Mortlach schreef:
Wat ik me ineens afvraag. Hoe kijk je aan tegen het gefuseerde chimpanseechromosoom in het menselijke genoom? Ik neem aan dat je daar mee bekend bent. Zo niet, een korte samenvatting: de mens heeft 1 chromosoom minder dan de grote mensapen. Een chromosoom verdwijnt niet zomaar, dus als de mens van de mensapen afstamt, moet je een gefuseerd chromosoom kunnen vinden. En dat vinden we: een chromosoom met in het midden twee stukken chromosoom die verder alleen maar voorkomen als afsluitstukken.
Is dat een argument of is dat bewijs? Als het geen bewijs is, prima, maar wat is de alternatieve verklaring dan? Als je de creationistische kant op wil, waarom zou God dan een chromosoom ontwerpen met twee 'middenstukken' en in het midden twee stukken sluitcode, en dan zeggen dat dat zeer goed was?
Hoe je het ook wendt of keert, je kunt lastig ontkennen dat deze vondst het niet verschrikkelijk doet lijken alsof de mens en de mensapen een gemeenschappelijke voorouder hebben. In ieder geval heeft de hypothese van de gemeenschappelijke afstamming een voorspelling gedaan en die voorspelling bleek waar.
Het is eigenlijk onverstelbaar dat tijdens mijn afwezigheid (wat ik na deze quote ongetwijfeld ook weer ga doen) nog steeds dezelfde idiote claims van de evo's weer geponeerd worden.Ze leren ook werkelijk helemaal niets.
Voor de chromosoom 2 fictie van Ken Miller verwijs ik naar een stuk wat Dr Borger heeft geschreven, dat plaats ik hier maar helemaal:The human chromosome 2
by Peter Borger (submitted for publication).
From a distance humans and chimpanzees look very similar. It is in fact this similarity that prompted Darwin to propose chimpanzees are our closest living relatives with whom we share a common ancestor quite recently. A close up look also reveals many similarities, and the word was man shares 99% of the genetic make up with his chimp cousin. The word was. In 2005 the chimpanzee genome project released the first genetic comparison of man and chimp. With astounding results: Man and chimp share far less sequences than ever expected. Science had to admit recently that the difference between man and chimp is 6.4% [1]. Despite the adjustment by over 5%, it can hardly be the right figure. After the realization of the first chimp-human whole genome comparison in 2005, the Chimpanzee Sequencing and Analysis Consortium stated:
“Best reciprocal nucleotide-level alignments of the chimpanzee and human genomes cover 2.4 gigabases (Gb) of high quality sequence, including 89 Mb from chromosome X and 7.5 from chromosome Y.” [2]
In other words, of the 2.85 Gb (=billion base pairs) human euchromatic DNA only 2.4 Gb formed a match with that of the chimpanzee. DNA sequences that do not match do not match because they are distinct sequences. Over 15% of the sequences do not match! The difference between man and his “closest relative” is now suddenly 15% plus 6.4% is more than 21 percent! Based on this figure, and the fact that man has unique protein-coding [3] and miRNA [4] genes for which standard evolutionary theory hasn’t the faintest origin clue, it is logically sound to reject common ancestry with chimpanzees. This also means that the structure and arrangement of human chromosome 2 has to be reinterpreted. The chromosome is said to be a fusion product of two ancestral primate chromosomes that are still separate in chimpanzees and is among the best molecular evidence of Darwinian common descent.
Comparing human and chimpanzee chromosomes its turns out there are 10 major chromosomal differences (5). Intra-chromosomal inversions are identified in nine human chromosomes: 1, 4, 5, 9, 12, 15, 16, 17 and 18. This means that a huge part within the chromosome was inverted head to toe, so that it now has the opposite orientation. In addition, there appears to be a fusion of chimpanzee chromosome 12 and 13, thus producing human chromosome 2 (5). It is this “fusion” located to chromosome 2q13-2q14.1 that has delighted evolutionists, as they claim it proves we have a common ancestor with chimpanzees. But is it compelling?
Remnants of telomeric DNA? In 2002, Fan et al analyzed the structure of >600 kb surrounding the fusion site and closely related sequences on other human chromosomes (6). Their analysis showed, what they call, “multiple subtelomeric duplications to chromosomes 1, 5, 8, 9, 10, 12, 19, 21, and 22” present in the fusion site. The sequences resembling telomeric DNA, which can also be found on several locations elsewhere in the human genome, are compelling evidence for the fusion. Isn’t it?
No, it is not compelling at all. In 2005, Hillier et al published the molecular sequence of human chromosome 2 and 4. The paper demonstrated that human chromosome 4 also has a 1.1 Mb (1.1 million base pairs) subtelomeric region (4q26) showing an abundance of subtelomeric duplications to human chromosomes 1-9, 11, 16, 19 and 20. Similar “not highly conserved” sequences could also be demonstrated in the mouse genome, but without “conclusive evidence” for an ancient fusion, (6; p729-730). Remarkably, chromosome 4 shows another region resembling non-functional subtelomeric sequences (4q32.3) that is highly conserved in mice (6; p730).
