Simon Wrote:
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> Hi bernard
>
> If non-coding parts of the genome are in effect
> activated by the prions to confer, say, a new
> disease resistance, and then through sexual
> reproduction this resistance is transferred, is
> that not effectively an alteration of the genes to
> confer a trait ?

This entire process has nothing to do with non-coding DNA. What we have is a genetic coding to produce a protein (a particular sequence of amino acids encoded in the DNA). This particular protein can fold into two (or more perhaps) 3-dimensional conformations. The normal folded conformation (call it A for ease of discussion) and a different folded conformation-- the prion (call it . The unusual properties of these prions is that they can in the proper conditions make all of conformation A convert to the prion conformation B. No thing in the geneome is activated, no coding or non coding DNA is activated. This does not confer disease resistance, in fact, prions ARE lethal diseases ("mad cow", "Jacob-Kreutzfeld", etc).


Whether or not you want to say
> its the phenotype rather than the genotype thats
> specifically changed, surely its is an
> evolutionary significant influence ? And surely
> such a mechanism is Lemarkian as well as Darwinian
> ?
What makes these systems interesting is that prions can pass on their conformations to other generations preent. This is a protein-to-protein inheritance it is not genetic and therefore by definition does not fall into the concept of Darwinian evolution which is a "change in the genotype and genome" it is also not Lamarkian because nothing new is acquired or "learned" in the process. The capacity to make prions is already (pre-existing) in the genetics of the yeast in question.

>
>
> But there's a bigger problem, Barton and other
> evolutionary biologists say. Most random mutations
> are deleterious, so how could processes that boost
> variability help organisms survive overall? In
> fact, says Barton, "a major problem in
> evolutionary biology is to explain why genetic
> variation is so abundant in nature."
>
>
> I realise there is plenty we don't about about
> what the role of non-coding DNA actually is,

non-coding DNA has noting to do with this.


but
> Lindquist has already shown that 'release' of
> mutations is controlled by HSP90 during times of
> environmental stress. In between these times
> HSP90 buffers the mutations and so they don't
> cause problems. So I don't really see what
> Bartons problem is.
>
No, Simon- I don't have the full paper (or the full New Scientist) but if you read what you wrote. First, HSP90 is what is called a chaperone protein- these are very common and are charectized by being 90 Kd in size, These help to regulate the transcriptions on the syntheses of proteins.

The point of Lindquist's and others is that it seems that in times of stress- organisms have developed mechanisms that produce more mutations and Barton's point is that this does not guarantee a successful adaptation because we know that most mutations are harmful rather than helpful. In normal times excess mutations so the potential problem does not occur.

This (and the other examples being pursued) resemble the strategy involved in our immune systems. Instead of developing a one-gene-one mutation-one disease approach, what the body has developed is a a generalized disease fighting machinery. The immune system is set up to fight any foreign substance (above a threshold size) that enters the body. it is extremely flexible and self programmming.

The same applies to the development of mutation developing machinery. Instead of just doing one mutation at a time. Here the DNA codes for a machine to generate mutations that kicks in when the organism is under stress. This is still controlled by genes , is Darwinian and does not oveerturn the new synthesis.
Bernard


> Simon
>
>
>