Target-Site and Metabolic Resistance Mechanisms to Penoxsulam in Barnyardgrass (Echinochloa crus-galli (L.) P. Beauv).

Abstract

Herbicide resistance identification is essential for effective chemical weed control. In this study, we quantified the differences in growth response between penoxsulam resistant (R) and sensitive (S) Echinochloa crus-galli populations, explored the changes in ALS, and performed genetic analyses to identify metabolic genes that are up-regulated by the application of penoxsulam and other common herbicides. The R population showed a 26.0-fold higher resistance to penoxsulam and varied resistance to most tested herbicides with indices ranging from 4.9 to 145.9. A Trp-574-Arg amino acid mutation in ALS and low penoxsulam ALS sensitivity were the main mechanisms underlying herbicide resistance. The penoxsulam resistance can be significantly reversed by two P450s inhibitors and one GST inhibitor. By RNA-Seq, thirty-six highly expressed contigs were selected, and 30 of them were up-regulated in the R population treated by penoxsulam. Many of these genes were significantly expressed when treated with pyroxsulam, metamifop, and quinclorac. These upregulated genes appear to be complementary for plant resistance to penoxsulam and other common herbicides.