Ralf Sommer – fenotypische plasticiteit

Fenotypische plasticiteit is gedefinieerd als de eigenschap van organismen om verschillende fenotypes te produceren in reactie op omgevingsvariatie. Intrinsically, phenotypic plasticity refers to all kinds of environmentally induced phenotypic variation and it can affect morphological, physiological, and behavioral aspects of an organism’s phenotype, but also its life history. Plasticity is a universal property of living things, because all organisms respond to genes and the environment alike; thus, plasticity is found throughout all domains of life. While botanists have long appreciated the environmental influence on plant morphology, plasticity was less valued in animal systems, although it is as widespread in animals as in plants. In addition, plasticity is known from bacteria, and even phage λ and other bacteriophages with their lytic (virulent) vs. lysogenic (temperate) life cycles. It is an interesting oddity of the history of biology that the first molecular process that was ever elucidated to near completion, the regulation of the lytic cycle in phage λ, represents an example of plasticity, even though it is rarely discussed as such.

Kan fenotypische plasticiteit door overerving worden overgebracht aan nakomelingen, waarbij veranderingen in erfelijk materiaal optreden? Sommer: In 1989, Mary Jane West-Eberhard published a review article entitled Phenotypic plasticity and the origin of diversity …, verder uitgewerkt … in her 2003 monograph Developmental Plasticity and Evolution. This monograph represented the most significant turning point in considering the role of plasticity in evolution by offering four unique contributions. First, it displayed an immense collection of polyphenisms. It showed “once and for all” (West-Eberhard 2003, p. vii) how pervasive alternative phenotypes and plasticity are in nature. This observation resulted in the important conclusion that organisms are universally responsive to the environment, similar to their responsiveness to genes. Een volkomen Einpassung van organismen in hun omgeving.

Het zijn de fenotypen die blootstaan aan natuurlijke selectie, zoals Waddington al benadrukte: Second, West-Eberhard argued that alternative phenotypes become developmentally and functionally independent subjects of selection. En Sommer zegt, – maar ik zie nog niet hoe -: The independent expression in different individuals and populations can therefore lead to evolutionary novelty and adaptation. Both of these conclusions, the universal interdependence between the environment and organisms, as well as selection independently targeting the alternative phenotypes of plasticity, were made possible by West-Eberhard’s liberate restriction on alternative phenotypes.

West-Eberhard stelt voor dat plasticiteit een manier is waarop nieuwe eigenschappen worden uitgeprobeerd, zonder dat ze eerst in de plaats (moeten) komen van oude eigenschappen: … the final contribution of the book was to propose plasticity as a major facilitator of novelty: “alternative (phenotypes) permit the elaboration of a new trait without eliminating an established one, thereby facilitating the evolution of new adaptive specializations” (West-Eberhard 2003, p.377). This idea resulted in the hypothesis that novelty in evolution is often associated with plasticity. Plasticity, with its inherent consideration of environmental and developmental influences on phenotypes, is therefore a logical extension to evolutionary theory that can overcome existing inconsistencies. In summary, Developmental Plasticity and Evolution represented a critique on evolutionary thought that simultaneously provided new hypotheses, which can be empirically tested. As will be discussed below, the confirmation of the facilitator hypothesis and the identification of associated molecular mechanisms are the most critical challenges for current and future plasticity research.

Er moet dan aan drie voorwaarden worden voldaan: First, the origin of novelty often starts with environmentally responsive and developmentally plastic traits. This proposal is also referred to as “plasticity first evolution” or the “flexible stem hypothesis”. Second, environmental responsiveness requires developmental reprogramming in the form of developmental switch genes. And third, pulses of plasticity are restricted in evolutionary time. Ultimately, plasticity, and with it environmental responsiveness, becomes genetically encoded, a phenomenon that is also known as “canalization,” “genetic accommodation,” or genetic assimilation with slightly different meanings. Sommer werkt de eerste voorwaarde  – novelty relies on plasticity – uit op basis van fylogenetische (re)constructies. Deze laat ik buiten beschouwing. Bij de tweede voorwaarde – developmental switch genes and the molecular basis of plasticity – geeft Sommer een interessant onderscheid:

