水稻叶绿体蛋白质合成抑制因子（MoSR）与蛋白酶抑制因子（MoDde1）调控轴：水稻白叶枯病敏感性的新型决定因素及可持续防控目标

Abstract

The transcription factor FgSR functions as a central regulator of ergosterol biosynthesis and 14α‐demethylation inhibitor (DMI) sensitivity in Fusarium graminearum , with its orthologous proteins being evolutionarily conserved within Sordariomycetes and Leotiomycetes fungi. In this study, we demonstrate that sterol regulators (SRs) differentially modulate DMI sensitivity across these fungal classes through divergent strategies involving key metabolic genes. In Magnaporthe oryzae , MoSR regulates DMI sensitivity through two distinct mechanisms: it directly modulates the transcription of ergosterol biosynthesis genes MoCYP51A and MoCYP51B , and binds to the DRE (DMI‐responsive element) motif to regulate MoDde1 ( Magnaporthe oryzae DMI detoxification enzyme 1), a gene encoding a cytochrome P450 monooxygenase involved in detoxification. Evolutionary analysis indicates that MoDde1 functions as a Sordariomycetes‐specific detoxification factor, capable of enzymatically degrading DMIs. Based on these findings, we developed a small‐molecule D1 targeting MoDde1 and engineered rice lines with reduced MoDde1 expression using host‐induced gene silencing (HIGS). Both approaches successfully suppressed the enzymatic activity and expression of MoDde1, respectively, demonstrating a promising sustainable strategy for controlling rice blast disease, particularly in conjunction with DMI fungicides. The transcription factor MoSR governs DMI fungicide sensitivity in Magnaporthe oryzae through dual regulation of ergosterol biosynthesis and the detoxification enzyme MoDde1. Targeting MoDde1 via a small‐molecule inhibitor or host‐induced gene silencing enhances DMI efficacy against rice blast, offering a sustainable disease management strategy.