An effector from ‘Candidatus Liberibacter asiaticus‘ targets the armadillo (ARM) repeated protein of Citrus sinensis to inhibit salicylic acid-mediated host immunity

1. CsARM26 subsequently degrades C Las0185 through the 26S proteasome pathway but exhibits minimal impact on C Las0185 pathogenicity. 2. CsARM26 citrus plants suppressed the accumulation of free salicylic acid (SA) and the expression of SA-associated genes. 3. An ARM repeated protein plays a role in the immune response to the C Las–citrus interaction, establishing a foundation for further investigation of the molecular mechanisms of C Las infection. Citrus Huanglongbing (HLB) has caused extensive damage to the global citrus industry. ‘ Candidatus Liberibacter asiaticus’ ( C Las), the primary causal agent of HLB, utilizes effectors to modulate host defense responses, though the mechanisms of these effectors remain unclear. This study demonstrates that the Citrus ARM repeated protein CsARM26 interacted with CLIBASIA_00185 ( C Las0185) in vivo and in vitro . C Las0185 enhanced the abundance of CsARM26, while CsARM26 destabilized the effector. Additionally, the transient co-expression of C Las0185 and CsARM26 facilitated infection by Xanthomonas citri subsp. citri . Moreover, transgenic CsARM26 citrus plants suppressed the accumulation of free salicylic acid (SA) and the expression of SA-associated genes. This study reveals that an ARM repeated protein plays a role in the immune response to the C Las–citrus interaction, establishing a foundation for further investigation of the molecular mechanisms of C Las infection.