Nonplastic developmental processes are hardwired against environmental fluctuations, whereas plastic processes are characterized by being able to sense and respond to environmental information. It has been proposed that developmental switch genes fulfill this function by first, sensing the environment and second, controlling alternative phenotypes. However, the identity of such developmental switch genes remained completely elusive for a long time. In developmental biology, so-called “genetic switch genes” are well known from various developmental pathways. For example, the proto-oncogene RAS in EGF/EGFR signal transduction, when permanently activated through a gain-of-function mutation, results in a conformational change that leads to the overexpression of certain cell fates (Han and Sternberg 1990). As part of more complex gene regulatory networks (GRNs), such signal transduction pathways control gene expression via individual or groups of transcription factors (Davidson 2006). However, it was unclear if genetic switch genes were part of “environmentally induced developmental switches” in the context of phenotypic plasticity. Similarly, the GRNs that control plastic phenotypes have not yet been identified. Therefore, testing this prediction, and identifying developmental switch genes and associated GRNs, were essential to confirm the significance of plasticity for evolution. Such endeavors require a model system approach with molecular and genetic investigations providing mechanistic insight. Onderzoek aan de nematode Pristionchus pacificus wijst in deze richting.

De derde voorwaarde – regimes of canalization, from genetic accommodation to assimilation – houdt in dat bepaalde fenotypische respons vastgelegd wordt in het genetisch materiaal. Onderzoek aan de Rundermestpillendraaier Ontophagus taurus (een mestkever) suggereert inderdaad dat polyphenisms are subject to selection, which will result in adaptive changes. Een ander voorbeeld dat Sommer geeft, gaat over pijlstaartvlinders: Heat-shock experiments at 42° in the sensitive period allowed a range of color morphs to be generated that can be selected for in experimental evolution settings. Within 13 generations, polyphenic and monophenic lines were selected that resulted in green and black morphs, respectively. When cultured under constant conditions between 20° and 33°, only the polyphenic line exhibited a strong threshold response with temperatures > 30°, showing a similar response to the heat-shock condition of 42°. Physiological studies revealed that the polyphenic line had higher juvenile hormone titers at higher temperatures, suggesting that changes in hormonal regulation may underlie the evolution of color polyphenism.

Genetic accommodation zoals hierboven beschreven, verschilt principieel van genetic assimilation en canalization: Genetic accommodation is a mechanism by which a phenotypic variation, originally induced by a mutation or an environmental change, becomes adaptive. In contrast, genetic assimilation results in the genetic fixation (canalization) of the novel trait, thereby eliminating its environmental responsiveness altogether.

Gerdien de Jong schreef vijftien jaar eerder over deze materie het artikel dat ik onder de Mexicaanse tetra aanhaalde. Zij noemt twee perspectieven op fenotypische plasticiteit: In the first view, phenotypic plasticity is a quantitative trait subject to selection and evolution and a property of the genotype. In this view, phenotypic plasticity might be of huge ecological importance but is a trait as any other trait as regards evolution. In the second view, phenotypic plasticity is a developmental process facilitating evolution. Here, phenotypic plasticity is an inherent property of the developing phenotype. In this second view, the most important question is not how phenotypic plasticity itself evolves, but how phenotypic plasticity changes development and thereby causes evolution. To rephrase and possibly overstate the divergence, phenotypic plasticity might be a trait subject to selection, or a developmental mechanism as important as selection in evolution. Het eerste perspectief zou ik Mendeliaans kunnen – hoe de trait tot stand komt, is niet het onderwerp, als er maar een erfelijke component is. Het tweede perspectief wil inzicht krijgen in de relatie tussen genotype en fenotype. Het belangrijkste dat De Jong laat zien, is dat deze perspectieven elkaar niet uitsluiten. Bij de derde voorwaarde die Sommer noemt, blijft selectie een rol spelen of is selectie niet uitgesloten.

Hoe zit dat nu met de evolutie van de Mexicaanse tetra? In het biologie-examen werd gesteld: Evolutie gaat sneller als epigenetische mechanismen een rol spelen. Dit is aangetoond bij een zoetwatervisje, de Mexicaanse tetra. Wat er sneller gaat, is dat het fenotype dat tot expressie komt, niet het gevolg is van mutaties, maar van epigenetische mechanismen:  Het snelle ontstaan van de oogloze dieren kan niet verklaard worden door nieuwe mutaties. Er zijn namelijk zo’n 15 tot 20 mutaties nodig voor het kleiner worden en verliezen van de ogen. Vervolgens treedt selectie op. Op deze wijze verloopt (micro-)evolutie sneller.

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