From: Josh Bembenek (jbembe@hotmail.com)
Date: Wed Jul 30 2003 - 15:13:00 EDT
The ability of systems to accumulate changes with Hsp90 and exhibit large
variations due to stress is quite an interesting mechanism hypothesized to
expand evolutionary pathways. This is one possible molecular mechanism that
could support Gould’s staltutory evolutionary change models (mass acting
RM&NS?). The following article deals with some parameters of this
mechanism. Could this be part of the indirect mechanism capable of building
IC in organisms?
Nature 424, 549 - 552 (31 July 2003); doi:10.1038/nature01765
Evolutionary capacitance as a general feature of complex gene networks
AVIV BERGMAN1,2 AND MARK L. SIEGAL1
1 Department of Biological Sciences, Stanford University, Stanford,
California 94305-5020, USA
2 Center for Computational Genetics and Biological Modeling, Stanford
University, Stanford, California 94305-5020, USA
Correspondence and requests for materials should be addressed to M.L.S.
(mlsiegal@stanford.edu).
An evolutionary capacitor buffers genotypic variation under normal
conditions, thereby promoting the accumulation of hidden polymorphism. But
it occasionally fails, thereby revealing this variation phenotypically. The
principal example of an evolutionary capacitor is Hsp90, a molecular
chaperone that targets an important set of signal transduction proteins.
Experiments in Drosophila and Arabidopsis have demonstrated three key
properties of Hsp90: (1) it suppresses phenotypic variation under normal
conditions and releases this variation when functionally compromised; (2)
its function is overwhelmed by environmental stress; and (3) it exerts
pleiotropic effects on key developmental processes. But whether these
properties necessarily make Hsp90 a significant and unique facilitator of
adaptation is unclear. Here we use numerical simulations of complex gene
networks, as well as genome-scale expression data from yeast single-gene
deletion strains, to present a mechanism that extends the scope of
evolutionary capacitance beyond the action of Hsp90 alone. We illustrate
that most, and perhaps all, genes reveal phenotypic variation when
functionally compromised, and that the availability of loss-of-function
mutations accelerates adaptation to a new optimum phenotype. However, this
effect does not require the mutations to be conditional on the environment.
Thus, there might exist a large class of evolutionary capacitors whose
effects on phenotypic variation complement the systemic, environment-induced
effects of Hsp90.
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