'Candidatus Liberibacter asiaticus' Effector SDE525 hijacks NACα to Suppress Jasmonic Acid-Mediated Immunity in...

Citrus huanglongbing (HLB), caused by the phloem-limited bacterium 'Candidatus Liberibacter asiaticus' (CLas), is one of the most destructive diseases in global citrus production. Here, we report the functional characterization of a core CLas effector, CLIBASIA_00525 named SDE525, that manipulates host immunity by targeting the citrus nascent polypeptide-associated complex alpha subunit (CsNACα). We confirmed that SDE525 is a secreted protein that localizes to the nucleus, cytoplasm, and plasma membrane. Notably, the effect of SDE525 exhibits host-specific context dependence: while its transient expression in the non-host Nicotiana benthamiana unexpectedly triggered immune responses, in its native host, sweet orange (Citrus sinensis), SDE525 interacted with CsNACα to modulate defence, as demonstrated by multiple independent assays. Integrated transcriptomic and metabolomic analyses revealed that this interaction reprograms the host's hormonal landscape, suppressing the jasmonic acid (JA) signalling pathway while simultaneously activating the salicylic acid (SA) pathway. Importantly, under transient overexpression conditions in citrus, this immune reprogramming enhanced resistance against the bacterial canker pathogen Xanthomonas citri subsp. citri-a phenomenon distinct from the susceptibility observed during authentic CLas infection. Our findings uncover a sophisticated mechanism by which a CLas effector rewires host defence signalling, providing fundamental insights into its pathogenesis with potential long-term implications for future HLB management.