Hi Bernard
Its always a pleasure to discuss things with you. You are never less than a gentleman. I hope you forgive the childish attitude I often take but its some kind of evolutionary survival instinct I rekon
bernard Wrote:
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>
> > So is DNA itself. Why do you seperate the
> > abilities of the evolution of DNA from the
> process
> > of evolution ? Surely evolution theory as a
> whole
> > does not make such a distinction in such a
> > specific way. If it does, and yet has such
> a
> > primitive understanding of the process, such
> as
> > mapping genome to production of specific
> function
> > and even more so feature, then it seems like
> > guesswork is taking president over evidence.
>
> I guess it is my failure to communicate. It is all
> part of evolution. I don't know is my point was
> that big a point. Essentially it was that in the
> process of generating the variety that then can be
> selected by interaction with the environment the
> DNA of organisms has not been limited to just
> making "silver-bullets", i.e. an allele that deals
> with only one selecting factor. Using the example
> of human disease as the stressor: the sickle cell
> gene, or thalassemia are specific mutations that
> respond to malaria. Humans also have a generalized
> multi-factorial, multi-gene machinery, the immune
> syatem, that can respond to a myriad of diseases.
> The immune syatem can respond physiologically to
> confer lifetime immunity to particular disease
> organisms but this specific immunity is not
> inherited. Only the immune system itself is
> inherited.
>
So are you suggesting the immune system is a 'fait a complete' and is no longer evolving ? Do you see why I'm saying that the ability of the immune system to generate lifetime immunity in the next generation is very much part and parcel of the bigger picture of evoution at a more fundamental level ?
> >
> > So you disasociate the fact DNA has evolved
> the
> > ability to generate these mutations with the
> > result of these mutations. Are you a closit
> > creationist ????
> >
> > LOL
> In the case of the yeast in question, as I
> understand it- There is a protein Sup35 that
> ordinarily is in a soluble conformation in this
> condition the gene is said to be . when this
> condition exists the function of Sup35 is to stop
> the gene's transcription machinery from
> transcribing the DNA of non-coding DNA. {You were
> partially right, and I was partially wrong.
> Non-coding DNA IS involved, but it is not involved
> in the genetic transmission of the prion).
I don't remember suggesting as much but I'll not press the point as its more than possible I was at least partially wrong
> There
> is also the involvement of another protein Hsp104
> in the process. If Hsp104 is present at low
> concentrations, it will catalyze a change in the
> conformation of Sup35 to an amyloid-like polymer--
> a prion. The cell in this condition is . When this
> happens, the normal functioning of Sup35 ceases
> and cells start to transcribe DNA from the
> non-coding DNA sections. This is what produces the
> "mutations" that in 20% of the time confer
> resistance to paraquat. In nature the appearance
> of is a transient occurrence that occurs
> spontaneoously about once every million cells . If
> Hsp104 is present at high concentrations or absent
> altogether, the conversion to prion does not
> occur.
>
> What I'm still not clear on and need to look at
> exactly how the authors prove the inheritance of
> the ability to make prions by daughter cells that
> did not have the ability originally.
Having a simple kind of mind I would suggest that there are bigger changes around function, and smaller ones that invoke these functions once they exist. It seems to me the ability to make the prions existed before, but that the result of the prions is evolutionary significant in terms of the overall genome.
> The claim is
> that this is not a transmission through DNA but
> rather by protein-to-protein. But, in my opinion,
> it might really be transmission of codes
> regulating the levels of Hsp104 protein.
>
But if the genes are shuffled in a particular way due to the prions that leaves certain genes activated that weren't before then there is some relationship between the different processes.
>
> Back to your point above. What I'm saying is that
> the production of proteins coded by the
> "non-coding DNA section" due to the disruption of
> Sup35 function and the subsequent responses to
> paraquat is analogous to the production of
> specific antigens (which are proteins just like
> the ones in the yeast except these are exquisitely
> tailored to the antobody in question) to measles
> by the immune system. We would not call the
> production of antigens to measles a "mutation" or
> even a "dormant gene" because that is just the
> carrying out of a programmed function.
The
> relevant evolutionary process is the one that led
> to the development of the immune system itself.
My point exactly, with the addition of a clear relationship in that gene transfer during reproduction is clearly affected even if the complete genome in this tiny one generation process is not itself actually altered in terms of how we read it as an isolated piece of code.
> In
> the case of the yeast, the relevant evolutionary
> process to look at is what Lindquist and I are
> focusing on-- the mechanism through which the
> function of Sup35 is disrupted by conversion into
> a prion, which makes the cell produce a
> scattershot of new proteins, and how this system
> is passed on to other generations.
>
It will definitely be interesting to follow the research into the whole prion/protein relationship with both DNA and neurons. I rekon some of the big upcoming discoveries in biology will be in this area myself.
Simon