Abstract

BackgroundMeiotic recombination rate has long been known to be phenotypically plastic. How plastic recombination evolves and is maintained remains controversial; though a leading model for the evolution of plastic recombination rests on the tenet that organismal fitness and recombination frequency are negatively correlated. Motivated by the mounting evidence that meiotic recombination frequencies increase in response to stress, here we test for a negative correlation between fitness and recombination frequency. Specifically, the fitness-associated recombination model (FAR) predicts that if stress increases meiotic recombination frequency, then increasing exposure to stressful conditions will yield an increasing magnitude of the recombinational response, while concomitantly decreasing fitness.ResultsWe use heat shock as a stressor to test this prediction in Drosophila melanogaster. We find that increased exposure to heat shock conditions is associated with a non-linear increase in meiotic recombination frequency. We also find an independent effect of heat shock on organismal fitness, with fitness decreasing with increased duration of thermal stress.ConclusionsOur results thus support the foundation of the FAR model for the evolution of plastic recombination. Our data also suggest that modulating recombination frequency is one mechanism by which organisms can rapidly respond to environmental cues and confer increased adaptive potential to their offspring.Electronic supplementary materialThe online version of this article (doi:10.1186/s12862-015-0452-8) contains supplementary material, which is available to authorized users.

Highlights

  • Meiotic recombination rate has long been known to be phenotypically plastic

  • Our results support the foundation of the fitness-associated recombination model (FAR) model for the evolution of plastic recombination and further suggest that modulating recombination frequency is one mechanism by which organisms can rapidly respond to environmental cues and confer increased adaptive potential to their offspring, which may be valuable in a variable environment

  • We leveraged classical genetic approaches to experimentally test a prediction of the fitness-associated recombination model for the evolution of plastic recombination

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Summary

Introduction

Meiotic recombination rate has long been known to be phenotypically plastic. How plastic recombination evolves and is maintained remains controversial; though a leading model for the evolution of plastic recombination rests on the tenet that organismal fitness and recombination frequency are negatively correlated. Motivated by the mounting evidence that meiotic recombination frequencies increase in response to stress, here we test for a negative correlation between fitness and recombination frequency. Defects in meiotic recombination have catastrophic consequences for the fitness of progeny [1, 2], underscoring the vital function of homologous recombination for the maintenance of organismal fitness. Meiotic recombination has another important function, which is to create novel combinations of alleles at linked loci. In this way, recombination can both facilitate adaptation as well as enable populations to purge deleterious alleles [3, 4]

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