What do these data mean? As a matter of fact it means nothing at all with respect to common descent. The sequences will, of course, be interpreted by our dear Darwinian opponents as the result of common ancestry with chimpanzees, but the fact that subtelomeric regions can be found also in other parts of the human and other genomes makes the conclusion merely conclusion jumping – not compelling at all. The fact that subtelomeric repetitive regions can be found scattered throughout the human genome merely reflects the nature of repetitive sequences, i.e. they easily duplicate and translocate. Why than do the sequences present in chromosome 2 qualify as evidence for a chromosome fusion, while similar sequences in chromosome 4 do not? Because it fits the Darwinian presupposition of an ancient fusion. We call this selective data interpretation.
And how do our Darwinian friends explain the conserved ancient subtelomeric sequences? As they are what Darwinians claim – remnants of ancient fusion sites – how could these sequences be conserved if they do not have an apparent function in humans?
Remnants of a centromere? Molecular biologists know that a fusion of two ancestral chromosomes would have produced human chromosome 2 with two centromeres. Currently, human chromosome 2 has only one centromere, so there must be molecular evidence for remnants of the other. In 1982, Yunis and Prakash studied the fusion site of chromosome 2 with a technique known as fluorescence in situ hybridization (FISH) and reported signs of the expected centromere (5). In 1992, another study also reported signs of the centromere (7). In 2005, after the complete sequencing of human chromose 2, we would have expected full, watertight proof of the ancestor’s centromere. However, even after intense scrutiny there are still only signs of the centromere. If signs of the centromere were already observed in 1982, why can it not be proved in the 2005 sequence analysis? Apparently, the site mutated with such high pace it is no longer recognizable as a centromere:
“During the formation of human chromosome 2, one of the two centromeres became inactivated (2q21, which corresponds to the centromere of chromosome 13) and the centromeric structure quickly deteriorated”.(6)
Why would it quickly deteriorate? Why would this region deteriorate faster than neutral? Did the centromere actively attract mutations? A close up scrutiny in 2005 showed the region that has been interpreted as the ancestor’s centromere to be built from sequences present in 10 additional human chromosomes (1, 7, 9, 10, 13, 14, 15, 18, 21 and 22) as well as a variety of other genetic repeat elements that were already in place before the alleged fusion occurred (6).
The fusion site revisited. The chimpanzee and human genome projects demonstrated that the fusion did not result in loss of protein coding genes. Instead, the human locus contains approximately 150 thousand additional base pairs not found in chimpanzee chromosome 12 and 13 (now also known as 2A and 2B). This is remarkable because why would a fusion result in more DNA? We would rather have expected the opposite: the fusion would have left the fused product with less DNA, since loss of DNA sequences is easily explained. The fact that humans have a unique 150 kb intervening sequence indicates it may have been deliberately planned (or: designed) into the human genome. It could also be proposed that the 150 kb DNA sequence demarcating the fusion site may have served as an adaptor sequence for bringing the chromosomes together and facilitate the fusion in human.
Another remarkable observation is that in the fusion region we find an inactivated cobalamin synthetase (CBWD) gene (8). Cobalamin synthetase is a protein that, in its active form, has the ability to synthesize vitamin B12, a crucial cofactor in the biosynthesis of nucleotides, the building blocks of DNA and RNA molecules. Deficiency during pregnancy and/or early childhood results in severe neurological defects, because of an impaired development of the brain. The Darwinian assumption is that the cobalamin synthetase gene was donated by bacteria a long time ago and afterwards it was inactivated. Nowadays, humans must rely on microorganisms in the colon and dietary intake (a substantial part come from meat and milk products) for their vitamin B12 supply. It is also of note that humans have several copies of inactivated cobalamin-synthetase-like genes on several locations in the genome, whereas chimpanzees only have one inactivated cobalamin synthetase gene. That the fusion must have occurred after man and chimp split is evident from the fact that the fusion is unique to humans:
“Because the fused chromosome is unique to humans and is fixed, the fusion must have occurred after the human-chimpanzee split, but before modern humans spread around the world, that is, between 6 and 1 million years ago.” [8]
The molecular analyses show we are more unique than we ever thought we were and this is in complete accordance with creation. We propose the fusion, if it really was a fusion after all, may have resulted from an intricate rearrangement or activation of repetitive genetic elements after the fall (as part of or executors of the curse following the fall) and inactivated the cobalamin synthetase gene (after the fall we had to eat meat!). The inactivation of the gene may have reduced people’s longevity in a similar way as the inactivation of the GULO gene which is crucial to vitamin C synthesis [9].
mortlach schreef:Ik heb trouwens nog nooit voorspellingen gezien die de creationistische hypothese heeft gedaan. (alleen 'voorspellingen achteraf' maar die tellen niet).
Weer een evo leugen, je weet dat er iemand in de bijbel las over paden in de zee en die later ook vond,dat weet je toch?
Waarom deze leugen?
Tot zover weer mijn inbreng voor een tijdje.
'Diegene die in evolutie geloven doen dat alleen om hun geweten te sussen'.
](./images/smilies/eusa_wall.gif "Brick wall")