‘Candidatus Liberibacter Asiaticus’ Effector SECP8 Subverts Salicylic Acid-Mediated Citrus Immunity via a Two-Pronged Impairment of CsTCP15 Dimerization

Abstract

Citrus Huanglongbing (HLB), a devastating disease caused by the unculturable bacterium ‘Candidatus Liberibacter asiaticus’ (CLas), poses a severe threat to global citrus production. CLas secretes effectors to suppress host immune responses and facilitate its colonisation. Previously, the CLas effector SECP8 (CLIBASIA_05330) has been identified as an immune inhibitor. However, its molecular mechanisms on host immune suppression remain unclear. This study identifies the citrus transcription factor CsTCP15 as a target of SECP8. Transgenic citrus plants overexpressing CsTCP15 enhanced resistance to CLas, whereas CsTCP15-RNAi interference plants became more susceptible, confirming its role as a positive immune regulator. Meanwhile, CsTCP15 was demonstrated to directly bind to cis-elements of salicylic acid (SA)-responsive genes CsPR5 and CsWRKY22, and overexpression of either gene strengthened citrus hairy roots' resistance against CLas. However, SECP8 directly interacts with CsTCP15 and inhibits its homodimerization. Concurrently, mSECP8 facilitates CsBRG3-mediated degradation and further prevents the dimerization of CsTCP15. This two-pronged interference eventually impairs the transcriptional activation of CsPR5 and CsWRKY22, thereby compromising salicylic acid-mediated immunity and promoting CLas infection. Our findings reveal a virulence strategy whereby a CLas effector manipulates a key host immune regulator to establish pathogenesis.