Thank you for an easily understood presentation. While in science we almost never refer to findings as proven or fact, the evidence is overwhelming that the process as presented or as presented with minor modifications is consistent with your conclusions.
Indeed the more we learn the more we see the glory of God in the workings of nature, be it on the molecular level or the astronomic.
Adam, Eve and human population genetics, Part 6: common ancestry, nested hierarchies, and parsimony | The BioLogos Forum
Thank you for an easily understood presentation. While in science we almost never refer to findings as proven or fact, the evidence is overwhelming that the process as presented or as presented with minor modifications is consistent with your conclusions.
I’ve actually written about the prestin protein before, which you might find informative:
The brief answer is that the prestin protein in bats and whales has been shaped, through natural selection, in two lineages to have similar (but not identical) features. Prestin is used in the auditory systems of all mammals, and in whales and bats this protein came under selection for use in echolocation in both lineages. We understand the mechanism, and it’s not at all surprising. Note that although the mutations are similar in the two lineages, they are not identical.
Your second objection is based on a paper that was widely panned back in 2009, and flew in the face of the evidence even then. The authors ignored genetic data, and instead tried to build a case on character traits like hair length (things we know can change easily in a short time frame). It’s a wonder it was even published, but it goes to show that in science even somewhat odd ideas will be entertained, even if they don’t fit the data of the time. What counts, however, is how the different models fare with new data - and the publication of the gorilla and orangutan genomes completely demolished that paper’s conclusions. At the DNA level, humans are most closely related to chimpanzees, then to gorillas, and then to orangutans.
Thank you, Dennis. This is one of the best blog series I’ve read on the evidence for common ancestry from genetics, and how evolution acts on populations, not individuals. Your comparisons to the evolution of language and your explanations of genetic mutations and nested hierarchies are building a solid framework for thinking about these things. I’m looking forward to the rest of the series. Please continue to post articles in this style so the concepts are accessible to people without deep expertise. I appreciate it when scientists can translate for the rest of us in such an engaging way. Keep it up!
hi again dr venema.
actually the prestin gene do have identical mutations between some bats and dolphins:
“Nevertheless, dolphins and porpoises share at least 14 derived amino acid sites in prestin with echolocating bats, including 10 shared with the highly specialised CF bats 2 and 3.”
so this evidence disprove any claim of share mutations=commondescent.
about the primate phylogeny- the problem is that even scientists dont know who is close to who. why we check this by genetic similarity and not by morphological similarity? according to this logic- even if fish and chimp was closest from genetic prespective, we will need to say in this case that chimp is more closer to fish then human?
Dr. Venema did not claim that “share mutations=commondescent” because that would be silly. His post is about patterns of shared mutations that inactivate genes. The paper you cite is about shared mutations that do not inactivate genes, and that perfectly correlate with physiology and behaviour. The paper provides evidence that the mutations were targets of positive selection. This case is a very, very rare example of presumed convergent evolution at the amino acid level. It is misleading to compare it to the olfactory receptor pseudogene story.
Convergent evolution is interesting but not surprising. Seeing it at the amino acid level is also interesting, but only surprising because it suggests that the adaptation (echolocation) depends on very specific protein shapes/configurations. In many other cases of convergence, the changes are different between the convergent lineages, suggesting that there are many ways to acquire the convergent phenotype. In the Prestin case, it looks like there are very few ways to get there.
You seem to think that the mutations are “the same,” but the authors of the paper only claim that there are identical mutations at the amino acid level. Have you looked at the DNA sequences? The accession numbers are provided in the paper.
actually its not matter if its in the amino acid level or dna. its still a lots of share mutations. here is another examples of share mutations in the dna level:
so the main point is that share mutations\phylogeny of pseudogenes doesnt mean commondescent.
It does matter whether you are talking about the DNA level or amino acids. There are often multiple possible changes in the DNA codon that can give the same amino acid. It’s the DNA that matters for this argument.
The main point is that your position isn’t determined by the evidence. It’s determined by your pre-committment to special creation of species. If that’s what you think you need to believe, fine, but you should admit to yourself that a literal interpretation of the Biblical account is the reason for your belief, not the evidence, because the evidence won’t lead to the conclusion that you want.
