Epigenetic Regulation of CYP72A385-Mediated Metabolic Resistance to Novel Auxin Herbicide Florpyrauxifen-benzyl in Echinochloa crus-galli (L.) P. Beauv.

Abstract

Weed's metabolic resistance to herbicides has undermined the sustainability of herbicides and global food security. Notably, we identified an Echinochloa crus-galli (L.) P. Beauv population (R) that evolved resistance to the never-used florpyrauxifen-benzyl, in which florpyrauxifen-benzyl was metabolized faster than the susceptible E. crus-galli population (S). RNA-seq identified potential metabolism-related genes, EcCYP72A385 and EcCYP85A1, whose expression in yeast exhibited the capacity to degrade florpyrauxifen-benzyl. Region-2 in the EcCYP72A385 promoter showed significant demethylation after florpyrauxifen-benzyl treatment in the R population. DNA methyltransferase inhibitors induce EcCYP72A385 overexpression in the S population and endow it with tolerance to florpyrauxifen-benzyl. Moreover, methyltransferase-like 7A (EcMETTL7A) was overexpressed in the S population and specifically bound to the EcCYP72A385 promoter. Transgenic EcCYP72A385 in Arabidopsis and Oryza sativa L. exhibited resistance to florpyrauxifen-benzyl, whereas EcMETTL7A transgenic plants were sensitive. Overall, EcCYP72A385 is the principal functional gene for conferring resistance to florpyrauxifen-benzyl and is regulated by EcMETTL7A in E. crus-galli.