The idea of genetic assimilation, that environmentally induced phenotypes may become genetically fixed and no longer require the original environmental stimulus, has had varied success through time in evolutionary biology research. Proposed by Waddington in the 1940s, it became an area of active empirical research mostly thanks to the efforts of its inventor and his collaborators. It was then attacked as of minor importance during the ‘‘hardening’’ of the neo-Darwinian synthesis and was relegated to a secondary role for decades. Recently, (...) several papers have appeared, mostly independently of each other, to explore the likelihood of genetic assimilation as a biological phenomenon and its potential importance to our understanding of evolution. In this article we briefly trace the history of the concept and then discuss theoretical models that have newly employed genetic assimilation in a variety of contexts. We propose a typical scenario of evolution of genetic assimilation via an intermediate stage of phenotypic plasticity and present potential examples of the same. We also discuss a conceptual map of current and future lines of research aimed at exploring the actual relevance of genetic assimilation for evolutionary biology. (shrink)

The phenomenon of ‘canalization’ ‐ the genetic capacity to buffer developmental pathways against mutational or environmental perturbations ‐ was first characterized in the late 1930s and early 1940s. Despite enormous subsequent progress in understanding the nature of the genetic material and the molecular basis of gene expression, there have been few attempts to interpret the classical work on canalization in molecular genetic terms. Some recent findings, however, bear on one form of canalization, ‘genetic canalization’, the stabilization of development against mutational (...) effects. These data indicate that co‐expressed paralogous genes can function as mutual ‘back‐up’ elements in developmental processes. Paralogues, however, are far from the only basis of canalization: other genetic sources can be readily envisaged and some of these are described here. The evolutionary questions about genetic canalization and the mechanistic questions about developmental instability that still need to be addressed are also briefly discussed. (shrink)

In describing the flawless regularity of developmental processes and the correlation between changes at certain genetic loci and changes in morphology, biologists frequently employ two metaphors: that genes ‘control’ development, and that genomes embody ‘programs’ for development. Although these metaphors have an admirable sharpness and punch, they lead, when taken literally, to highly distorted pictures of developmental processes. A more balanced, and useful, view of the role of genes in development is that they act as suppliers of the material needs (...) of development and, in some instances, as context‐dependent catalysts of cellular changes, rather than as ‘controllers’ of developmental progress and direction. The consequences of adopting this alternative view of development are discussed. (shrink)

A founder event occurs when a new population is established from a small number of individuals drawn from a large ancestral population. Mayr proposed that genetic drift in an isolated founder population could alter the selective forces in an epistatic system, an observation supported by recent studies. Carson argued that a period of relaxed selection could occur when a founder population is in an open ecological niche, allowing rapid population growth after the founder event. Selectable genetic variation can actually increase (...) during this founder‐flush phase due to recombination, enhanced survival of advantageous mutations, and the conversion of non‐additive genetic variance into additive variance in an epistatic system, another empirically confirmed prediction. Templeton combined the theories of Mayr and Carson with population genetic models to predict the conditions under which founder events can contribute to speciation, and these predictions are strongly confirmed by the empirical literature. Much of the criticism of founder speciation is based upon equating founder speciation to an adaptive peak shift opposed by selection. However, Mayr, Carson and Templeton all modeled a positive interaction of selection and drift, and Templeton showed that founder speciation is incompatible with peak‐shift conditions. Although rare, founder speciation can have a disproportionate importance in adaptive innovation and radiation, and examples are given to show that “rare” does not mean “unimportant” in evolution. Founder speciation also interacts with other speciation mechanisms such that a speciation event is not a one‐dimensional process due to either selection alone or drift alone. BioEssays 30:470–479, 2008. © 2008 Wiley Periodicals, Inc. (shrink)

Epistasis plays an important role in the genetic architecture of common human diseases and can be viewed from two perspectives, biological and statistical, each derived from and leading to different assumptions and research strategies. Biological epistasis is the result of physical interactions among biomolecules within gene regulatory networks and biochemical pathways in an individual such that the effect of a gene on a phenotype is dependent on one or more other genes. In contrast, statistical epistasis is defined as deviation from (...) additivity in a mathematical model summarizing the relationship between multilocus genotypes and phenotypic variation in a population. The goal of this essay is to review definitions and examples of biological and statistical epistasis and to explore the relationship between the two. Specifically, we present and discuss the following two questions in the context of human health and disease. First, when does statistical evidence of epistasis in human populations imply underlying biomolecular interactions in the etiology of disease? Second, when do biomolecular interactions produce patterns of statistical epistasis in human populations?Answers to these two reciprocal questions will provide an important framework for using genetic information to improve our ability to diagnose, prevent and treat common human diseases. We propose that systems biology will provide the necessary information for addressing these questions and that model systems such as bacteria, yeast and digital organisms will be a useful place to start. BioEssays 27:637–646, 2005. © 2005 Wiley Periodicals, Inc. (shrink)