CsWRKY33 Integrates Immune Signalling and Metabolic Reprogramming to Enhance Tea Plant Resistance Against <i>Colletotrichum camelliae</i>

Tea anthracnose, caused by Colletotrichum camelliae, poses a serious threat to tea yield and quality. While certain transcription factors have been implicated in stress responses, the core transcriptional networks governing immunity in tea plants remain largely elusive. In this study, we identify CsWRKY33 as a central regulator that orchestrates immune responses and metabolic reprogramming during C. camelliae infection in tea plants. Transcriptome analysis revealed that CsWRKY33 is significantly induced upon fungal challenge and functions downstream of both pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). Mechanistically, protein-promoter affinity experiments demonstrated that CsWRKY33 directly binds to W-box motifs in the promoters of key immune genes, including CsSERK2, CsMPK3, CsCDPK32, CsPR1B, CsWIN2 and CsRPM1. Dual-luciferase assays and functional validations further confirmed that CsWRKY33 activates its expression, forming a positive feedback loop that amplifies immune signalling. Concurrently, CsWRKY33 modulates primary metabolism by repressing photosynthetic genes such as CsRCA and enhances secondary metabolism by directly activating phenylpropanoid pathway genes such as CsPAL and CsCAD1. These coordinated transcriptional programmes reallocate energy and resources toward defence, thereby enhancing resistance. We propose a working model in which CsWRKY33 serves as a transcriptional hub linking immune activation with metabolic adjustment to facilitate efficient defence. This study provides new insights into WRKY-mediated immunity in perennial woody plants and highlights CsWRKY33 as a promising target for molecular breeding of anthracnose-resistant tea cultivars.