that number.
Fine with me.
Yup, I saw that. But the 98% estimate didn't include indels, at least not the 98% estimate mentioned in that paper. 1.23%-2% divergence was estimated for substitutions in aligned sequences by earlier studies, and for the same measure of divergence, these authors came up with 1.44%. No, this is not the overall divergence, all mutations included.
I think we can agree on that and move on now.
Far more common than previously thought, you mean? Yes, but what is the significance of that? If our small amount of sequence divergence translates to relatively big differences in the products, it only becomes easier to reconcile the levels of genetic and phenotypic difference between humans and chimps.
Where does gene expression come into this? I thought we were talking about sequence divergence??
Furthermore, what are you trying to argue with these expression data? (I don't know if you addressed the mouse Huntington's expression data in another post, so don't respond if you already did.)
I didn't miss it (remember, that's where I went with the "mob" and pointed out that gene gain/loss differences can't be compared with nucleotide-level differences). I thought the discussion has drifted away from the duplication/loss study long ago, but if you really want to return to it, go ahead.
I'm not sure what you're referring to. Care to elaborate?
This seems a common communication problem with you. I say something about data you use or an argument you make, and then you reply with something that doesn't directly address what I wrote and doesn't make it clear what (if anything) it does address. Maybe it's just me, or maybe it's you having problems conveying your point.
I am going to bow out on making comments in the thread, for one reason that I never did care much for genetics.
Couple of comments tho. Since I am not looking at the details of the genetics discussion maybe some other aspects are more clear to me.
Most obvious is that the reason for what looks like a communication problem is that this is not a fair and honest discussion.
One, is that mk makes fallacious assertions, and will take no responsibility to correct, acknowledge, or stop doing it.
Another is that he is, as he has stated, coming from a mind set, paradigm if you like, that all scientists are hopelessly biased and incapable of ever doing objective work.
By the same token, (as he stated) no creationist can-.he says- ever get published and no matter how valid their work is, it will be ignored because it is from that source and they dont buy into the great a priori assumption of the evos.
Also that human being are not apes, that they are a special creation and that this is Truth.
Basically you seem to be arguing against the Truth of the Bible, but talking about genetics.
If that is worth discussing, it would still be a much cleaner discussion if it stayed on topic, with a moratorium on all the dissertations on the perceived personal qualities of others.
as in-
"That's not the case and the rationalization you are using as a characterature is more of a performance then a valid criticism. This is how it works, responding to the OP is generally a string of ad hominem attacks undermining any visage of credibility on the part of the creationist. This is usually followed by a series of pedantic and circular questions chosen for the dramatic effect rather then their substantive content. Then enters the scientific type who will cherry pick a few points and if pressed will even make a few substantive points. This individual will be limited to the point made previously by the evolutionists who make the initial contact which is Naraoia's primary difficulty except he is probably not aware of it."
So you have completely forgotten the OP and the paper this thread is based on I see.
Didn't that paper estimate a 6% difference, which would mean 94% identity, not 96%?
Interesting...your point?
That even though most of the morphological change is crammed into the last third of our lineage, the same need not be the case for the genetic change.
Just the ERVs in general, not just comparing the ones known to be the same.
You might want to refresh my memory, then. It's a bit patchy on ERVs.
I have no idea what you are talking about or why you have ignored the carefully prepared and detailed measurements of the various skulls.
Carefully prepared and detailed measurements of the various skulls?
The dataset in this study is a carefully prepared and detailed measurement. Of not just a few skulls, but hundreds of them belonging to diverse hominin taxa, all the way from 3.2 Mya to 10 000 years ago. Note this, from the summary:
Originally Posted by De Miguel & Henneberg 2001
When hominid CC by taxon with date as a covariate is subjected to ANOVA, taxon is responsible for 5% of the variance while date is responsible for the main portion, (89%). The relationship between CC and date is best characterised as a gradual time trend. It is proven by the ANOVA test for linearity, by G test for trend and by ASReml fitting of a linear function. The line of best fit to this time trend is a double exponential curve which explains 90% of the total variance in CC:
Key point to note: taxon accounts for only a tiny amount of variation - when the creature lived matters more than where it falls taxonomically. Now there might be an issue with specimens of uncertain affinities, but I wouldn't think it's so large that it could reverse the relative explanatory power of age and taxon (maybe a separate coding for H. erectus and ergaster would be useful, though; while I'm not aware of a major difference in their distribution of cranial capacities, that doesn't mean there isn't a difference).
