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

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.