Metribuzin Resistance in a Wild Radish (Raphanus raphanistrum) Population via Both psbA Gene Mutation and Enhanced Metabolism

This paper identifies multiple mechanisms: as well as psbA gene mutation, there is a non-target site resistance mechanism of enhanced metabolism.

We expect multiple mechanisms of herbicide resistance as evident here in both target site psbA gene mutation and non-target site enhanced metabolism resistance.

In his current studies, Huan Lu is documenting that this non-target site enhanced metabolism resistance endows resistance to other very different herbicides. This information will become available in Huan’s next publication.

Abstract

There have been many studies on target-site resistance (TSR) to PSII-inhibiting herbicides, but only a few on the non-target-site resistance (NTSR). Here, we reported both TSR and NTSR to metribuzin in a wild radish population.

Dose−response studies revealed a higher level of resistance to metribuzin in the resistant (R) compared to the susceptible (S) population. Sequencing of the target psbA gene revealed the known Ser-264-Gly mutation in R plants. In addition, a higher level of [14C]-metribuzin metabolism and, consequently, a lower level of [14C] translocation were also detected in the R plants.

These results demonstrated that both psbA gene mutation and enhanced metabolism contribute to metribuzin resistance in this wild radish population. Furthermore, this resistant population showed resistance to ALS-inhibiting herbicides due to multiple ALS gene mutations.

This is the first report in wild radish of metabolic herbicide resistance, in addition to the target-site psbA gene mutation.