Anyway, this could easily mean that whatever the precise lineage of H. sapiens is, a similar time trend applies to it.
If you say so.
Great, way to address a point!
Do you accept that averages on their own mean sod all, or do you not? If not, why? If yes, please stop giving me average cranial capacities as if they were a better indicator of trends than a detailed data set of two and a half hundred individual skulls.
I thought you were a biologist that understood that a molecular basis was crucial.
I am a not-yet-biologist, and I understand that you can study natural selection without looking at DNA.
It's a nice bonus if you find the genetic culprit for a particular change - but it is rather difficult if the change is in a massively polygenic trait that's difficult to experiment on... you don't genetically manipulate humans just to study how a gene affects their brain development.
It sucks if it turns out that you can't explain the change with genetics - but again, the change being in a trait under highly complicated genetic influences, it's not so easy to say whether you can or can't explain it!
Overall, though, if you observe that certain changes can occur under selection, you'd be daft to declare that they can't just because you don't know what's going on at the molecular level.
Granted, I haven't heard of an example of observed evolution in brain size in particular, but there are plenty of examples of selection at work. Chihuahuas I brought up because they are a spectacular and "condensed" example. Very different from their wolf ancestors (both morphologically and behaviourally, I think), but this difference was achieved entirely without knowledge of the underlying genetics, let alone conscious genetic manipulation. And whatever genes did it, it clearly worked.
As for the human brain, again, variation within modern humans is orders of magnitude larger than what would be required to get from australopiths to us in three, two or even half a million years. All you need to do is chop off the lower tail of the distribution in each generation, and so long as there are brain size-affecting mutations, the average will keep creeping upwards.
Sure, that only takes into account brain size, but are the differences between human and other ape brains really qualitative, or are they just differences of degree? (New cell types? New structures that are organised in novel ways? Or is it just extra lumps of the old cells and a little more cell adhesion?)
When you are talking about 18 substations in a regulatory gene that is only 118 nucleotides long and has not allowed more then two in 400 million years it is.
No, a tripling in 2 my never is the same as a doubling in 0.5 my. You shifted the goalposts and now you try to weasel out of it by bringing in a completely different argument.
Which, by the way, is fallacious if you are hung up on the contrast between the long conservation and the rapid divergence of HAR1, because that would only be odd if the selection on HAR1 was constant over the whole time period in question.
First you want to be touchy about how we do the statistics and then you want to talk in generalities. Typical.
How is a concrete experiment based on your specifications "generalities"?
How about a real comparison:
Listing unqualified average values from arbitrarily chosen species counts as a real comparison as opposed to a dataset of all published measurements of hominin skulls between 10 000 and 3.2 million years of age?
I assume you realize that natural selection cannot account for the actual divergence:
There is tentative evidence from in-depth analysis of divergence and diversity that natural selection is not the major contributor to the large-scale patterns of genetic variability in humans Nature 437, 69-87 (1 September 2005)
I assume you realise that what you quote says no such thing?
The quote (which, in fact, cites the conclusions of other papers) apparently refers to patterns of variation across different regions of the genome within the human species. Presumably, if natural selection is not the major contributor, it's drift...
*checks citations*
Ow, differential mutation rate, it seems. Both studies cited there (Hellmann et al. 2003 and Lercher & Hurst 2002) investigate the influence of local recombination rates on diversity in particular genomic regions, and the first one concludes that "regions that experience less recombination have reduced divergence to chimpanzee and to baboon, as well as lower levels of diversity. This observation suggests that mutation and recombination are associated processes in humans, so that the positive correlation between diversity and recombination may have a purely neutral explanation."
The paragraph also doesn't discuss whether selection can explain divergence per se, but the regional variation in divergence. As to that, they conclude that regional variation in mutation rates is probably a better explanation.
How does that undermine human-chimp common ancestry again?
I don't think that's actually a problem but artificial insemination could prove that one way or the other. There are a lot of cross overs and bottle necks involved, it's hard to say.
I see. So why do you question the genetic basis of selection when it comes to your own species? Do I smell double standards?
Just a mean average, I didn't expect you to follow.
How flattering of you. Just so we're clear about my meaning:
"Where does that come from" means "what's your source". If one of your earlier references contained that estimate, I missed it.
"What does 'the same' mean" means... what it says. Is it the same at orthologous positions, same as in no substitutions or indels, same as in has an orthologue in the other species... what? I thought you realised by now that there are two many kinds of similarity and difference for you to be able to simply say "the same" and expect everyone to understand what you mean. That's asking us to read your mind.
