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thesciguy

06/05/07 4:10 PM

#64214 RE: frogdreaming #64206

Frog-

Unfortunately there are ten times as many parts as previously thought.

There are, in fact, about 3X FEWER parts than previously predicted. Prior to the completion of the HGP, there was an estimated 100,000 genes in the human genome. It turns out there are only about 30,000.

The reason that we can't seem to find the causal elements that result in specific traits is that we are limiting our review to the 'parts' that we have on our list.

Stop the presses! Do you mean to suggest, that YOU know (understand) the REASON we are having a harder time than predicted correlating specific genetic variants to specific disease. Please, by all means, tell us! You owe it to the rest of humanity to put us on the right track. (At least give us a hint where to look).

I try to discuss, "the relationship between gene variants and traits", you argue the difference between "inheritance and disease" as though those topics are not direct subsets of "variants and traits".

Cute Frog, but my distinction was in response to your inability to differentiate between inheritance and disease in the context of Mendel. Next time, copy the reference so that I don't need to go round-and-round with you. Here it is: Mendel's work was motivated by the desire to understand the mechanism of inheritance, not disease.

Sciguy, I'm sorry but you seem intent on trying to hide behind words when we are trying to discuss concepts.

On the contrary, I am trying to focus the discussion. You have a tendency to pick nits (your words from a previous post). It is essential to understand, define and differentiate the terms we are attempting to discuss, something that you try very hard to manipulate to create an "advantage" or a level of understanding, which does not exist.

Thanks for the reference. I'll read it and explain it to you in a subsequent post.

Good luck.





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thesciguy

06/05/07 4:42 PM

#64216 RE: frogdreaming #64206

Frog-

What is your opinion and reaction to the fairly recent discovery that instead of the one tenth of one percent variation between individuals that was compiled by the genome project, the actual variances are much larger than that and were 'missed' by false assumptions made in the genome project process? Variances that are also 'invisible' to SNP analysis methods?

They are not 'missed', or 'invisible'. (Can you even define what that means?) You misunderstood the paper. Here's the reference: http://www.nature.com/nature/journal/v444/n7118/abs/nature05329.html

I'll summarize for you (I don't actually expect you to read it- and I know you didn't. I did). CNVs only ADD to the multidimensional analysis use to correlate coarse-grained genetic variance with disease. Knowledge of CNVs lends SUPPORT for using AIMs, SNPs, HapMaps, etc.. as a tool for genetic analysis of disease. Knowledge and understanding of CNVs is GOOD for advancing this "infant" technology.

Light a candle, Frog.

Good Luck.