Muller ( 1932 ), however, thought that the evolutionary selection would act Zygotes will have a better chance of survival than " A 1 a", and If necessary, no effect will be produced, i.e. Work required of them, then any inactivation of one of a pair of genes would lead to aĬan just oxidize all of a certain substrate as fast as it is formed, its inactivation will "If we imagine a race whose genes were only just doing the Haldane interpreted dominance in metabolic terms, but adoptedįisher's view that weak selective evolutionary forces acting on heterozygoteswould be sufficient to maintain the What sustains the enzyme activity in a wild-type homozygote at It is in the case of non-rate-limiting enzymes that a furtherĮxplanation must be sought. Rate-limiting enzyme (E 1) the margin could indeed be a simple consequence of the evolution Some have argued that thisĬan be explained entirely in metabolic terms ( Kacser & Burns, Inhibition provides another " margin of safety"Īllowing a heterozygote to maintain the wild-type phenotype.Ī major problem with what we might now call the margin-of-safety theory, is in determining what selectiveįorces would have created and sustained the margins of safety. The reaction rate would become the same as in the homozygote. This would increase the activity per molecule of E 1, so that The most common of these isĮnd-product inhibition (Fig. However, in general, rate-limiting enzymes are subject toĬomplex controls by products of intermediary metabolism. In the case of the rate-limiting enzyme E 1, halving of gene-productĬoncentration ( X to X' in Fig. ![]() It can be seen that the situation with the non-rate-limiting enzymes (E 2,Į 3) corresponds to the " margin-of-safety" To become B, subsequent chemical modifications by E 2 and E 3ĭo not influence the rate of accumulation of the end-product D. Has squeezed through the " bottle-neck" E l This quantity of enzyme would correspond to point Y on a plot of reaction There isĪmple enzyme to accommodate fluctuations in availability of the substrates BĪnd C (the products of E l and E 2, respectively). The ascending limbs of the corresponding substrate dose-response curves (Fig. 1).Įnzymes E 2 and E 3, the normal substrate concentration corresponds to Plot of reaction rate versus enzyme concentration (Fig. Plateau of the dose-response curve, so that enzyme concentration, and not substrateĬoncentration, is rate limiting. The in vivo concentration of A must, by definition, correspond with the In the case of the rate-limiting enzyme E l The vertical arrows indicate the normal substrateĬoncentration existing in vivo. Presented here provides a better basis for understanding the possible role of heat-shockįigure 3 shows hypothetical in vivo substrate dose-response curvesįor the three steps in the pathway. The latter has been provided by Kacser & Burns ( 1980 ). Or " physiological" theory ( Haldane, 1930 Muller,ġ932 Wright, 1977 ), should receive closer scrutiny. Subpopulation, only the wild-type phenotype is observed in heterozygotes.Īgainst the generality of Fisher's theory ( Charlesworth, 1979 Orr,Īppropriate that an alternative theory, the " dose-response" Modification by the products of other genes (modifier genes) eventually, followingĮvolutionary selection acting on the heterozygote That heterozygotes begin with codominant expression of alleles, which are then subject to Much debate, notably the classic dual between Fisher and Wright. ![]() Possible mechanisms of dominance have been the subject of W ild-type alleles are usually dominant over deleterious Proteins occurring in the heat-shock response would have provided a sufficient selectiveįorce for the margin of safety to have evolved. This paper proposes that the rapid decrease in quantity of most normal Response evolved very early as part of an intracellular system for self/not-selfĭiscrimination. The author has proposed elsewhere that the heat-shock Safety is some unspecified " extreme environment The selective force postulated to lead to the evolution of this margin of Heterozygotes with only one copy of a wild-type allele still have sufficient product for ![]() ![]() Of safety" in the quantity of wild-type gene product so that Theory under which dominance is an incidental consequence of selection acting on the Heterozygote population, and a mutant homozygote population.ĭominance would evolve by selection acting on the heterozygote subpopulation has lost Such alleles possible populations include a wild-type homozygote population, a Alleles are usually dominant over deleterious mutant alleles.
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