- THIS ARTICLE
- Full Text (PDF)
- Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via HighWire
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Clark, A. G.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Clark, A. G.
Genetics, Vol 129, 909-923, Copyright © 1991
INVESTIGATIONS |
Mutation-Selection Balance and Metabolic Control Theory
A. G. Clark
Department of Biology and Genetics Program, Pennsylvania State University, University Park, Pennsylvania 16802
The evolution of metabolic control is examined with models that unify approaches of classical quantitative genetics and metabolic control theory. The quantitative traits considered are the activities of enzymes embedded within metabolic pathways. In the models, polygenic mutation alters the enzyme activities (V(max)/K(m)) according to prescribed distributions, and the population evolves following classical haploid viability selection. Stabilizing selection operates on global properties of the metabolic pathway, including either flux or metabolite pool concentration. Analytical results and numerical simulations demonstrate several important properties of these characters, including skewed, non-Gaussian equilibrium distributions, and an expected positive correlation between activities of enzymes flanking a substrate pool undergoing stabilizing selection. The house-of-cards approximation proved to be accurate in predicting the equilibrium distribution of allelic effects for a biologically reasonable segment of the parameter space. Further experimental and theoretical work is needed before a clear assessment can be made whether the observed variance in enzyme activities is explicable by a mutation-selection balance, and this system provides an excellent opportunity for such a test.
This article has been cited by other articles:
 |
|
 |
|
  K. L. Montooth, K. T. Siebenthall, and A. G. Clark Membrane lipid physiology and toxin catabolism underlie ethanol and acetic acid tolerance in Drosophila melanogaster J. Exp. Biol., October 1, 2006; 209(19): 3837 - 3850. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. C. Bagheri and G. P. Wagner Evolution of Dominance in Metabolic Pathways Genetics, November 1, 2004; 168(3): 1713 - 1735. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Bierne, A. Tsitrone, and P. David An Inbreeding Model of Associative Overdominance During a Population Bottleneck Genetics, August 1, 2000; 155(4): 1981 - 1990. [Abstract] [Full Text]
|
|
|
|
|
|
B. Bost, C. Dillmann, and D. de Vienne Fluxes and Metabolic Pools as Model Traits for Quantitative Genetics. I. The L-Shaped Distribution of Gene Effects Genetics, December 1, 1999; 153(4): 2001 - 2012. [Abstract] [Full Text]
|
|
|
|
 |
|
 B Oliver, J Singer, V Laget, G Pennetta, and D Pauli Function of Drosophila ovo+ in germ-line sex determination depends on X-chromosome number Development, January 11, 1994; 120(11): 3185 - 3195. [Abstract] [PDF]
|
|