LAUSR

During the past decade, one of the most novel findings emerging from herbicide-resistance research was gene amplification as a resistance mechanism. Although amplification of genes— including genes encoding detoxifying enzymes as well as genes encoding the target site itself— has been known to confer insecticide resistance for some time (reviewed by Bass and Field), such a mechanism was not reported for herbicide resistance until 2010. In that report, Gaines et al. showed in glyphosate-resistant Palmer amaranth (Amaranthus palmeri) massive amplification (over 100 copies in some plants) of the EPSPS gene, which encodes 5-enolypyruvylshikimate-3phosphate synthase, the target site of glyphosate. Follow-up research has not yet elucidated the mechanism by which such amplification has occurred in Palmer amaranth, although the amplified region is now known to be surprisingly large (possibly >300 kb) and contains multiple genes in addition to EPSPS. A very recent report found that numerous, geographically separated populations contained the same amplicon, suggesting that such amplification is a rare event and may have occurred only once in Palmer amaranth. EPSPS amplification has since been found in glyphosate-resistant biotypes of several additional species, including both grass and broadleaf weeds (e.g., Lolium perenne, Amaranthus tuberculatus, and Kochia scoparia). Cytogenetic analysis has revealed differences in the patterns of gene amplification among species. Whereas the initial report in Palmer amaranth showed seemingly random insertions of EPSPS throughout the genome, tandem amplification accounted for most or all of the EPSPS amplification found in K. scoparia and A.