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      Cooperation between phenotypic plasticity and genetic mutations can account for the cumulative selection in evolution

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          Abstract

          We propose the cooperative model of phenotype-driven evolution, in which natural selection operates on a phenotype caused by both genetic and epigenetic factors. The conventional theory of evolutionary synthesis assumes that a phenotypic value ( P) is the sum of genotypic value ( G) and environmental deviation ( E), P= G+ E, where E is the fluctuations of the phenotype among individuals in the absence of environmental changes. In contrast, the cooperative model assumes that an evolution is triggered by an environmental change and individuals respond to the change by phenotypic plasticity (epigenetic changes). The phenotypic plasticity, while essentially qualitative, is denoted by a quantitative value F which is modeled as a normal random variable like E, but with a much larger variance. Thus, the fundamental equation of the cooperative model is given as P= G+ F where F includes the effect of E. Computer simulations using a genetic algorithm demonstrated that the cooperative model realized much faster evolution than the evolutionary synthesis. This accelerated evolution was found to be due to the cumulative evolution made possible by a ratchet mechanism due to the epigenetic contribution to the phenotypic value. The cooperative model can well account for the phenomenon of genetic assimilation, which, in turn, suggests the mechanism of cumulative selection. The cooperative model may also serve as a theoretical basis to understand various ideas and phenomena of the phenotype-driven evolution such as genetic assimilation, the theory of facilitated phenotypic variation, and epigenetic inheritance over generations.

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          Most cited references38

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          Introduction to Quantitative Genetics

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            The biology of chromatin remodeling complexes.

            The packaging of chromosomal DNA by nucleosomes condenses and organizes the genome, but occludes many regulatory DNA elements. However, this constraint also allows nucleosomes and other chromatin components to actively participate in the regulation of transcription, chromosome segregation, DNA replication, and DNA repair. To enable dynamic access to packaged DNA and to tailor nucleosome composition in chromosomal regions, cells have evolved a set of specialized chromatin remodeling complexes (remodelers). Remodelers use the energy of ATP hydrolysis to move, destabilize, eject, or restructure nucleosomes. Here, we address many aspects of remodeler biology: their targeting, mechanism, regulation, shared and unique properties, and specialization for particular biological processes. We also address roles for remodelers in development, cancer, and human syndromes.
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              Phenotypic plasticity's impacts on diversification and speciation.

              Phenotypic plasticity (the ability of a single genotype to produce multiple phenotypes in response to variation in the environment) is commonplace. Yet its evolutionary significance remains controversial, especially in regard to whether and how it impacts diversification and speciation. Here, we review recent theory on how plasticity promotes: (i) the origin of novel phenotypes, (ii) divergence among populations and species, (iii) the formation of new species and (iv) adaptive radiation. We also discuss the latest empirical support for each of these evolutionary pathways to diversification and identify potentially profitable areas for future research. Generally, phenotypic plasticity can play a largely underappreciated role in driving diversification and speciation. Copyright (c) 2010 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Biophysics (Nagoya-shi)
                Biophysics (Nagoya-shi)
                biop
                Biophysics
                The Biophysical Society of Japan (BSJ)
                1349-2942
                2014
                17 December 2014
                : 10
                : 99-108
                Affiliations
                [1 ]Institute for Protein Research, Osaka University, 3-2 Yamadaoka, Suita, Osaka 565-0871, Japan
                Author notes
                Corresponding author: Akira R. Kinjo, Institute for Protein Research, Osaka University, 3-2 Yamadaoka, Suita, Osaka 565-0871, Japan. e-mail: akinjo@ 123456protein.osaka-u.ac.jp
                Article
                10_99
                10.2142/biophysics.10.99
                4629657
                27493504
                80cef410-1e94-424d-b836-d382babf13e3
                ©2014 THE BIOPHYSICAL SOCIETY OF JAPAN
                History
                : 16 June 2014
                : 11 November 2014
                Categories
                Hypotheses and Perspectives

                epigenetics,genetic assimilation,rapid evolution,environmental change,computer simulation

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