96,580 research outputs found

    Fluctuating population dynamics promotes the evolution of phenotypic plasticity

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    An increasing number of studies are showing evidence in support of sympatric speciation. One basic question remains, however. When a population has undergone a branching in its phenotype, is this due to an evolutionary branching in the underlying genotype or due to phenotypic plasticity modifying a single genotype? Thus, phenotypic plasticity has come to be viewed as a trait subject to selection, just like any other phenotypic character1,2. Here we present a model addressing the conditions under which a predator phenotype experiencing selection for two alternative optimal phenotypes gives rise to genetically based phenotypic branching or to phenotypic plasticity, allowing the corresponding genotype to give rise to two alternative, well-adapted phenotypes.
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    Phenotypic flexibility and the evolution of organismal design

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    Evolutionary biologists often use phenotypic differences between species and between individuals to gain an understanding of organismal design. The focus of much recent attention has been on developmental plasticity – the environmentally induced variability during development within a single genotype. The phenotypic variation expressed by single reproductively mature organisms throughout their life, traditionally the subject of many physiological studies, has remained underexploited in evolutionary biology. Phenotypic flexibility, the reversible within-individual variation, is a function of environmental conditions varying predictably (e.g. with season), or of more stochastic fluctuations in the environment. Here, we provide a common framework to bring the different categories of phenotypic plasticity together, and emphasize perspectives on adaptation that reversible types of plasticity might provide. We argue that better recognition and use of the various levels of phenotypic variation will increase the scope for phenotypic experimentation, comparison and integration.

    The conceptual structure of evolutionary biology: A framework from phenotypic plasticity

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    In this review, I approach the role of phenotypic plasticity as a key aspect of the conceptual framework of evolutionary biology. The concept of phenotypic plasticity is related to other relevant concepts of contemporary research in evolutionary biology, such as assimilation, genetic accommodation and canalization, evolutionary robustness, evolvability, evolutionary capacitance and niche construction. Although not always adaptive, phenotypic plasticity can promote the integration of these concepts to represent some of the dynamics of evolution, which can be visualized through the use of a conceptual map. Although the use of conceptual maps is common in areas of knowledge such as psychology and education, their application in evolutionary biology can lead to a better understanding of the processes and conceptual interactions of the complex dynamics of evolution. The conceptual map I present here includes environmental variability and variation, phenotypic plasticity and natural selection as key concepts in evolutionary biology. The evolution of phenotypic plasticity is important to ecology at all levels of organization, from morphological, physiological and behavioral adaptations that influence the distribution and abundance of populations to the structuring of assemblages and communities and the flow of energy through trophic levels. Consequently, phenotypic plasticity is important for maintaining ecological processes and interactions that influence the complexity of biological diversity. In addition, because it is a typical occurrence and manifests itself through environmental variation in conditions and resources, plasticity must be taken into account in the development of management and conservation strategies at local and global levels

    A multi-phenotypic cancer model with cell plasticity

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    The conventional cancer stem cell (CSC) theory indicates a hierarchy of CSCs and non-stem cancer cells (NSCCs), that is, CSCs can differentiate into NSCCs but not vice versa. However, an alternative paradigm of CSC theory with reversible cell plasticity among cancer cells has received much attention very recently. Here we present a generalized multi-phenotypic cancer model by integrating cell plasticity with the conventional hierarchical structure of cancer cells. We prove that under very weak assumption, the nonlinear dynamics of multi-phenotypic proportions in our model has only one stable steady state and no stable limit cycle. This result theoretically explains the phenotypic equilibrium phenomena reported in various cancer cell lines. Furthermore, according to the transient analysis of our model, it is found that cancer cell plasticity plays an essential role in maintaining the phenotypic diversity in cancer especially during the transient dynamics. Two biological examples with experimental data show that the phenotypic conversions from NCSSs to CSCs greatly contribute to the transient growth of CSCs proportion shortly after the drastic reduction of it. In particular, an interesting overshooting phenomenon of CSCs proportion arises in three-phenotypic example. Our work may pave the way for modeling and analyzing the multi-phenotypic cell population dynamics with cell plasticity.Comment: 29 pages,6 figure

    Testing mechanisms of Bergmann’s rule: Phenotypic decline but no genetic change in body size in three posserine bird populations

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    Bergmann’s rule predicts a decrease in body size with increasing temperature and has much empirical support. Surprisingly, we know very little about whether “Bergmann size clines” are due to a genetic response or are a consequence of phenotypic plasticity. Here, we use data on body size (mass and tarsus length) from three long-term (1979–2008) study populations of great tits (Parus major) that experienced a temperature increase to examine mechanisms behind Bergmann’s rule. We show that adult body mass decreased over the study period in all populations and that tarsus length increased in one population. Both body mass and tarsus length were heritable and under weak positive directional selection, predicting an increase, rather than a decrease, in body mass. There was no support for microevolutionary change, and thus the observed declines in body mass were likely a result of phenotypic plasticity. Interestingly, this plasticity was not in direct response to temperature changes but seemed to be due to changes in prey dynamics. Our results caution against interpreting recent phenotypic body size declines as adaptive evolutionary responses to temperature changes and highlight the importance of considering alternative environmental factors when testing size clines.

    Phenotipic integration does not constrain phenotypic plasticity: differential plasticity of traits is associated to their integration across environments

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    ResearchUnderstanding constraints to phenotypic plasticity is key given its role on the response of organisms to environmental change. It has been suggested that phenotypic integration, the structure of trait covariation, could limit trait plasticity. However, the relationship between plasticity and integration is far from resolved. Using a database of functional plasticity to drought of a Mediterranean shrub that included 20 ecophysiological traits, we assessed environmentally-induced changes in phenotypic integration and whether integration constrained the expression of plasticity, accounting for the within-environment phenotypic variation of traits. Furthermore, we provide the first test of the association between differential trait plasticity and trait integration across an optimum and a stressful environment. Phenotypic plasticity was positively associated with phenotypic integration in both environments, but this relationship was lost when phenotypic variation was considered. The similarity in the plastic response of two traits predicted their integration across environments, with integrated traits having more similar plasticity. Such variation in the plasticity of traits partly explained the lower phenotypic integration found in the stressful environment. We found no evidence that integration may constitute an internal constraint to plasticity. Rather, we present the first empirical demonstration that differences in plastic responses may involve a major reorganization of the relationships among traits, and challenge the notion that stress generally induces a tighter phenotypeinfo:eu-repo/semantics/publishedVersio
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