Mei, Yalin

ABSTRACT The selective autophagy receptor NEIGHBOUR OF BRCA1 (NBR1) is a key regulator of plant immunity, but its role against bacterial pathogens remains poorly understood. Here, we demonstrated that overexpression of CsNBR1 confers citrus resistance to huanglongbing (HLB) caused by ‘ Candidatus Liberibacter asiaticus’ ( C Las). CsNBR1 can interact with multiple virulence effector proteins of C Las, including SDE5115, SDE1, SDE19 and SDE5, leading to their degradation via the autophagic pathway. In addition, expression of CsNBR1 in Nicotiana benthamiana mitigated the leaf curling and dwarfing phenotypes triggered by SDE1 by reducing the protein content of SDE1. These findings reveal that CsNBR1 positively regulates citrus defence against C Las by degrading its effector proteins via selective autophagy, providing both mechanistic insights and a potential target for resistance breeding.

ABSTRACT Ubiquitin‐proteasome is a conserved mechanism that regulates cellular responses and disease resistance in plants. However, the regulatory role of ubiquitin‐proteasome in the pathogenicity of “ Candidatus Liberibacter asiaticus” ( C Las), the causal agent of citrus huanglongbing (HLB), one of the most serious citrus diseases, remains poorly defined. In this study, we demonstrated that CLIBASIA_04250 (SDE4250) suppresses 26S proteasome activity in citrus, leading to a reduction in salicylic acid (SA) levels and downregulation of SA‐responsive genes. Further investigation revealed that SDE4250 specifically targets the citrus 26S proteasome non‐ATPase regulatory subunit 4 homologue (CsRPN10) and enhances its degradation via the 26S proteasome pathway. Moreover, overexpression of CsRPN10 inhibited C Las proliferation in citrus hairy roots, which was accompanied by a significant accumulation of SA content and upregulation of related defence genes. Collectively, our findings indicate that SDE4250 targets the citrus 26S proteasome to disrupt SA‐mediated citrus immunity.