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  Topic: Evolution of the horse; a problem for Darwinism?, For Daniel Smith to present his argument< Next Oldest | Next Newest >  
JAM



Posts: 517
Joined: July 2007

(Permalink) Posted: Oct. 14 2007,00:01   

Quote (Daniel Smith @ Oct. 13 2007,23:32)
My hypothesis does not predict a flat line - except within a lineage.  By "lineage" I mean either the same species or very closely related species.  As an example I would think something along the lines of the African vs. Asian elephant.  This is why I said that the test needs to be done within the lineage to test my hypothesis.

I already gave you a URL for such a pair--rat vs. mouse. You, predictably, completely ignored the data.
   
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But orthologous regions are regions that are thought to be homologous due to speciation - which is assumed to have occurred by an accumulation of mutations - isn't that correct?    

Not even close. All orthologs are homologs, but not all homologs are orthologs. Orthologs are not merely homologous, but have the same function. Operationally, we're only really sure about these when we have complete genome sequences or when we rescue a mouse mutant with its human ortholog as a transgene. There are orthologous stretches along huge segments of chromosomes, in which gene order is preserved. This is called synteny. How do you explain that?
     
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Isn't it my hypothesis we're testing?    

We're testing both at once.
     
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What demands?      
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You must show me that the evidence supports this assumed buildup of random mutations first, then we can move on from there.

That's a petulant demand.
     
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My hypothesis predicts that there is no buildup of random mutations within the genome - even in non-coding sites.  Isn't that what we're testing?

Not quite. Your hypothesis predicts that identity will be no different in coding vs. noncoding sites. Predictions are made about observable data, but we both know that you're desperate to avoid that.

You really oughta figure out that "random" only refers to fitness before going on these rants.
 
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Speaking of predictions, I have another one for you:
It's my prediction that random mutations are only neutral or deleterious - never advantageous.

That's not a prediction, it's a hypothesis. Come on, man, this isn't that difficult. Predictions are made ABOUT DIRECTLY OBSERVABLE THINGS.

Let's see if you can grasp this at the second-grade level:
1) The hypothesis that my dog understands the meaning of the word "sit" predicts that that my dog WON'T sit when I say "fit" or "tit" or "sib" or "hit" in the same tone of voice and with the same body language.
2) The hypothesis that my dog does not understand the meaning of the word "sit" predicts that that my dog WILL sit when I say "fit" or "tit" or "sib" or "hit" in the same tone of voice and with the same body language.

Do you get it yet? The prediction is about what you directly observe--whether the dog sits or not.
 
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All advantageous mutations are non-random and are therefore experimentally repeatable.

"Non-random"=/="experimentally repeatable," Daniel. If one does sufficient trials, the random becomes not only repeatable, but predicted. Maybe you should read a primer on the Poisson distribution.
 
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"Therefore, I predict that anytime Acromobacter guttatus Sp. K172 is subjected to an environment where it must consume nylon to survive, the same frame shift will occur, resulting in Flavobacterium Sp. KI72."

That's meaningless without numbers, but that's probably what you were aiming for.

  
  1733 replies since Sep. 18 2007,15:27 < Next Oldest | Next Newest >  

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