There aren’t just a few shared mutations between species like humans, chimps and gorillas. There are millions of them, and that’s counting only the complex mutations like sizable insertions and deletions. And its not just in pseudogenes. There are shared complex mutations all over the place, sometimes even in coding regions. Of course each species also has some species-specific mutations that have occurred since they diverged. For transposon insertions there are a few thousand that are specific to each species, but millions that are shared, which indicates a very long shared history before they diverged. And occasionally you will see simple point mutations that did occur twice independently, say in human and gorilla but not chimp, but they are a very low percentage of the total.
If you are really interested, it’s not that hard to use the genome browser web sites. Get the human sequence, pick a segment at random and look at the corresponding chimp and gorilla sequences in the same region. For simplicity, it should be a region that isn’t part of a large segmental duplication. If you want to see a sample of that kind of thing, look at the figure at http://biomattersarising.blogspot.com/2014/12/transposable-elements-and-common.html
first- there is 20 amino acid and only 4 dna bases. so the ratio is1\5. its mean that 14 shared amino acid is like 70 shared dna bases!
2)my position determined by the evidence and not by belief. im actually former evolutionist. what is the evidence? i will give you 2 of them:
1)we know that a self replicat motor need a de signer. the flagellum is a self replicat motor. then the flagellum need a designer.
2)there is no step wise from complex system to another. so if we will have a self replicat car (for example)’ it will not evolve into somthing like f15. so there is not step wise also in living systems that are no less complex.
"And occasionally you will see simple point mutations that did occur twice independently, say in human and gorilla but not chimp, but they are a very low percentage of the total. "
actually there is milions of them:
You’ve missed the point of Pgarrison’s explanation of your mistake on the shared DNA vs shared amino acids. 14 amino acids in common does not mean 14 x 3 shared DNA bases - far from it. There are many ways to code for most of the amino acids - for example, the amino acid leucine can be coded for by six possible codons: CTT, CTA, CTG, CTC, TTA or TTG. In cases of convergent evolution (independent mutations leading to the same features) we see convergence at the amino acid level but often different DNA sequences underneath, as expected by independent events.
The post you linked to claiming repeated mutations in GULO is also wrong. The original paper (done by a group in Japan with little to no expertise in evolutionary biology) claimed that there were many repeated mutations. They were wrong - not because they did the sequencing wrong, but because they did the interpretation wrong. They assumed that the rat sequence was ancestral and that humans and guinea pigs independently mutated at several locations to the same DNA letter. In reality, the shared DNA sequences between human and guinea pig were ancestral, and the rat had mutated away from the ancestral sequence. Their erroneous conclusions were picked up and trumpeted by young and old-earth creationists (such as Reasons to Believe), but they’re simply wrong. The original study was published in a Japanese journal of vitaminology - hardly a reputable source for information on evolution.
You can read more about the GULO shared mutation issue, and why the anti-evolutionary claims based on it are wrong here:
The other examples claimed in your sources (such as the remainder of the examples in the creation.com article, and the Discovery Institute / ID article, are also understood and expected when one understands that evolution is a population-level phenomenon. The claim is that some DNA sequences in humans do not most closely match chimpanzees, but rather other apes (e.g. gorillas). One example in the creation.com article has a sequence where gorillas and chimps match more closely than either does to human.
These examples are real, but the interpretation offered (that they are the result of independent mutations, or that they confound phylogenies) is incorrect. These are the expected results of what happens when large populations undergo speciation. Have you noticed that these examples invariably use another very close relative to humans (i.e. other apes)? There is a reason for this - the lineages leading to present-day humans, chimpanzees and gorillas separated from each other in a relatively short timespan, and did so as large populations (around 50,000 for each common population at the point of separation). As a result , we expect this sort of thing - if we didn’t see it it would be a problem for evolution, actually.
The effect producing these patterns is called incomplete lineage sorting. We will actually be covering this next in this series in the context of using it to determine population sizes. I’ve also written about it before, which you might find helpful:
When you cover this again, it may be a good idea to include the maths (the theory behind this (theory of coalescent trees) was worked out in 1982) which predicts:
That for Humans, Chimps and Gorillas:
- In 70% of sequences Humans and Chimps are most similar
- In 15% of sequences Chimps and Gorillas are most similar to each other
- In 15% of sequences Humans and Gorillas are most similar to each other
This is almost exactly what they found with the publication of the Gorilla genome
thanks for your response dr venema.
