PMID: 20598394;PMCID: PMC3198833;Abstract:
Why isn't random variation always deleterious? Are there factors that sometimes make adaptation easier? Biological systems are extraordinarily robust to perturbation by mutations, recombination and the environment. It has been proposed that this robustness might make them more evolvable. Robustness to mutation allows genetic variation to accumulate in a cryptic state. Switching mechanisms known as evolutionary capacitors mean that the amount of heritable phenotypic variation available can be correlated to the degree of stress and hence to the novelty of the environment and remaining potential for adaptation. There have been two somewhat separate literatures relating robustness to evolvability. One has focused on molecular phenotypes and new mutations, the other on morphology and cryptic genetic variation. Here, we review both literatures, and show that the true distinction is whether recombination rates are high or low. In both cases, the evidence supports the claim that robustness promotes evolvability. © 2010 Elsevier Ltd.
PMID: 24228631;PMCID: PMC3849687;
PMID: 15240505;PMCID: PMC1304395;
PMID: 17206583;PMCID: PMC1766558;Abstract:
Adaptive plasticity allows populations to adjust rapidly to environmental change. If this is useful only rarely, plasticity may undergo mutational degradation and be lost from a population. We consider a population of constant size N undergoing loss of plasticity at functional mutation rate m and with selective advantage s associated with loss. Environmental change events occur at rate θ per generation, killing all individuals that lack plasticity. The expected time until loss of plasticity in a fluctuating environment is always at least τ, the expected time until loss of plasticity in a static environment. When mN > 1 and Nθ ≫ 1, we find that plasticity will be maintained for an average of at least 108 generations in a single population, provided τ > 18/θ. In a metapopulation, plasticity is retained under the more lenient condition τ > 1.3/θ, irrespective of mN, for a modest number of demes. We calculate both exact and approximate solutions for τ and find that it is linearly dependent only on the logarithm of N, and so, surprisingly, both the population size and the number of demes in the metapopulation make little difference to the retention of plasticity. Instead, τ is dominated by the term 1/(m + s/2). © 2007 by The University of Chicago.
PMID: 19521499;PMCID: PMC2686163;Abstract:
The [PSI+] prion may enhance evolvability by revealing previously cryptic genetic variation, but it is unclear whether such evolvability properties could be favored by natural selection. Sex inhibits the evolution of other putative evolvability mechanisms, such as mutator alleles. This paper explores whether sex also prevents natural selection from favoring modifier alleles that facilitate [PSI+] formation. Sex may permit the spread of "cheater" alleles that acquire the benefits of [PSI +] through mating without incurring the cost of producing [PSI+] at times when it is not adaptive. Using recent quantitative estimates of the frequency of sex in Saccharomyces paradoxus, we calculate that natural selection for evolvability can drive the evolution of the [PSI+] system, so long as yeast populations occasionally require complex adaptations involving synergistic epistasis between two loci. If adaptations are always simple and require substitution at only a single locus, then the [PSI+] system is not favored by natural selection. Obligate sex might inhibit the evolution of [PSI+]-like systems in other species. © 2009 Griswold, Masel.
