bernard Wrote:
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>
> 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).
>


Have you considered that although New Scientist may not be as highbrow as the journals you frequent, it may be more up to date ? You clearly have more specialisation in this area than me, I'm a generalist and like to keep up with quantum physics, cosmology, cognition etc etc so can never match a specialist. But I'd like to hear your response to the rest of the New Scientist article and the paper it references before I reply to that;

Quote

Now Lindquist has shown that in yeast at least there is another way that adaptive traits can be passed on, involving a combination of genetic and epigenetic inheritance. And it is triggered by prions, proteins that can change shape, assuming a conformation which coaxes other proteins to form that shape, too.

Lindquist examined the role of a protein called Sup35 in the yeast Saccharomyces cerevisiae which normally makes certain that "junk" regions of the genome are not used to make proteins. When Sup35 forms a prion it becomes sloppy in its work, allowing proteins to be made from previously unused pieces of DNA.

Lindquist's team showed that a surprising proportion of yeast cells containing Sup35 prions, about 20 per cent, acquired new adaptive powers, such as resistance to the herbicide paraquat. Using sophisticated genetic techniques, her team was then able to remove the prion and show that the resistance also disappears. No change had occurred in the cell's DNA. Instead the presence of the Sup35 prion meant that unused portions of the yeast genome were switched on to code for new protein regions that conferred resistance to the herbicide.

But even more surprising was what happened when these cells were mated to another strain with no paraquat resistance. Some of the progeny quickly acquired the ability to resist the herbicide - even when they did not contain the prion (Nature, DOI: 10.1038/nature02885). Lindquist believes that the reshuffling of genes that occurs in sexual reproduction allowed new genetic combinations to form that are resistant to the drug. "Without the prion, these cells would not have survived to mate and find those new genetic combinations," she says. So the epigenetic inheritance supported by prions provided a route for selection of new gene combinations, mating Larmarckian and Darwinian notions of evolution.

Even so, prion researcher Yuri Chernoff of the Georgia Institute of Technology in Atlanta says it remains unclear whether this type of evolution occurs outside the laboratory, and in organisms other than yeast. "But that does not diminish the importance of this work in revealing a specific mechanism for this type of inheritance." Lindquist points out that the Sup35 protein seems to have retained its ability to turn into a prion over some 400 million years of fungal evolution, suggesting the prion provided some advantage.

Experts already think other epigenetic mechanisms may have shaped the evolution of more complex organisms (New Scientist, 28 November 1998, p 26). "I wouldn't be surprised if this happens in people as well. This is the tip of the iceberg," Lindquist says.

>
> 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.


Bernard I expected more from you than that excuse DNA itself contains within it the ability to adapt (and you don't need to go to the Dawkins Selfish Gene exteme to accept that. So it has a pre-existing capacity to mutate and evolve for survival. If you don't realise why that is appropriate to your comments I will elucidate further :-)

Something new IS acquired. After reproduction the genes produce a different organism in that it has traits that its predeccessor did not have (whether or not they had the mechanism to produce that trait in the first place is irrelevant (or on the other hand extremely relevant) to your argument. You have decided that a small part of the whole process is the only one to consider relevant when more and more evidence is suggesting a more complex process at work. If I didn't have problems with the way the term is used in the US, I would even suggest attributes of the process that are intelligent, even beautiful.


>
> >
> >
> > 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.
>


No Bernard If mutations build up slowly over time and then when certain factors kick in which stimulate the release of these mutations (via HSP90 mechanisms) then sure, the genes that were not best adapted (at the risk of using Dawkins extreme philosophy) would cause their "host" to die, but in a circumstance where most of the species are dying anyway. A few release a combination of genes that both leads to traits that overcome the current difficulties, and are compatible (at the very least for one generation) with the current species. I may have a simplistic view on all this but if something makes sense to me then its up to you to persuade me otherwise. You haven't done so yet




>
> 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.
>


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.


> 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
>


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