:“14amino acids in common does not mean 14 x 3 shared DNA bases - far from it. There are many ways to code for most of the amino acids -”-
yes, i know that. but the chance is the same. the chance for specific amino acid is 1\20. the chance for specific nucleotied is 1\4. so from pure chance prespective, without any selection involve, is more rare to get the same amino acid compare to the same dna base. simple calculation…
“In cases of convergent evolution (independent mutations leading to the same features) we see convergence at the amino acid level but often different DNA sequences underneath, as expected by independent events”-
not always. see here for example:
““This means that vocal learning birds and humans are more similar to each other for these genes in song and speech brain areas than other birds and primates are to them,” Jarvis said.”
about the gulo- you said:
“They assumed that the rat sequence was ancestral and that humans and guinea pigs independently mutated at several locations to the same DNA letter. In reality, the shared DNA sequences between human and guinea pig were ancestral, and the rat had mutated away from the ancestral sequence.”-
its unlikely for 3 reasons:
- the rat population is huge, so the fixation time for new mutation will take more time in the rat genome then the cavia one
2)beneficial mutations is much more rare then neutral one. so the molecular clock for the first(rat in this case) is much more slower
- you assume that evolution is true: therfore you claim that the rat sequance was changed. but if evolution isnt true- then it is not changed.
now about the ils model- first, if its true that for a 6 my split(human-chimp) we will get 15% different(like “aceofspades” claim)then its mean that for a split before about 50 my we will get a different of 100% in the genome. but we know that it is not true. even human and banana share near 50%. so somthing is wrong here.
secondly- with the ils model we can explain any phylogenetic contradiction. so how can we know when is convergent evolution and when it the ils?
about the evolution in general- again: we know that a gps cant evolve into a cell-phone(even if they will have a self replicat system). so we know that one kind of animal cant evolve into another.
I don’t know how to say this without sounding abrasive (I’m not intending to be). You don’t understand what you are reading, and taking quotes from a news article isn’t going to be useful unless you understand the science behind it. The convergence between birds and humans with respect to speech/song is not at the DNA sequence level of individual genes. It’s in how those genes, in general, are expressed (make into protein in certain times and places). There are similarities there, but the individual DNA sequences underlying those general similarities of expression are different. Many different DNA sequences can lead to (broadly similar) patterns of gene expression.
As for your comments on GULO, I can’t really understand what you are arguing for. Note - I don’t “assume” evolution. I accept the overwhelming evidence for common ancestry. It’s not an assumption, it’s based on the evidence. Perhaps re-read the post I linked to on the topic.
Your question on ILS and phylogenies is a better one. We expect ILS for close relatives, and we expect a pattern (roughly) as follows:
The highest level of identity with our closest relative. (chimpanzees)
Based on population size and time since speciation, we predict a certain amount of our DNA will more closely match our next closest relative (gorilla).
This pattern will continue, with ever-smaller amounts of DNA matching more distantly-related organisms. For example, around 0.8% of our genome matches orangutans more closely than other great apes.
so, it’s not an arbitrary pattern, it’s a pattern that interlocks with other lines of evidence we have (we have the highest overall similarity to chimps, then gorillas, then orangutans, and so on).
Lastly, we do not have 50% genome identity with bananas. For some very, very highly-conserved genes, we might approach that figure at an amino acid level (not DNA), but not for an overall genome score.
I’m not sure I’ll reply to other comments, but I hope you (and others) find this helpful.
hi again dr venema.
it may be my final response also
“There are similarities there, but the individual DNA sequences underlying those general similarities of are different.”-
here is more clear example
“We estimate that 113 convergent changes are distributed across all 13 mitochondrial protein-coding genes; this is ≈44 more convergent changes (presumably nonneutral) than predicted by empirically observed convergence levels between other branches over the entire tree, and ≈73 more than predicted by evolutionary model-based expectations.”
and again- even if it was in the amino acid level its not so different from dna level.
"As for your comments on GULO, I can’t really understand what you are arguing for
i will try to explain it again. you claim that the rat sequance was changed and not the cavia sequance. so i explain that its very unlikely because the molecular “clock” of the rat gulo is expact to be more slower then the cavia one. but there is no need for this because i show above a lots of convergent changes without commondescent.
. Note - I don’t “assume” evolution. I accept the overwhelming evidence for common"
ancestry. It’s not an assumption, it’s based on the evidence."-
science base on facts and not by belief. the fact is that we never seen an animal evolve a new complex systme like flagellum or eyes. according to the evolution its take milions of years. so its indeed a belief and not part of science because we cant test this claim in experiment.
“so, it’s not an arbitrary pattern, it’s a pattern that interlocks with other lines of evidence we have (we have the highest overall similarity to chimps, then gorillas, then orangutans, and so on).”-
this is again the phylogenetic tree. but like i said before- the morphological tree contradict the genetic one(and even the fossil one from what i remember). so according to what tree we should follow?