With that in mind, do you want to give it another go?
Dear trust me when I say, its not worth worrying about. You wont find any.
Way to be scientific, there.
It's not important anyway even though I have gotten a lot of millage out of that particular argument evolutionists have no answer for.
Can anyone help me translate this sentence?
Just listen to me one time, that is all I ask. I want to know what makes butterflies, birds and arctic wildlife adapt to changing conditions.
You read scientific literature, don't you? Have you tried anything other than human/chimp genetics? I'm sure there is a lot out there that could help you.
I can't give you concrete studies off the top of my head, but one specific example that's quite well-known is Pitx1 enhancer evolution and pelvic spine size in sticklebacks. I think there was also a genetic study of the famous beak of the famous finch a while ago. I've already mentioned teosinte and maize, though I can't remember if anyone looked at the actual loci or just estimated how many there are.
And then there's the textbook example of sickle-cell trait and its heterozygous advantage.
If you've seen all of this before, then give me some time and I could try to dig up something more obscure... though I don't think I know any more papers on the genetics of adaptation than you do.
Wait!
I think I can give you a precise citation, and it was your mentioning Arctic wildlife that reminded me of that. Here is one on the way lactate dehydrogenase adapted to functioning in extreme cold in Antarctic fish:
Fields PA, Somero GN (1998) Hot spots in cold adaptation: Localized increases in conformational flexibility in lactate dehydrogenase A4 orthologs of Antarctic notothenioid fishes. PNAS95:11476-11481
Adaptation, check, molecular mechanism, check.
I want to know what those molecular mechanisms are, even if it's speculative. That is the only reason I continue to pursue these discussions because every great once in a while I find another piece of the puzzle.
That's a worthy goal.
They are the effects of mutations on the human brain right?
Yes (though IIRC in both cases, a "disease allele" is only a risk factor), and if their only negative effect manifests long after humans typically stop reproducing, they aren't truly deleterious in the evolutionary sense.
__________________ "There is much we do not understand about the history of life, and the same will be true of our grandchildren. But, then, if we knew all there was to know, scientific interest would cease. Textbooks may portray science as a codification of facts, but it is really a disciplined way of asking about the unknown." - A.H. Knoll, Life on a Young Planet
"Come on, put your bloody thinking caps on!" - Dr Tony Prave, geology lecture
Argh, I so want to just take one of MK's posts and do a long detailed rebuttal of it. His stuff is almost as good as RB's statement that metatherian mammals hyperevolved from their eutherian "counterparts" to repopulate the world after the Flood.
I'll do it later this week when I have a day off.
__________________ Slug's 1st Law of YECism- Genesis 1-9 must be interpreted literally. Slug's 2nd Law of YECism- Any other verses can be interpreted liberally to support the 1st Law. Slug's 3rd Law of YECism- Make up any extra-Biblical claim, no matter how wild, to wave-away evidence in violation of the 1st Law.
"If God sent a wind from space, and blew waters off the surface, for example, the waters would go down. Just as if you take a cup full of water over a sink, and blow hard on it, a lot will go out of the cup. Elementary." -dad ^This statement nullifies his own argument by comparing a "present state" event to a "past state" event!
Forgive me but I am in the middle of a move and I am unable to respond to your posts as I want to. I find you responses as entertaining as I find them challenging and I assure you I will be responding as soon as I am able.
Don't take this wrong but you remind me of Jet Black. She was someone I imagined as a professor type in a rumpled tweed jacket and horn rimmed glasses. Imagine my supprise to find that she was an Asian gal with a pretty but serious smile. For some reason woman make great biologists and seem to have a real talent for genetics.
Don't lose patience just yet. I'll get to your posts as soon as I am able.
Grace and peace,
Mark
__________________
“Gärtner, by the results of these transformation experiments, was led to oppose the opinion of those naturalists who dispute the stability of plant species and believe in a continuous evolution of vegetation. He perceives in the complete transformation of one species into another an indubitable proof that species are fixed with limits beyond which they cannot change.” (G. Mendel)
Argh, I so want to just take one of MK's posts and do a long detailed rebuttal of it. His stuff is almost as good as RB's statement that metatherian mammals hyperevolved from their eutherian "counterparts" to repopulate the world after the Flood.
I'll do it later this week when I have a day off.
Cool! We can talk about the fossils some more. Your not a lot of fun when it comes to the biology and genetics stuff but your a hoot when it comes to fossils. I'll get the thread started in a couple of days and you can jump in when you are interested.
