Proposed model for JA-mediated SAK-dependent anthracnose resistance. (IMAGE)
Caption
Proposed model for JA-mediated SAK-dependent anthracnose resistance. Upon C. camelliae infection, pathogen attack triggers differential JA signaling responses between tea cultivars. In the resistant cultivar Zijuan (ZJ), enhanced JA accumulation leads to stronger activation of the transcription factor CsMYC2.1, which directly binds to the CsNOMT promoter and activates its expression. Elevated CsNOMT expression drives increased SAK biosynthesis through the methylation of naringenin. The accumulated SAK acts as a potent phytoalexin, providing enhanced antifungal activity against anthracnose pathogens and contributing to the disease-resistant phenotype. In contrast, the susceptible cultivar Longjing 43 (LJ43) exhibits weaker JA signaling, resulting in lower CsMYC2.1 activation, reduced CsNOMT expression, minimal SAK accumulation, and consequently increased susceptibility to anthracnose infection. This model illustrates how cultivar-specific differences in JA signaling efficiency determine the strength of the CsMYC2.1–CsNOMT–SAK defense axis, ultimately controlling disease resistance outcomes in tea plants.
Credit
Horticulture Research
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CC BY