“Lastly, we do not have 50% genome identity with bananas”
not according to this source:
"The genes of organisms that look very different are surprisingly similar. For example, human DNA sequences are over 95% identical to chimpanzee sequences and around 50% identical to banana sequences. "
do you have another source?
even so- according to the claim here of “15% prediction” we will need to find a 100%changes in the genomes of 2 animals that split before 50 my… we know that isnt true- then its wrong.
have a nice day
dscccc, “the molecular tree contradict the genetic one”
The molecular tree is the genetic tree. It is possible to infer trees for individual genes which sometimes don’t agree with the tree inferred from whole genome sequences or from large sets of gene sequences for various reasons, including the incomplete lineage sorting mentioned by Dennis, but they are all molecular genetic trees.
You quote a paper which says in the title that the degree of convergence is unusual, so it’s not a general explanation for any similarity which is seen in different genomes. They made clear that the convergence seen was due to similar selection at high temperature, and that not all the mutations were convergent. That virus has a very small genome - only a few genes, which overlap with each other. As a consequence there are not that many possibilities for mutations to optimize for a new condition, so it’s not too surprising that some of them should repeat in an experiment with enough repetitions.
You don’t think evolution happened at all, so why do you think convergence by selection somehow accounts for similarities in genomes? Even if it was all by selection, that wouldn’t support your rejection of evolution. You would be invoking evolution to disprove evolution.
“so its indeed a belief and not part of science because we cant test this claim in experiment.”
Just before you made this statement you were arguing based on the observed sequences of mammals. Those were observations, not experiments. You need to make up your mind whether inferences from observations (based on understanding gained from experiments on present day organisms) are part of science or not. You can’t have it both ways. Those of us who have actually been scientists are clear that this is part of science, and declaring that it isn’t is just a rhetorical strategy, not a serious argument. You can’t do experiments with stars, planets, black holes, etc. in astronomy - that doesn’t keep it from being a science.
“1) the rat population is huge, so the fixation time for new mutation will take more time in the rat genome then the cavia one”
It doesn’t matter. Huge numbers of neutral mutations happen in a population. A small proportion of them get fixed by chance. There has been plenty of time for fixation of a few neutral mutations in the GULO gene in rats.
“Almost always” is what you need to account for the similarities between genomes. An occasional parallel occurrence of the same mutation in different species (the technical term is homoplasy) can’t come anywhere near to accounting for what we see. I have seen a paper describing independent insertions of a transposon at the same site in 2 different species, but even then it wasn’t the same kind of transposon, so the events were easily distinguished.
“even so- according to the claim here of “15% prediction” we will need to find a 100%changes in the genomes of 2 animals that split before 50 my… we know that isnt true- then its wrong.”
This isn’t how this works. The multiplication isn’t valid. The 15% is not a prediction based on how many mutations are expected in a given period of time. It has to do with the fact that two speciation events occurred close to each other in time, with the relative times estimated from coalescence theory.
Of course, mutations do accumulate with time. Mammals have a lot of similarities in sequences that have no functional effect, that are the result of recent common descent, but if you go as far as comparing a bird and a mammal there is little sequence similarity outside of coding and regulatory sequences. There are blocks of similar gene order, and of course it’s easy to detect the similarity in sequences that code for most RNAs and proteins and some regulatory sequences. Dennis was right that the mammalian and plant genomes are not 50% identical. That article was probably referring to the most highly conserved genes, but those are a very small portion of either genome.
There’s not any possible biological mechanism for the repeating of millions of complex mutations in multiple species. Targeted mutation can’t do it, because enzymes are just not that accurate (and there’s no evidence for it anyway.) Natural selection can’t do it, because in complex organisms there are way too many ways for it accomplish similar functional results. Whichever one happens first is going to be selected.
I have to agree with Dennis that, if you are really interested in this stuff, you are going to have to go beyond news articles and creationist websites and take some college courses in molecular biology, or if you are capable of teaching yourself, get good textbooks in genetics, biochemistry, population genetics etc. and work your way through them.
