Glyphosate resistance: state of knowledge

Abstract

Studies of mechanisms of resistance to glyphosate have increased current understanding of herbicide resistance mechanisms. Thus far, single-codon non-synonymous mutations of EPSPS (5-enolypyruvylshikimate-3-phosphate synthase) have been rare and, relative to other herbicide mode of action target-site mutations, unconventionally weak in magnitude for resistance to glyphosate. However, it is possible that weeds will emerge with non-synonymous mutations of two codons of EPSPS to produce an enzyme endowing greater resistance to glyphosate. Today, target-gene duplication is a common glyphosate resistance mechanism and could become a fundamental process for developing any resistance trait. Based on competition and substrate selectivity studies in several species, rapid vacuole sequestration of glyphosate occurs via a transporter mechanism. Conversely, as the chloroplast requires transporters for uptake of important metabolites, transporters associated with the two plastid membranes may separately, or together, successfully block glyphosate delivery. A model based on finite glyphosate dose and limiting time required for chloroplast loading sets the stage for understanding how uniquely different mechanisms can contribute to overall glyphosate resistance.

Figure 1

A theoretical cellular-level model of glyphosate uptake and distribution for (A) a normal, glyphosate-susceptible source cell and (B) a glyphosate-resistant source cell using the vacuole to sequester glyphosate. The units for glyphosate are relative concentration, with a theoretical chloroplast minimum inhibitory concentration (25) indicated by a red line, and a chloroplast glyphosate concentration (35) consistent with saturated inhibition indicated by a dashed blue line.