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

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.