Non-target Site Mechanisms of Resistance to Herbicides

Evolution of resistance in weeds to herbicides is threatening world agricultural production. Weed management has become more complicated with the development of non-target site resistance (NTSR) to herbicides in weeds. The NTSR mechanisms can be caused by herbicide metabolism, altered patterns of translocation, and herbicide absorption/penetration. Metabolism of herbicides consists of an activation phase and then a conjugation phase, though in some cases no activation phase is needed. The activation phase mainly involves the addition of functional groups to herbicide molecules using enzymes such as cytochrome P-450. Transcriptome-wide gene expression has shown that genes which encode for several cytochrome P-450s are upregulated in weeds resistant to ACCase-inhibitor and ALS-inhibitor herbicides. In the conjugated phase, several studies have shown that two important types of enzyme, glutathione S-transferases and glucosyltransferases, play crucial roles in conferring resistance to herbicides. An altered pattern of translocation can also play a crucial role in conferring NTSR to weeds. With glyphosate and paraquat, it has been shown that altered patterns of translocation are due to sequestration of the herbicide into vacuoles. However, some other little known mechanisms such as “hyper-sensitive” reactions, impaired translocation, and root exudation can affect the patterns of herbicide translocation within resistant weeds. The molecular understanding of NTSR mechanisms is still in its infancy. Recent developments in techniques such as high-throughput DNA/RNA sequencing technologies will soon allow further insights into the NTSR mechanisms in weeds. This information is essential for developing strategies to overcome weeds with the NTSR mechanisms.