Abstract

The repeated evolution of herbicide resistance has been cited as an example of genetic parallelism, wherein separate species or genetic lineages utilize the same genetic solution in response to selection. However, most studies that investigate the genetic basis of herbicide resistance examine the potential for changes in the protein targeted by the herbicide rather than considering genome-wide changes. We used a population genomics screen and targeted exome re-sequencing to uncover the potential genetic basis of glyphosate resistance in the common morning glory, Ipomoea purpurea, and to determine if genetic parallelism underlies the repeated evolution of resistance across replicate resistant populations. We found no evidence for changes in 5‐enolpyruvylshikimate‐3‐phosphate synthase (EPSPS), glyphosate’s target protein, that were associated with resistance, and instead identified five genomic regions that showed evidence of selection. Within these regions, genes involved in herbicide detoxification—cytochrome P450s, ABC transporters, and glycosyltransferases—are enriched and exhibit signs of selective sweeps. One region under selection shows parallel changes across all assayed resistant populations whereas other regions exhibit signs of divergence. Thus, while it appears that the physiological mechanism of resistance in this species is likely the same among resistant populations, we find patterns of both similar and divergent selection across separate resistant populations at particular loci.

Highlights

  • The evolution of pesticide resistance is a key example of rapid evolution in response to strong, human-mediated selection [1]

  • Because there are relatively few examples underscoring the genetic basis of non-target-site resistance (NTSR) in herbicide resistant plants, it is currently unclear if cases of herbicide resistance via NTSR support the idea of extreme genetic parallelism

  • Within the five genomic regions enriched with outlier loci, we identified genes involved in the herbicide detoxification pathway, suggesting that glyphosate resistance is caused by herbicide metabolism in I. purpurea

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Summary

Introduction

The evolution of pesticide resistance is a key example of rapid evolution in response to strong, human-mediated selection [1]. Due to the widespread use of insecticides and herbicides in agriculture, multiple resistant pest populations often exist across the landscape [2,3,4] These repeated examples of resistance allow for questions about the level at which parallel adaptation occurs [5,6,7]—e.g., are parallel resistant phenotypes in separate lineages due to parallel changes at the developmental, physiological, or genetic level? We understand very little about the potential for parallel genetic responses that may occur across the genome beyond the potential for changes within the (most often) single genes responsible for TSR This is problematic as many weed species exhibit non-target-site resistance (NTSR) [11], which is caused by any physiological mechanism that is not due to TSR. Because there are relatively few examples underscoring the genetic basis of NTSR in herbicide resistant plants, it is currently unclear if cases of herbicide resistance via NTSR support the idea of extreme genetic parallelism

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