Recent advances in deciphering metabolic herbicide resistance mechanisms

Authors: Nandula, Vijay

Submitted to: Taylor and Francis Group
Publication Type: Book / Chapter
Publication Acceptance Date: 4/10/2018
Publication Date: 5/14/2018
Citation: Nandula, V.K. 2018. Recent advances in deciphering metabolic herbicide resistance mechanisms. In: Jugulam, Mithila, editor. Biology, Physiology and Molecuar Biology of Weeds. CRC Press, Taylor and Francis Group. p. 144-155.

Interpretive Summary:

Technical Abstract: The next and most important phase after the confirmation of herbicide resistance in a weed population is the deciphering of the underlying resistance mechanism(s). The mechanism of resistance to an herbicide in a weed population can greatly determine the effectiveness of resistance management strategies. In general, five modes of herbicide resistance have been identified in weeds: (1) altered target site due to a mutation at the site of herbicide action resulting in complete or partial lack of inhibition; (2) metabolic deactivation, whereby the herbicide active ingredient is transformed to nonphytotoxic metabolites; (3) reduced absorption and/or translocation that results in restricted movement of lethal levels of herbicide to point/site of action; (4) sequestration/compartmentation by which a herbicide is immobilized away from the site of action in cell organelles such as vacuoles or cell walls; and (5) gene amplification/over-expression of the target site with consequent dilution of the herbicide in relation to the target site (Nandula 2010). Among these, mutation at target site and gene amplification are target site based, and metabolic deactivation, differential absorption/translocation, and sequestration are classified as non-target site-based resistances (NTSR). This article summarizes current understanding of metabolic resistance in weeds by providing a history of related research, reporting recent advances, and identifying future research opportunities. Herbicide metabolism in plants, crops and weeds, is brought about by the action of enzyme systems such as cytochrome P450 monoxygenases, glutathione S-transferases, and glycosyl transferases. These enzymes deactivate herbicide molecules by modifying side chains, which then are conjugated to biochemical moieties such as sugar and amino acid residues. Some of these conjugates are further deposited in vacuoles and cell walls. A three-step procedure is proposed, based on the use of the ‘omics’ (genomics, transcriptomics, proteomics or metabolomics), to decipher the genetic bases of NTSR.