Selfing, Local Mate Competition, and Reinforcement.

Published

Journal Article

Reinforcement can contribute to speciation by increasing the strength of prezygotic isolating mechanisms. Theoretical analyses over the past two decades have demonstrated that conditions for reinforcement are not unduly restrictive, and empirical investigations have documented over a dozen likely cases, indicating that it may be a reasonably common phenomenon in nature. Largely uncharacterized, however, is the diversity of biological scenarios that can create the reduced hybrid fitness that drives reinforcement. Here I examine one such scenario-the evolution of the "selfing syndrome" (a suite of characters including reductions in flower size and in nectar, pollen, and scent production) in highly selfing plant species. Using a four-locus model, where the loci are (1) a discrimination locus, (2) a target-of-discimination locus, (3) a pollen-production locus, and (4) a selfing-rate locus, I determine the conditions under which this syndrome can favor reinforcement, an increase in discrimination through change at locus 1, in an outcrossing species that experiences gene flow from a highly selfing species. In the absence of both linkage disequilibrium between loci and pollen discounting, reinforcement can occur, but only in a very small fraction of the parameter combinations examined. Moderate linkage ([Formula: see text]) between one pair of loci increases this fraction moderately, depending on which two loci are linked. Pollen discounting (a reduction in pollen exported to other plants due to increased selfing), by contrast, can increase the fraction of parameter combinations that result in reinforcement substantially. The evolution of reduced pollen production in highly selfing species thus facilitates reinforcement, especially if substantial pollen discounting is associated with selfing.

Full Text

Duke Authors

Cited Authors

  • Rausher, MD

Published Date

  • February 2017

Published In

Volume / Issue

  • 189 / 2

Start / End Page

  • 87 - 104

PubMed ID

  • 28107056

Pubmed Central ID

  • 28107056

Electronic International Standard Serial Number (EISSN)

  • 1537-5323

International Standard Serial Number (ISSN)

  • 0003-0147

Digital Object Identifier (DOI)

  • 10.1086/690009

Language

  • eng