Metabolism-based herbicide resistance (MHR) is now widespread in many weeds and particularly problematic in wild grasses competing with cereal crops.  In the UK, MHR in black-grass (Alopecurus myosuroides) is now a major problem affecting arable agriculture in much of the most productive growing areas, resulting in serious crop losses due to the loss of control with registered graminicides.  Over the last 20 years our group have studied the biochemistry and molecular genetics of MHR in black-grass and have recently discovered a key regulator of this problematic trait.   We determined that all populations of black-grass demonstrating MHR, showed elevated levels of expression of a specific phi (F)-class glutathione transferase (GST) we have termed AmGSTF1.   Unlike the GSTs we have worked with previously in crops and weeds, AmGSTF1 showed little detoxifying activity toward herbicides.  Instead, as demonstrated in transgenesis experiments,  we have determined that this protein has a regulatory function which is independent of its catalytic activity, that causes an up-regulation of protective antioxidant and detoxification biochemical responses which leads to resistance to herbicides.  Intriguingly, AmGSTF1's role in MHR has many parallels with the protective regulatory function of an evolutionarily distinct pi class GST found in drug resistant tumors in humans.  Selective use of chemicals known to disrupt the drug resisting activity of the human GST through covalent and inhibitory action, were also shown to act on AmGSTF1 and synergise herbicides in MHR black-grass.   The molecular basis of AmGSTF1's causative role in MHR is currently under investigation, though it is clear from transcriptomic and metabolomics studies that it is but part  of a wider and more complex resistance phenotype.  To this end we are currently investigating the potential for molecular diagnostics to be employed as a monitoring tool to mitigate against herbicide resistance in both existing and emerging MHR black-grass populations.

New insights into the molecular basis of metabolism-based herbicide resistance in weeds

248th National Meeting (2014)

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