Genomic structural variation and herbicide resistance

The coinciding increase in genomics resources for weedy plant species and herbicide resistance evolution has led to a rapid expansion of our understanding of the relationship between genomic structural variation and herbicide resistance mechanisms. Since the first discovery of 5-enolpyruvylshikimate-3-phosphate synthase ( EPSPS) copy number variation conferring glyphosate resistance in Amaranthus palmeri, we have seen rapid convergent evolution of the same herbicide-resistance mechanism in eleven diverse weed species by a variety of unique structural variant-generating mechanisms. These mechanisms include extrachromosomal circular DNA replication, unequal crossing over, and subtelomeric duplication. More recently, target-site duplication has been found to cause resistance for other herbicides with different modes of action, including acetyl-CoA carboxylase (ACCase) inhibitors and glutamine synthetase inhibitors. Additionally, the first transposon-generated structural variants that confer herbicide resistances are beginning to be discovered. This review summarizes our current understanding of structural variation in agronomic weed genomes as it relates to herbicide resistance and emphasizes necessary future research to clarify the size, nature, and mechanisms that give rise to genomic structural variation. While we limit our review to herbicide resistance traits, this work also highlights the importance of structural variation as a critical component of total genetic diversity and its importance for the rapid evolution of novel traits.