Stress is an omnipresent factor in wild conditions, but has not been fully appreciated in evolutionary theory. One of the most consistent trends recorded in analyses of phenotypic response to stress is an increase in phenotypic variation. It has been suggested that the major cause for this phenomenon is disruption of homeostatic processes under stressful conditions, inducing an increase either in genetic variance, in the frequency of developmental random errors as measured by fluctuating asymmetry (FA),or both. This challenges one of the major issues addressed by quantitative genetic, that is, the validity of the predictive models of phenotypic evolution. These models are indeed based on the assumption that matrix of genetic variance (G matrix) is consistent across environments. Departure from this assumption might cause strong biases on the conclusions of the models, and thus challenge our ability to predict evolution. The molecular and genetic bases of the buffering processes presumably impaired by stress remain mostly obscure. Heat Shock Protein 90 (Hsp90) is a good candidate for such buffering mechanism. The aim of this project is:
(1) to investigate the genetic bases of the increase of phenotypic variation under stressful conditions, using an approach combining geometric morph metrics and quantitative genetics. Particular attention will be paid to the effects of temperature on the structure of the G matrix. We will investigate the hypothesis that genes different from those involved in genetic variance under usual temperature are responsible for the predicted increase in genetic variance under stressful conditions.
(2) Comparing the effects of environmental stress and those of several mutations of Hsp90,we will investigate the putative role of Hsp90 in the phenotypic and genetic stress responses. The wings of Drosophilae melanogaster are a particularly suitable model to investigate these mechanisms.
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