Journal of Plant Protection Research (Jun 2021)
Tolerance of Brazilian bean cultivars to protoporphyrinogen oxidase inhibiting-herbicides
Abstract
The high sensitivity of beans to herbicides is one of the limiting factors regarding the management of dicot weeds in bean crops. Protoporphyrinogen oxidase (PPO) inhibition is an important mechanism of action that has unregistered molecules with potential use in bean crops. The objectives of this study were to investigate the tolerance of Brazilian bean cultivars to distinct PPO inhibitors and to determine the existence of cross-tolerance in cultivars to the different PPO inhibitor chemical groups. In the first and second experiments, the BRSMG Talismã, Jalo Precoce, BRS Esplendor, and IPR 81 cultivars were subjected to saflufenacil doses pre- (0, 9.6, 14.1, 20.5, 30.0, and 43.8 g a.i. ‧ ha–1) and post-emergence (0, 0.7, 1.0, 1.5, 2.1, and 3.1 g a.i. ‧ ha–1). In the third experiment, the tolerance of 28 bean genotypes to saflufenacil (20.5 g a.i. ‧ ha–1) in pre-emergence was determined. In the fourth, fifth, sixth and seventh experiments, we investigated the cross-tolerance of bean to the fomesafen, flumioxazin, sulfentrazone, and saflufenacil herbicides, respectively. Even very low saflufenacil doses in post-emergence caused plants of all cultivars to die rapidly; therefore, the tolerance was much lower at this application time than in pre-emergence. There was high tolerance variability to saflufenacil among the 28 cultivars. The bean tolerance to fomesafen, flumioxazin, sulfentrazone, and saflufenacil applied pre-emergence depended on the cultivar and dose. Fomesafen was highlighted owing to its higher selectivity in relation to the different cultivars. No cross-tolerance pattern to the PPO inhibitor chemical groups applied in pre-emergence was observed among the evaluated bean cultivars. The results of this study could be of significance to farmers and technical assistance personnel, as well as for future research on cultivar breeding and the elucidation of biochemical and genetic mechanisms involved in herbicide tolerance.
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