The "Logic" of the creationist....

dear JP,You state:
"It, too, says nothing of the numbers of mutations required."Actually it just depends on the gene or DNA region of the primates one studies. There are genes that are (almost) identical between chimp and human, but there are also genes that are very, very distinct (indicating a directed mechanism). If you have a careful look at the chromosomes and DNA sequences of both species it is highly questionable whether a random mechanism is involved. One might as well assume creation.Peter

dear SLPx,I will look into my weird-stuff-literature and I will let you know what gene I referred to (it was a very recent Nature or Science article). Next, we can calculate a bit on it and find out what mechanism is involved. I go for a non-random/directed mechanism. I presume you go for randomness and selection.best wishes,
Peter

dear SLPx,The article I refered to can be found in:
Nature 2001 Oct 4;413(6855),p514-9.Let's have a carefull look at this gene family and whether a random non-directed mechanism can hold.Positive selection of a gene family during the emergence of humans and African apes, by johnson ME et al.Gene duplication followed by adaptive evolution is one of the primary forces for the emergence of new gene function. Here we describe the recent proliferation, transposition and selection of a 20-kilobase (kb) duplicated segment throughout 15 Mb of the short arm of human chromosome 16. The dispersal of this segment was accompanied by considerable variation in chromosomal-map location and copy number among hominoid species. In humans, we identified a gene family (morpheus) within the duplicated segment. Comparison of putative protein-encoding exons revealed the most extreme case of positive selection among hominoids. The major episode of enhanced amino-acid replacement occurred after the separation of human and great-ape lineages from the orangutan. Positive selection continued to alter amino-acid composition after the divergence of human and chimpanzee lineages. The rapidity and bias for amino-acid-altering nucleotide changes suggest adaptive evolution of the morpheus gene family during the emergence of humans and African apes. Moreover, some genes emerge and evolve very rapidly, generating copies that bear little similarity to their ancestral precursors. Consequently, a small fraction of human genes may not possess discernible orthologues within the genomes of model organisms.For your information:
PMID: 11586358 [PubMed - indexed for MEDLINE]I recommend anyone who wants to participate in the discussion to read the article very carefully. I will soon send in my comments that demontrate where it clashes with NDT.For now, focus your attention to the latter two sentences of the abstract. Will this paper provide a cover for future genes that will not be found in the great apes, but will be present in the human genome?Best wishes,Peter[This message has been edited by peter borger, 08-15-2002]

Dear SLPx,In response to:quote:
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Originally posted by peter borger:
dear JP,
You state:
"It, too, says nothing of the numbers of mutations required."Actually it just depends on the gene or DNA region of the primates one studies. There are genes that are (almost) identical between chimp and human, but there are also genes that are very, very distinct (indicating a directed mechanism). If you have a careful look at the chromosomes and DNA sequences of both species it is highly questionable whether a random mechanism is involved. One might as well assume creation.Peter--------------------------------------------------------------------------------You wrote:Actually, n o it doesn't.I say:
Well, as demonstrated by the reference: IT DOES, your statement was not correct.And:
"Perhaps you can provide us with some examples of what you speak."I say:
This reference is the first one that was published. Since only the minor part of chimps genes is known there will (for sure) follow more. These genes will provide a severe problem for the putative non-random mechanism of NDT. As explained below.And you said:
"What you see as a 'directed mechanism' those with experience see as the result of either selection of the physicochemical properties of the DNA sequence in question."I say:
Maybe you could be clearer on the putative physicochemical properties of DNA sequence in question.And you state:
"More undue extrapolations."I say:
"Who is doing the undue extrapolations? Why are evolutionists allowed to do unwarranted extrapolations all the time, then?"And:
Concerning the Nature article:It should be noted that fifteen copies of the duplicated segment were found in humans. (I also wonder whether duplications are randomly introduced or also non-randomly, directed).The authors state: "Sequence comparison of putative proteins from two full length human transcripts showed 81% amino acid sequence identity"And, the authors state: "...the corresponding NON-CODING portions of genomic DNA were 98.1% identical"Furthermore the authors state that: "We found NO significant sequence similarities to this gene in other organisms..."They conclude that: "These data suggest either that the exonic regions were HYPERMUTABLE or that amino acid changes had been selected for."{I agree on HYPERMUTABLE. Here, SELECTION is only a matter of believe. I am sure that the mechanism underlying hyper-mutability is directed by protein and/or RNA.}My comments:
If genes emerge and evolve rapidly giving rise to genes with little/no similarity to ancestral precursors, than how did they come into being?
According to NDT an original LCR16a gene region (where did it come from, anyway?) duplicated several times. Duplications give rise to IDENTICAL regions and if it encodes a protein it will specify the same protein. After duplication the genes/DNA regions are redundant. Redundant regions accumulate mutations at a neutral rate. Mutation rate is approx 10exp(-10) - 10exp(-9)/nucleotide/year. In the gene random accumulation of mutations will occur with an incidence of approx 1.5 exp(-6). That is 1.5-15 nucleotides per million years in this approx 2000 bp gene. In 6 million year there will be only 9-90 nucleotides to be different. That is a lousy 0.5-5 promille. It doesn’t matter whether selection acts or not, since the generation of mutations is a random process (according to NDT). It indicates that you need a very large population, and it has been demonstrated with the ZFY region (that provides another major problem for evolution theory) that only minor populations of humans had to be present.It should be noted that sequences similar to LCR16 are present in all great apes but the gene is specific for humans: the authors did not find a match in other organisms.NDT does not have an explanation for this gene. According to theory, a common ancestor for chimp and human lived 5-6 million years ago. In 5-6 million years random accumulation in redundant genes cannot give rise to new genes. It already takes approx 150 million years for a gene to arise from a duplication that has approx 20% sequence identity (see the actinin genes). What we see is that the LCR16 region has attracted/accumulated mutations in a much defined area: the coding region. Notably, there are 15 similar LCR16 regions, but only one of them accumulated the mutations. So, the authors are right in claiming that the region is hypermutable --the gene in particular--and indicates a non-random mechanism. However, they cannot introduce a non-random mechanism since it would violate NDT.In addition, if you have a careful look at table 3 you will find out that exon 4 demonstrates more variation WITHIN chimpanzee species than BETWEEN human and chimp.Finally, we find NEGATIVE selection for exon 2 within Hylobates subspecies (table 2).So, could you please tell me what kind of evolution is it that we observe in this region?Best wishes,Peter

