Abstract Watermelon fusarium wilt is a soil-borne disease that seriously affects watermelon yield and economic benefits. Our previous study found that salicylic acid (SA) plays an essential role in regulating watermelon roots against the Fusarium wilt (FW), but the molecular mechanism is still unclear. Therefore, in this experiment, the molecular mechanism of how SA manipulate watermelon immune system to against FW was explored by transcriptome analysis, combined with chlorophyll fluorescence images, phytohormone content quantification, RT-qPCR verification and promoter prediction analysis. The plant phenotyping and pathway enrichment analyses revealed that exogenous SA activates watermelon plants against Fusarium oxysporum f. sp. niveum (FON) infection at early stage (3 dpi) by inducing other phytohormones and enriching resistance genes to keep the citrate cycle working. Furthermore, DEGS comparison, RT-qPCR verification and promoter sequences analyses demonstrated that the CIPER10, CIMYB59, CIMYB44, CIPYL4, CIAGP31, and CIACO3 genes play significant roles in against FON infection by signal network between SA and abscisic acid (ABA), jasmonic acid (JA), and ethylene (ET). Collectively, the findings suggested that SA manipulate watermelon immune system to maintaining the citrate cycle via activating a phytohormone crosstalk.
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Yang et al. (2024) studied this question.
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