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      Condition-dependent sex: who does it, when and why?

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      Philosophical Transactions of the Royal Society B: Biological Sciences
      The Royal Society

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          Abstract

          <p class="first" id="d5003466e135">We review the phenomenon of condition-dependent sex—where individuals' condition affects the likelihood that they will reproduce sexually rather than asexually. In recent years, condition-dependent sex has been studied both theoretically and empirically. Empirical results in microbes, fungi and plants support the theoretical prediction that negative condition-dependent sex, in which individuals in poor condition are more likely to reproduce sexually, can be evolutionarily advantageous under a wide range of settings. Here, we review the evidence for condition-dependent sex and its potential implications for the long-term survival and adaptability of populations. We conclude by asking why condition-dependent sex is not more commonly observed, and by considering generalizations of condition-dependent sex that might apply even for obligate sexuals. </p><p id="d5003466e137">This article is part of the themed issue ‘Weird sex: the underappreciated diversity of sexual reproduction’. </p>

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          Most cited references78

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          Integrons: agents of bacterial evolution.

          Integrons are assembly platforms - DNA elements that acquire open reading frames embedded in exogenous gene cassettes and convert them to functional genes by ensuring their correct expression. They were first identified by virtue of their important role in the spread of antibiotic-resistance genes. More recently, our understanding of their importance in bacterial genome evolution has broadened with the discovery of larger integron structures, termed superintegrons. These DNA elements contain hundreds of accessory genes and constitute a significant fraction of the genomes of many bacterial species. Here, the basic biology of integrons and superintegrons, their evolutionary history and the evidence for the existence of a novel recombination pathway is reviewed.
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            Deleterious mutations and the evolution of sexual reproduction.

            The origin and maintenance of sexual reproduction continues to be an important problem in evolutionary biology. If the deleterious mutation rate per genome per generation is greater than 1, then the greater efficiency of selection against these mutations in sexual populations may be responsible for the evolution of sex and related phenomena. In modern human populations detrimental mutations with small individual effects are probably accumulating faster than they are being eliminated by selection.
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              Mutation as a stress response and the regulation of evolvability.

              Our concept of a stable genome is evolving to one in which genomes are plastic and responsive to environmental changes. Growing evidence shows that a variety of environmental stresses induce genomic instability in bacteria, yeast, and human cancer cells, generating occasional fitter mutants and potentially accelerating adaptive evolution. The emerging molecular mechanisms of stress-induced mutagenesis vary but share telling common components that underscore two common themes. The first is the regulation of mutagenesis in time by cellular stress responses, which promote random mutations specifically when cells are poorly adapted to their environments, i.e., when they are stressed. A second theme is the possible restriction of random mutagenesis in genomic space, achieved via coupling of mutation-generating machinery to local events such as DNA-break repair or transcription. Such localization may minimize accumulation of deleterious mutations in the genomes of rare fitter mutants, and promote local concerted evolution. Although mutagenesis induced by stresses other than direct damage to DNA was previously controversial, evidence for the existence of various stress-induced mutagenesis programs is now overwhelming and widespread. Such mechanisms probably fuel evolution of microbial pathogenesis and antibiotic-resistance, and tumor progression and chemotherapy resistance, all of which occur under stress, driven by mutations. The emerging commonalities in stress-induced-mutation mechanisms provide hope for new therapeutic interventions for all of these processes.
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                Author and article information

                Journal
                Philosophical Transactions of the Royal Society B: Biological Sciences
                Phil. Trans. R. Soc. B
                The Royal Society
                0962-8436
                1471-2970
                September 12 2016
                September 12 2016
                : 371
                : 1706
                : 20150539
                Article
                10.1098/rstb.2015.0539
                5031623
                27619702
                12733417-4677-4f5a-8320-70dd9d307981
                © 2016
                History

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