Marcio Pie pointed us to a fascinating article that up to this moment no one
has responded to. The silence on the part of the Christian apologists, most
noteably the ID folk who believe that irreducibly complex systems can't
arise without divine help, seems rather odd. The article that Marcio pointed
us to has gone a long way toward explaining how such systems can arise--yet
the apologists ignore this article. IMO this is an extremely important
article in the creation/evolution debate.
Marcio wrote:
> An interesting article came out recently in Nature on how a prion may
> improve the "evolvability" of yeast. This may have some relevance
> regarding some ID hypotheses. I'd love to hear your comments on this.
And then cited the first paragraph:
> Nature 407, 477 - 483 (2000)
>
> A yeast prion provides a mechanism for genetic variation and phenotypic
> diversity
>
> HEATHER L. TRUE AND SUSAN L. LINDQUIST
>
> A major enigma in evolutionary biology is that new forms or functions
> often require the concerted effects of several independent genetic
> changes. It is unclear how such changes might accumulate when they are
> likely to be deleterious individually and be lost by selective pressure.
> The Saccharomyces cerevisiae prion [PSI+] is an epigenetic modifier of the
> fidelity of translation termination, but its impact on yeast biology has
> been unclear. Here we show that [PSI+] provides the means to uncover
> hidden genetic variation and produce new heritable phenotypes. Moreover,
> in each of the seven genetic backgrounds tested, the constellation of
> phenotypes produced was unique. We propose that the epigenetic and
> metastable nature of [PSI+] inheritance allows yeast cells to exploit
> pre-existing genetic variation to thrive in fluctuating environments.
> Further, the capacity of [PSI+] to convert previously neutral genetic
> variation to a non-neutral state may facilitate the evolution of new
> traits.
>
The second paragraph tells us a bit about how this happens:
“Here we report that a protein-based element of inheritance (a prion) in
the yeast Sacharomyces cerevisiae provides a means to expose this and other
types of silent protein-coding information. The prion [PSI+] reduces the
fidelity with which ribosomes terminate translation at stop codons in a
metastable, heritable manner. The reduction in translational fidelity caused
by [PSI+] is routinely monitored by the production of active products from
genetic markers containing stop-codon mutations.” Heather L. True and Susan
L. Lindquist, “A Yeast Prion Provides a Mechanism For Genetic Variation and
Phenotypic Diversity,” Nature, 407(2000):477-483, p. 477
This prion seems to make the protein manufacturing facility--the
ribosome--pay less attention to the instructions to stop reading the gene.
This means that the data on the genome past the gene will be read. It may be
nonsense or it may be something good. In any event, the prion causes parts
of the genome which are not normally sampled to be tested for useful
codings. If useful proteins are found in these stranded parts of the genome,
then they manufactured and put out into the cell. If several proteins (from
different parts of the genome) are needed to work in concert in order for
the cell to survive, the prion allows them to be found and used. The prion,
by causing the stop codons to be ignored, allow a period of testing of many,
many novel places in the genome.
True and Lindquist then tell how this mechanism causes new evolution. They
write:
“We have demonstrated that the [PSI+] element of the yeast S. cerevisiae
provides a means to unveil silent genetic information to produce new
heritable phenotypes. IN the context of an individual cell, [PSI+] allows
alternative heritable phenotypes to be encoded by a single genome. In the
context of diverging populations it provides a vast array of new phenotypic
states with unique growth advantages and disadvantages. We propose that the
epigenetic and metastable nature of [PSI+], associated with the fundamental
process of translation, potentiates survival in a fluctuating environment
and provides a conduit for the evolution of new traits.
“Yeast cells spontaneously switch from the [psi-] to the PSI+] state, with
rates generally varying between 1 in 10^5 to 1 in 10^7. Thus, once a
population has reached an appreciable size, some of its genetically
identical members will have acquired a new, heritable phenotype. If the
environment does not favour this phenotype, the loss of these cells will
have a minimal impact on the fitness of that genotype. If the environment
does favour it, the original genotype can thrive even if the original
phenotype is disfavored. Once the progeny with the new phenotype have
reached sufficient densities the spontaneous appearance of [psi-]
derivatives will ensure that the original phenotype is available should the
environment change.”
“[PSI+] allows cells to occupy a new niche without foregoing their capacity
to occupy the old. If the new phenotype remains advantageous, the size of
the growing population increases the likelihood that mutations will arise to
eliminate stop codons that are relevant to the phenotype and require [PSI+]
for read-through. These would make that phenotype more robust and fix the
trait; cells would retain the phenotype upon reversion to the [psi-] state
(presumably normal translation fidelity will generally be favoured in
nature). By this mechanism, [PSI+] could facilitate the evolution of new
traits.” Heather L. True and Susan L. Lindquist, “A Yeast Prion Provides a
Mechanism For Genetic Variation and Phenotypic Diversity,” Nature,
407(2000):477-483, p. 481- 482
Thus, if the environment requires these novel proteins in order to survive,
cells without them will die but cells with them and with the positive prion
state will live. Eventually mutation will remove the stop codons which
normally prevent the manufacture of these novel proteins.
This mechanism answers has huge implications for Behe's claim. Michael
writes:
"Well, for starters, a system that is irreducibly complex. By irreducibly
complex I mean a single system composed of several well-matched, interacting
parts that contribute to the basic function, wherein the removal of any one
of the parts causes the system to effectively cease functioning. An
irreducibly complex system cannot be produced directly (that is, by
continuously improving the initial function, which continues to work by the
same mechanism) by slight, successive modifications of a precursor system
because any precursor to an irreducibly complex system that is missing a
part is by definition nonfunctional." ~ Michael J. Behe, Darwin's Black Box,
(New York: The Free Press, 1996), p. 39
Even if Behe is correct, that such systems can't arise by small independent
changes, this mechanism allows for such systems to arise all at once by
natural causes. Thus, irreducibly complex systems can't be considered
indicative of designers--either intelligent alien life forms or divine
beings. This mechanism effectively refutes the use of complex systems to
infer design.
Behe can no longer claim that as the number of working components increase,
the likelihood of a natural route to the system goes down. Behe claimed,
"Even if a system is irreducibly complex (and thus cannot have been
produced directly), however, one can not definitively rule out the
possibility of an indirect, circuitous route. As the complexity of an
interacting system increases, though, the likelihood of such an indirect
route drops precipitously. And as the number of unexplained, irreducibly
complex biological systems increases, our confidence that Darwin's criterion
of failure has been met skyrockets toward the maximum that science allows."
~ Michael J. Behe, Darwin's Black Box, (New York: The Free Press, 1996), p.
40
The prion system allows lots of different places on the genome to be tested
for useful codings. And given the fact (that I pointed out earlier) that
useful codings are found at a rate of 10^-13 in randomly made sequences, one
must realize that such a mechanism will allow for this search process to be
successful!
The ID group needs to cease looking for evidence of design in biological
systems. It isn't there. While I believe that the universe is designed, I
simply don't think that biological systems are capable of yielding evidence
for design. As such, we should be honest with ourselves and our readers.
Thank you Marcio for pointing out this article and its importance. Why have
the anti-evolutionary apologists not pointed it out first?
glenn
see http://www.flash.net/~mortongr/dmd.htm
for lots of creation/evolution information
>
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