Dear Percy,I have some comments on the human ZFY region:It was very surprising that within the samples obtained from human subpopulations NO polymorphisms were detected whatsoever. On the contrary, inspection of the corresponding homologous intron region in the primates reveals that several variable sites are distributed throughout the intron and include at least 39 substitutions (21 transitions and 14 transversions) and 4 insertion/deletion (indel) mutations. Thus, at least 5% variation in this region is observed between human and primates.The complete absence of variation in the ZFY region in humans is very awkward, and, according to the authors, cannot be ascribed to a chance alone (= random mechanism).Introns are thought to be subject to neutral evolution, and variation within the human population is predicted on neutral positions. Confronted with the peculiar situation of the absence of variation, the authors must apply statistics to define an era when the common ancestor of all males lived. They estimate that ‘Y-chromosome Adam’ lived around 270.000 (range 0-800.000) years before present.It should be noted that the non-variant intron sequences in the ZFY region provides a severe problem for evolution biologists, since molecular rules demand some neutral evolution: variation on silent positions. But, he authors state that "the invariance likely may results from a selective sweep, a recent origin of modern Homo sapiens, or a historically small effective male population sizes". Let us have a look what this evolutionary jargon means.Humans have 46 chromosomes. One set of 23 chromosomes is inherited from the mother, including the sex-determining chromosome X. The other set of 23 chromosomes is obtained from the father, and may include either an X- or a Y chromosome. Females have two 22 pairs of autosomal and one pair of X chromosomes. Therefore, all genes are backed up by an additional copy. In contrast, males have one X chromosome and a Y chromosome. Genetic information on these chromosomes is present as single non-allelic genes, meaning that these genes are not backed up by genes present on other chromosomes.
Because the X and Y chromosome have little sequence homology there is no recombination possible between the major part of these chromosomes, and most of the genes on the Y chromosome will behave as one linked genetic group. Hence, if an advantageous mutation occurs in a gene on the Y chromosome it will drag with it all the non-recombining parts of the chromosome. A rapid, natural selection driven fixation of any advantageous gene on the Y chromosome would therefore result in loss of variance throughout the entire Y chromosome (Svante Paabo in Nature). Because all non-recombining DNA sequences of the Y chromosome are replaced in a single sweep, this vision predicts that variability should be absent in all linked non-recombining Y chromosome genes.A recent study in mice on the non-coding region flanking the SRY gene, which is directly responsible for inducing maleness, is revealing in this matter. The study compared the amount of variation within the species and related it to the amount of variation among species. Then, the authors compared this ratio to the ratio for a rapidly changing region in the mitochondrial DNA obtained in the same way.If any of the two regions were subject to a selective sweep, it would be demonstrated by a reduced variation within species. It was found, however, that the non-coding region of the SRY gene changed at a neutral rate. It implicates that, because of linkage of the major part of the Y chromosomal genes, the entire non-recombining part of the Y chromosome changes at a neutral rate. Therefore, it is unlikely that natural selection acts upon the Y chromosome. More recently, similar findings were observed in human.But if natural selection did not act upon the Y chromosome the high degree of variability of the Y chromosome between primates apparently defies the theory of evolution, since the coding region of the SRY gene is very stable within a species, whereas considerable variation is observed between distinct species (again!)."Some part of the SRY protein show such high degree of variability between distinct primate species that one must conclude that part of the protein has no function at all, or that the gene is subject to directional selection (!)", says evolution biologist Svante Pbo in Nature. However, directional selection is only demonstrated in cases involving intergenomic conflict, such as occur between host and pathogen, but is has never been observed for non-immune system related protein coding genes.The only remaining scientific explanation of the variability in the Y chromosome between species is by the mechanism of NEUTRAL EVOLUTION. Yet, the observation that more replacement substitutions than synonymous substitutions are present between species suggests that a neutral mechanism is not likely to be responsible for variation among species. The ultimate hypothesis evolutionists propose is that "these regions have been retained throughout the primate lineage without any requirement for sequence conservation, implying that the SRY protein is [] the HMG box alone".But that doesn't solve the problem. It would still imply that the SRY protein is expected to evolve at a neutral rate! The peculiar thing about the SRY proteins was, however, that they are much more variable than predicted by neutral evolution. To properly understand this one has to assume selection on neutral positions (= neutral selection!!). (OR: a NON-RANDOM mechanism of mutations).I can imagine that evolutionary biologists really get frustrated solving the riddles around the SRY region. Despite several ad hoc hypotheses it all ends in a paradox. Apparently, there is no explanation for the high degree of dissimilarity of SRY region between distinct primates within the current evolutionary paradigm.Best wishes,Peter