Cool beans, catch you later,
Mark
__________________
“Gärtner, by the results of these transformation experiments, was led to oppose the opinion of those naturalists who dispute the stability of plant species and believe in a continuous evolution of vegetation. He perceives in the complete transformation of one species into another an indubitable proof that species are fixed with limits beyond which they cannot change.” (G. Mendel)
Argh, I so want to just take one of MK's posts and do a long detailed rebuttal of it. His stuff is almost as good as RB's statement that metatherian mammals hyperevolved from their eutherian "counterparts" to repopulate the world after the Flood.
I'll do it later this week when I have a day off.
Please do. I have about a million deadlines and then exams coming up, and I really shouldn't be procrastinating on CF before the end of May.
(Of course, I will keep procrastinating, whatever I say about deadlines, but it would still be nice to have someone else willing to dissect long posts )
Originally Posted by mark kennedy
Naraoia,
Forgive me but I am in the middle of a move and I am unable to respond to your posts as I want to. I find you responses as entertaining as I find them challenging and I assure you I will be responding as soon as I am able.
Don't worry. In fact I'm relieved that I'll have time to do other things besides posting in this thread )
For some reason woman make great biologists and seem to have a real talent for genetics.
And all generalisations are false
__________________ "There is much we do not understand about the history of life, and the same will be true of our grandchildren. But, then, if we knew all there was to know, scientific interest would cease. Textbooks may portray science as a codification of facts, but it is really a disciplined way of asking about the unknown." - A.H. Knoll, Life on a Young Planet
"Come on, put your bloody thinking caps on!" - Dr Tony Prave, geology lecture
By the way, I found the New Scientist feature on personality. The article is here, but it needs subscription, so relevant part quoted:
Originally Posted by New Scientist, 9 February 2008
For example, there are two common forms of the serotonin transporter gene which codes for the substance that removes the mood-affecting neurotransmitter serotonin from the gaps between neurons. People with at least one copy of the short form of the gene have higher neuroticism scores than people with two copies of the long form. The genetic findings also correlate with the neuroscientific ones. In the brain scanner, individuals with one or more short forms of the gene show a greater spike of amygdala activity when they are presented with a fearful face than do individuals with two long forms.
It seems that an earlier article (13 September 2003) covered this in more detail, and it mentions another example, a dopamine receptor whose alleles correlate with extroversion.
If you are interested, I hunted down papers:
Lesch KP et al. (1996) Association of anxiety-related traits with a polymorphism in the serotonin transporter gene regulatory region. Science 274:1527-1531
(However, I looked at the related links on PubMed, and found some controversy. This study didn't find an association, this one did. So it seems you need detailed reading to make up your mind about this example.)
Ebstein RP et al. (1996) Dopamine D4 receptor (D4DR) exon III polymorphism associated with the human personality trait of Novelty Seeking. Nature Genetics12:78-80
and
Benjamin J et al. (1996) Population and familial association between the D4 dopamine receptor gene and measures of Novelty Seeking. Nature Genetics 12:81−84
In all fairness, the 2003 New Scientist article mentions that later meta-analyses (for example, here) of these studies found the evidence to be wanting - but also that newer researchdoes support an association of certain loci with neuroticism scores...
__________________ "There is much we do not understand about the history of life, and the same will be true of our grandchildren. But, then, if we knew all there was to know, scientific interest would cease. Textbooks may portray science as a codification of facts, but it is really a disciplined way of asking about the unknown." - A.H. Knoll, Life on a Young Planet
"Come on, put your bloody thinking caps on!" - Dr Tony Prave, geology lecture
In all fairness, the 2003 New Scientist article mentions that later meta-analyses (for example, here) of these studies found the evidence to be wanting - but also that newer researchdoes support an association of certain loci with neuroticism scores...
Association studies of genes with complex traits had a miserable rate of successful replication (see Genet Med. 2002 Mar-Apr;4(2):45-61 for the situation with disease association studies). It's reasonable to assume that most such reports were wrong. (This is no longer the case, with the advent of whole genome association studies, but it was true when these studies were done.)
Thanks. It did seem like a horribly messy subject even at a brief glance...
__________________ "There is much we do not understand about the history of life, and the same will be true of our grandchildren. But, then, if we knew all there was to know, scientific interest would cease. Textbooks may portray science as a codification of facts, but it is really a disciplined way of asking about the unknown." - A.H. Knoll, Life on a Young Planet
"Come on, put your bloody thinking caps on!" - Dr Tony Prave, geology lecture
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