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H2O2‐Dependent Methyl Jasmonate Regulates H2S‐Induced Resistance to Fusarium oxysporum f. sp. niveum Race 2 in Citrullus lanatus

Shiyu Li,Tongshu Zhao,Ning Chang,Yi Chen,Qi Wang,Zhongyuan Wang,Chunhua Wei,Jianxiang Ma,Yong Zhang,Xian Zhang,Hao Li

Published 2025 in Plant, Cell and Environment

ABSTRACT

Fusarium wilt, caused by Fusarium oxysporum (Fo), is a destructive fungal disease that reduces crop yield and quality. Hydrogen sulphide (H2S), a critical signalling molecule, modulates plant defence responses; however, its role and mechanism in combating Fo remain elusive. This study reveals that exogenous NaHS (an H2S donor) enhances watermelon resistance to Fusarium oxysporum f. sp. niveum race 2 (FON2), accompanied by elevated hydrogen peroxide (H2O2) and methyl jasmonate (MeJA) levels. Exogenous H2O2 and MeJA also enhance FON2 resistance. Conversely, silencing respiratory burst oxidase homologue F (ClRBOHF) and jasmonic acid carboxyl methyltransferase (ClJMT), key genes for H2O2 and MeJA biosynthesis, respectively, inhibits NaHS‐induced resistance to FON2. Deletion of l‐cysteine desulfhydrase (ClLCD), a pivotal gene for H2S generation, reduces FON2 resistance, but this reduction is restored by H2O2 or MeJA supplementation. Upon FON2 infection, exogenous H2O2 elevates MeJA levels; however, silencing ClRBOHF suppresses NaHS‐induced MeJA accumulation. Furthermore, silencing ClClJMT inhibits H2O2‐induced FON2 resistance, while MeJA supplementation rescues the reduced resistance caused by ClRBOHF silencing. Collectively, these findings demonstrate that H2O2‐dependent MeJA plays a crucial role in regulating H2S‐induced watermelon resistance to FON2. The growing focus on reducing pesticide use highlights the potential of this mechanism for combating Fo sustainably.

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