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Old 09-16-2002, 09:02 PM   #21
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Quote:
Originally posted by Doubting Didymus:
<strong>

Undisputed: that human chromosome 23 is the product of a fusion event.

We can certainly find corroborating studies for these, but where will it end? At 2 verified papers? 3 papers? just where have you set your standard for corroboration?</strong>
Part of the difficulty in having a sober discussion is that you people keep using words like "undisputed". Why is it necessary to be so emphatic? Perhaps it is because you aren't as confident as you'd like to be. Anyway....

Do you mean human chromsome 2? Which one do you consider to be #23: X or Y?

I have only seen one paper on #2. Do you have others?

Vanderzyden

[ September 16, 2002: Message edited by: Vanderzyden ]</p>
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Old 09-16-2002, 09:22 PM   #22
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sorry, typo.

But I think 'undisputed' is the appropriate term, so I will stand by it.

I think its funny when people say 'why are you so emphatic about that, perhaps you are not so confident after all'. There is just a small possibility that I simply think I am right.

Quote:
I have only seen one paper on #2
My question was: how many do you want? this is not a flippant question. I am confident that the combined research skills of the posters here will bring to light as many papers as you please. As I say, it is not disputed among the majority of biologists.

(please note: as per your previous request that I cease to point out ironies in your posts, I have tried to ignore the fact that you have previously spent time attacking scientific writings for using tentative language, yet you do the opposite here, and attack me for using emphatic language. Perhaps we should stop using any language at all?)

[ September 16, 2002: Message edited by: Doubting Didymus ]</p>
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Old 09-16-2002, 09:45 PM   #23
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Okay, I think I have found the page most of the human chromosome fusion info we have all been looking from has been drawn from, so lets start with the journal references there.

( the page is <a href="http://www.gate.net/~rwms/hum_ape_chrom.html" target="_blank">here</a>, and has probably been shown to you by many others

1. Yunis, J. J., Sawyer, J.R., Dunham, K., The striking resemblance of high-resolution g-banded chromosomes of man and chimpanzee. Science, Vol. 208, 6 June 1980, pp. 1145 - 1148


2. Yunis, J. J., Prakash, O., The origin of man: a chromosomal pictorial legacy. Science, Vol 215, 19 March 1982, pp. 1525 - 1530


3. IJdo JW, Baldini A, Ward DC, Reeders ST, Wells RA, Origin of human chromosome 2: an ancestral telomere-telomere fusion. Proc Natl Acad Sci U S A 1991 Oct 15;88(20):9051-5


I have not been able to find full text versions.

Note that these are mostly over ten years old. This is not sinister, It is just that the fusion of Chromosome # 2 has not been controvertial for some time.

I assume you need more, or different, journal refs, however. How many do you need, and of what kind?
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Old 09-16-2002, 09:51 PM   #24
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My apologies to monkenstick, this chromosome fusion information is off topic. I will now seek articles on the truly basic premise of genetic homology. Perhaps monkenstick can reference his own opening post? (unless it is original work).

Note that I make no claim to expertise in genetic fields. This should demonstrate that even relative laymen should be able to corroborate such basic studies as these.

Incidentally, do you have any reliable references AT ALL that challenge these premises?
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Old 09-16-2002, 10:01 PM   #25
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vanderzyden, what do you want "corroborated"

are you denying that these are the correct sequences?

they're posted to genbank at NCBI if you want to check them

<a href="http://www.ncbi.nlm.nih.gov/" target="_blank">http://www.ncbi.nlm.nih.gov/</a>

[ September 16, 2002: Message edited by: monkenstick ]</p>
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Old 09-16-2002, 10:07 PM   #26
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Vander's point is that a single paper might be wrong, and he is sort of right about that, but we could probably sit here all day posting different papers with the same conclusion.

We need to know from vanderzyden how much of what kinds of papers he needs.
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Old 09-16-2002, 10:12 PM   #27
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a single paper is no good to vander? How about three?

Quote:
: Proc Natl Acad Sci U S A 1989 Dec;86(23):9412-6
Related Articles, Links


Urate oxidase: primary structure and evolutionary implications.

Wu XW, Lee CC, Muzny DM, Caskey CT.

Verna and Marrs McLean Department of Biochemistry, Baylor College of Medicine, Houston, TX 77030.

Urate oxidase, or uricase (EC 1.7.3.3), is a peroxisomal enzyme that catalyzes the oxidation of uric acid to allantoin in most mammals. In humans and certain other primates, however, the enzyme has been lost by some unknown mechanism. To identify the molecular basis for this loss, urate oxidase cDNA clones were isolated from pig, mouse, and baboon, and their DNA sequences were determined. The mouse urate oxidase open reading frame encodes a 303-amino acid polypeptide, while the pig and baboon urate oxidase cDNAs encode a 304- amino acid polypeptide due to a single codon deletion/insertion event. The authenticity of this single additional codon was confirmed by sequencing the mouse and pig genomic copies of the gene. The urate oxidase sequence contains a domain similar to the type 2 copper binding motif found in other copper binding proteins, suggesting that the copper ion in urate oxidase is coordinated as a type 2 structure. Based upon a comparison of the NH2-terminal peptide and deduced sequences, we propose that the maturation of pig urate oxidase involves the posttranslational cleavage of a six-amino acid peptide. Two nonsense mutations were found in the human urate oxidase gene, which confirms, at the molecular level, that the urate oxidase gene in humans is nonfunctional. The sequence comparisons favor the hypothesis that the loss of urate oxidase in humans is due to a sudden mutational event rather than a progressive mutational process.
and

Quote:
Mol Biol Evol 2002 May;19(5):640-53
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Loss of urate oxidase activity in hominoids and its evolutionary implications.

