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Developmental Noise (developmental + noise)
Selected AbstractsTrait variability and stress: canalization, developmental stability and the need for a broad approachECOLOGY LETTERS, Issue 2 2001Hoffmann Trait variability (particularly fluctuating asymmetry) may provide a general measure of environmental stress applicable across taxa but consistent empirical support is lacking. Historically, stress effects were considered to act independently on trait canalization, developmental noise and trait size. However, in trait comparisons these processes are often assumed to be associated. Here we reconsider this issue and implications for detecting stress effects using trait variability. Published studies that consider multiple environments report little association between the effects of environmental variation on trait canalization and on developmental noise measured as fluctuating asymmetry, sug-gesting that environmental effects often act independently on these processes. To further test the usefulness of trait variability as an indicator of stress, comparisons across environ-ments should take a broad approach and report on several measures of trait variability, rather than focusing on only one index of fluctuating asymmetry as is commonly done. [source] THE EVOLUTION OF ENVIRONMENTAL AND GENETIC SEX DETERMINATION IN FLUCTUATING ENVIRONMENTSEVOLUTION, Issue 12 2003Tom J. M. Van Dooren Abstract Twenty years ago, Bulmer and Bull suggested that disruptive selection, produced by environmental fluctuations, can result in an evolutionary transition from environmental sex determination (ESD) to genetic sex determination (GSD). We investigated the feasibility of such a process, using mutation-limited adaptive dynamics and individual-based computer simulations. Our model describes the evolution of a reaction norm for sex determination in a metapopulation setting with partial migration and variation in an environmental variable both within and between local patches. The reaction norm represents the probability of becoming a female as a function of environmental state and was modeled as a sigmoid function with two parameters, one giving the location (i.e., the value of the environmental variable for which an individual has equal chance of becoming either sex) and the other giving the slope of the reaction norm for that environment. The slope can be interpreted as being set by the level of developmental noise in morph determination, with less noise giving a steeper slope and a more switchlike reaction norm. We found convergence stable reaction norms with intermediate to large amounts of developmental noise for conditions characterized by low migration rates, small differential competitive advantages between the sexes over environments, and little variation between individual environments within patches compared to variation between patches. We also considered reaction norms with the slope parameter constrained to a high value, corresponding to little developmental noise. For these we found evolutionary branching in the location parameter and a transition from ESD toward GSD, analogous to the original analysis by Bulmer and Bull. Further evolutionary change, including dominance evolution, produced a polymorphism acting as a GSD system with heterogamety. Our results point to the role of developmental noise in the evolution of sex determination. [source] Incidental neurodevelopmental episodes in the etiology of schizophrenia: An expanded model involving epigenetics and developmentCLINICAL GENETICS, Issue 6 2004SM Singh Epidemiological data favors genetic predisposition for schizophrenia, a common and complex mental disorder in most populations. Search for the genes involved using candidate genes, positional cloning, and chromosomal aberrations including triplet repeat expansions have established a number of susceptibility loci and genomic sites but no causal gene(s) with a proven mechanism of action. Recent genome-wide gene expression studies on brains from schizophrenia patients and their matched controls have identified a number of genes that show an alteration in expression in the diseased brains. Although it is not possible to offer a cause and effect association between altered gene expression and disease, such observations support a neurodevelopmental model in schizophrenia. Here, we offer a mechanism of this disease, which takes into account the role of developmental noise and diversions of the neural system. It suggests that the final outcome of a neural developmental process is not fixed and exact. Rather it develops with a variation around the mean. More important, the phenotypic consequence may cross the norm as a result of fortuitous and/or epigenetic events. As a result, a normal genotype may develop as abnormal with a disease phenotype. More important, susceptible genotypes may have reduced penetrance and develop as a normal phenocopy. The incidental episodes in neurodevelopment will explain the frequency of schizophrenia in most populations and high discordance of monozygotic twins. [source] | ||||||||||