. "5 The Frailty of Adaptive Hypotheses for the Origins of Organismal Complexity--MICHAEL LYNCH." In the Light of Evolution: Volume 1. Adaptation and Complex Design. Washington, DC: The National Academies Press, 2007.
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In the Light of Evolution, Volume I: Adaptation and Complex Design
As in the case of subfunction fission and duplicate-gene subfunctionalization, the probability of establishment of these types of changes will depend on Ng. This is because a redundantly regulated allele has a weak mutational advantage equal to the rate of loss of a regulatory site (ul); one such mutation will result in the nonfunctionalization of either a self-regulated or an upstream-dependent allele, but will leave the function of a redundantly regulated allele unaltered. If 1/Ng > u1, such an advantage will be too small to be influenced by selection, and the population will evolve to an allelic state that simply depends on the relative rates of gain and loss of regulatory sites (ug and ul in Fig. 5.3). In contrast, if 1/Ng < u1, the accumulation of upstream-dependent alleles will be inhibited by their weak mutational burden and their lack of function in genetic backgrounds that fail to support A–B crosstalk. Thus, whereas small Ng may promote the passive elongation of genetic pathways, large Ng has the opposite effect. This does not mean that the augmentation of obligatory pathways cannot occur in very large populations, but if such changes are to occur, they must be of immediate selective advantage.
All replicating populations are capable of evolution, but it has recently been argued that some species are better at it than others, with natural selection directly advancing features of genomic architecture, genetic networks, and developmental pathways to promote the future ability of a species to adaptively evolve. Such speculation, which is almost entirely restricted to molecular and cell biologists and those who study digital organisms (e.g., Gerhart and Kirschner, 1997; Kirschner and Gerhart, 1998, 2005; Rutherford and Lindquist, 1998; True and Lindquist, 2000; Caporale, 2003; Earl and Deem, 2004; Bloom et al., 2006; Federici and Downing, 2006), has been subject to considerable criticism by evolutionary biologists (e.g., Williams, 1966; Dickinson and Seger, 1999; Partridge and Barton, 2000; Brookfield, 2001; Sniegowski and Murphy, 2006). The term evolvability has long been in use in quantitative genetics, where it has a precise definition closely related to the concept of heritability, i.e., the relative amount of standing variation that is subject to a response to natural selection (Houle, 1992; Lynch and Walsh, 1998). However, the above-mentioned authors use the word in a rather different way, loosely defining evolvability to be the ability of a lineage to generate useful adaptive variation via mutational flexibility. Regardless of the definition, the idea that variation in evolvability exists among species is secure, as it has long been known that organisms and classes of traits vary in their propensities to respond to natural selection (Falconer and Mackay, 1996). Less secure is the idea that the ability to evolve itself is actively promoted by directional selection. Four reasons for skepticism follow.