Oda M, Satta Y, Takenaka O, Takahata N.

Department of Biosystems Science, Graduate University for Advanced Studies (Sokendai), Hayama, Kanagawa, Japan. Primate Research Institute, Kyoto University, Inuyama, Aichi, Japan.

We have determined and compared the promoter, coding, and intronic sequences of the urate oxidase (Uox) gene of various primate species. Although we confirm the previous observation that the inactivation of the gene in the clade of the human and the great apes results from a single CGA to TGA nonsense mutation in exon 2, we find that the inactivation in the gibbon lineage results from an independent nonsense mutation at a different CGA codon in exon 2 or from either one-base deletion in exon 3 or one-base insertion in exon 5, contrary to the previous claim that the cause is a 13-bp deletion in exon 2. We also find that compared with other organisms, the primate functional Uox gene is exceptional in terms of usage of CGA codons which are prone to TGA nonsense mutations. Nevertheless, we demonstrate rather strong selective constraint against nonsynonymous sites of the functional Uox gene and argue that this observation is consistent with the fact that the Uox gene is unique in the genome and evolutionarily conserved not only among animals but also among eukaryotes. Another finding that there are a few substitutions in the cis-acting element or CAAT-box (or both) of primate functional Uox genes may explain the lowered transcriptional activity. We suggest that although the inactivation of the hominoid Uox gene was caused by independent nonsense or frameshift mutations, the gene has taken a two-step deterioration process, first in the promoter and second in the coding region during primate evolution. It is also argued that the high concentration of uric acid in the blood of humans and nonhuman primates has developed molecular coevolution with the xanthine oxidoreductase in purine metabolism. However, it remains to be answered whether loss of Uox activity in hominoids is related to protection from oxidative damage and the prolonged life span.

PMID: 11961098 [PubMed - in process]
and

Quote:
: Cytogenet Cell Genet 1992;61(2):121-2
Related Articles, Links


Localization of the human urate oxidase gene (UOX) to 1p22.

Yeldandi AV, Patel YD, Liao M, Kao FT, Rao MS, Reddy JK, Le Beau MM.

Department of Pathology, Northwestern University Medical School, Chicago, IL 60611.

The human urate oxidase (E.C.1.7.3.3) gene, UOX, is assigned to chromosome 1 by Southern analysis of human x hamster cell hybrids. Using fluorescent in situ hybridization, we have mapped this gene to 1p22.

MeSH Terms:

Animal
Blotting, Southern
Chromosome Mapping
Chromosomes, Human, Pair 1*
DNA/isolation & purification
DNA/genetics
Hamsters
Human
Hybrid Cells
Karyotyping
Restriction Mapping
Support, Non-U.S. Gov't
Support, U.S. Gov't, P.H.S.
Urate Oxidase/genetics*


Gene Symbols:

UOX


Substances:

Urate Oxidase
DNA


Grant support:

CA42557/CA/NCI
GM23750/GM/NIGMS


PMID: 1395718 [PubMed - indexed for MEDLINE]
Now vanderzyden, your delaying tactics aside, what is your explanation for this evidence?
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Old 09-16-2002, 10:18 PM   #28
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More to the point: there may be confusion of just why genetic homology is 'evidence' for the theory of evolution. The evidence supports the theory in this case because the theory of evolution EXPLAINS the data. (we are genetically similar to chimpanzees because our species diverged recently).

I am yet to see a competeing theory that explains the data better. the common design theory explanation: that the genes are similar because the designer chose a similar plan, does not hold up. It does not explain why there are similarities in non-functional 'junk' DNA.

Would you agree that the theory that best explains the data is the better theory?
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Old 09-16-2002, 10:20 PM   #29
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Thank you, monken. I couldn't bloody find them.

(personally I find pubmed a bugger to use, but I'm sure I just need more practice)

It's kind of tricky to dig up articles for things that have been accepted for decades, isn't it? Does anyone know where I might look for the original article that suggested 99% genetic homology (circa 1975, I believe).

[ September 16, 2002: Message edited by: Doubting Didymus ]</p>
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Old 09-16-2002, 10:29 PM   #30
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to save Vander the trouble of checking and seeing that they do indeed corroborate eachother, a blast alignment of the sequences derived from the first and third papers yields a difference of 1 nucleotide, an A-&gt;T transversion at residue number 368

comparisons between the first and the second paper yield 100 percent homology between the sequences posted on genbank.

The final corroboration comes from a genome blast of contig sequence from the human genome project - its 100 percent homologous.

what a shame vander, you'll actually have to adress the evidence, rather than call its accuracy into question

[ September 17, 2002: Message edited by: monkenstick ]</p>
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