I meant to add that I used to work with a family of proteins that was fairly well conserved and widely distributed in various organisms, including plants and microbes. If you looked at the gene from a mammal and compared it to that from plants or microbes, there would usually be ~20-25% identity at the protein level. 25% identity at the DNA level is what you what you expect for no relation at all (ignoring the effects of GC%.) When you make comparisons at those distances, the conservation is mostly due to functional requirements, since the common ancestor was over a billion years ago. That means a lot of mutations have happened at positions that don’t have much functional constraint on them. In comparisons where the specific reaction catalyzed by the protein was different, the 3D structure of the two proteins would still be very similar, but you often couldn’t detect any protein sequence similarity at all beyond a few positions that contributed directly to the catalysis.
“I have to agree with Dennis that, if you are really interested in this
stuff, you are going to have to go beyond news articles and creationist
websites and take some college courses in molecular biology, or if you
are capable of teaching yourself, get good textbooks in genetics,
biochemistry, population genetics etc. and work your way through them.”
Or, if you’re so inclined, you could start here:
“The molecular tree is the genetic tree.”-
yep. of course that i mean the morphologic one. i fix it…
“You quote a paper which says in the title that the degree of convergence is unusual, so it’s not a general explanation for any similarity which is seen in different genomes.”-
not realy. this article claim that is very unlikely that 12 mutaions will happen independenly in those sites. so i show that its very likely…
“Just before you made this statement you were arguing based on the observed sequences of mammals. Those were observations, not experiments.”-
its not part of evolution. one of the main part of the evolution theory is that complex system can evolve step wise. there is no experiment that show its possible. so all the experiments so far prove creation and not evolution.
“t. You can’t do experiments with stars, planets, black holes, etc. in astronomy - that doesn’t keep it from being a science”-
yes. but we can test some of those field . the evolution theory we cant…
" Huge numbers of neutral mutations happen in a population. A small proportion of them get fixed by chance. There has been plenty of time for fixation of a few neutral mutations in the GULO gene in rats"-
maybe. but we still have the same mutations in both cavia and human but not rat. so according to this- the rat clock is more speedy. but we know its not true because the rest of the exon is not share. so we have a problem here .
"Dennis was right that the mammalian and plant genomes are not 50% identical. That article was probably referring to the most highly conserved genes "-
maybe. do you have another source?.
“There’s not any possible biological mechanism for the repeating of millions of complex mutations in multiple species.”-
first: who is talking about milions? secondly: if all the genomes made by the same designer- then even bilions bases can be in the same sites.
about books. i actually read a lots of them…
“so i show that its very likely…”
I don’t know what you are talking about. You didn’t show anything. You said evolution can’t be studied in experiments, and you reference a paper that describes experiments in evolution of a virus. You claim that parallel amino acid residues means parallel mutation, but if the codon is different, it’s not really parallel. It came about by a different mutation pathway, which in the virus in the experiment was clearly because the selection was always for growth at the same temperature. This is a fundamental misunderstanding, which you simply refuse to give up.
“so all the experiments so far prove creation and not evolution.”
“Proof” is a concept that applies in math and logic, not science. You mean “support” or “demonstrate.” But no experiment can support special creation directly, because you can’t run creation again. And in fact many experiments support evolution, including the ones in the phiX174 paper you referenced. You say experiments can support aspects of astronomy. The same is true for evolution, both in terms of experiments in short term evolution and observations of wild populations. Speciation has been directly observed in plants. Dogs and other domesticated species changed their anatomy and behavior recently in evolutionary terms. The behavioral differences, including not fearing humans and barking were duplicated by artificial selection in foxes over a small number of generations. There have been many papers in the last few years on changes in genomes of domesticated species from their wild ancestors. There is a vast literature out there on evolution in the lab, in domesticated species and in wild species which you can search on PubMed or other sites. When you declare the experiments “prove” creation, you are just echoing the creationist sites. You should go roaming around in the biology literature, or at least Dennis’s material here before coming to such a certain conclusion.
“we still have the same mutations in both cavia and human, so according to this- the rat clock is more speedy”
This has nothing to do with a mutation clock, except that there has been plenty of time for mutations to occur and be fixed in all those genomes. You are assuming that the mutations were in the cavia and human, which is not the simple (parsimonious) interpretation. The thing to do is to look at what other mammalian species the sequence is available for. If they all have the same nucleotide at those positions as cavia and human, that makes it even more likely that that is the ancestral sequence and the mutations happened in the rat.
“maybe. do you have another source?”
The source I have is years of comparing sequences in my own research. You could look up plant genome papers pretty easily, but they won’t tell you what the overall DNA sequence identity level is with mammals. Nobody thinks that plants and mammals have a recent common ancestor, so the question isn’t very interesting. You could look up the banana genome on the web, pick a few segments of a few thousand bp outside of genes and without internal repeats and run them against the human genome on a genome browser. My guess is that nothing will match above about 30% identity (~25% would be random.) The only matches you see would probably be in short repetitive sequences “microsatellites.” There would be matches between conserved RNA or protein coding genes, but for protein coding genes they would easier to detect by comparing protein sequences to translated DNA (one of the options on the search services.)
“first: who is talking about milions?”
I am. That’s what the evidence is. Look at the original human genome paper (it’s free.) There is a section on transposable element insertions with a table that gives the numbers of each type. Only about half a percent of those (a few thousand out of over 3 million) are not shared between the human and chimp genomes. That’s in later papers after the chimp genome was sequenced. And this doesn’t include thousands of retrotransposed gene copies and fragments of mitochondrial DNA inserted in the same locations in the two genomes or many thousands of shared haplotypes (patterns of small mutations in an interval short enough that recombination hasn’t separated them,) small insertions and deletions.
“if all the genomes made by the same designer- then even bilions bases can be in the same sites.”
It’s quite true that you can account for the evidence with miracles. But you can account for any conceivable set of evidence by invoking miracles. So how do you tell? If you prefer to invoke miracles, that’s fine, but then there’s no reason to bother with science at all. No matter what is observed, you have it accounted for. You can just believe what you want and spend your time on something else. But why would God make it all by special creations and make it look as if it happened by common descent?
I suppose your response will be that it doesn’t look like common descent, but 98% of the professional biologists, Christian or not, think that it does. (The other 2%, as far as I can tell, are like you in being committed to special creation.) There is no great conspiracy. After working with them for 35 years, I’d say they really are a pretty bright bunch of people - some of them are amazingly brilliant. They are just curious; they work hard; criticize each other’s work, and they want to find out how the world works.
hi again pgarrison.
"You said evolution can’t be studied in experiments, and you reference a paper that describes experiments in evolution of a virus. "-
not realy. not any change is evolution. the evolution theory claim that a complex systems like eyes ot flagellum can evolve step wise. there is no even one experiment that can show its possible…
for example: take the lenski experiment: its need only 2 mutations to get citrit digest in oxigen environment. the gene(protein actually) that can digest citrit jump near promoter that can be activated by on(from what i remember). its like to move an abs system from into the car to outside the car. now the car get be more protect to carshs. but it isnt a new complex system like a new gps or dvd to the car.
so again- can you show that a complex system will evolve? do you think for example that a gps can evolve step wise from a cell-phone if we have a self replicat gps with dna?
“You claim that parallel amino acid residues means parallel mutation, but if the codon is different, it’s not really parallel.”-
but its still parallel in the amino acid level. from a rendom prespective- the chance to get the same 10 amino acid is about 20^10. in the dna level the chance is about 4^10. so the chance to get the same amino acid is much lower then dna bases.
i also gave an example of dna level.
" which in the virus in the experiment was clearly because the selection was always for growth at the same temperature. This is a fundamental misunderstanding, which you simply refuse to give up"-
so what? its still convergent…
." “But no experiment can support special creation directly, because you can’t run creation again.”-
not realy. first- the creation model predict that a dog will stay as dog even for bilions of years. but evolution predict that it will be change into another family. so all the experiment so far support creation and not evolution.
secondly -we can prove that the creation model is right. how? let me ask you this: do you think that a self replicat robot with dna is a proof of design or not?
“Speciation has been directly observed in plants. Dogs and other domesticated species changed their anatomy and behavior recently in evolutionary terms.”-
again- dog stay as dog and doesnt evolve any new complex system.
“Only about half a percent of those (a few thousand out of over 3 million) are not shared between the human and chimp genomes. That’s in later papers after the chimp genome was sequenced. And this doesn’t include thousands of retrotransposed gene copies and fragments of mitochondrial DNA inserted in the same locations”
actually retrotransposons(or transposon if its matter) are functional:
“TEs make up a large fraction of the C-value of eukaryotic cells. They are generally considered non-coding DNA, although it has been shown that TEs are important in genome function and evolution. In Oxytricha, which has a unique genetic system, they play a critical role in development”
so again- they may be a result of commondesginer.
" “but 98% the professional biologists, Christian or not, think that it does. (The other 2%, as far as I can tell, are like you in being committed to special creation”-
100% of chemists thought there is no quasicrystal in the past. but they all wrong. its also a logical fallacy:
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