ABSTRACT
Citrus Huanglongbing (HLB), caused by ‘
Candidatus
Liberibacter asiaticus’ (
Ca
Las), is the most devastating disease affecting the global citrus industry. Here, we reported that the
Ca
Las effector SDE70 promotes HLB pathogenicity by targeting the citrus ubiquitination pathway. Transgenic expression of
SDE70
in Wanjincheng orange (
Citrus sinensis
Osbeck) accelerated early
Ca
Las proliferation, aggravated HLB symptoms, and increased susceptibility to citrus canker induced by
Xanthomonas citri
subsp.
citri
(
Xcc
). These results demonstrate that SDE70 functions as a broad‐spectrum suppressor of citrus immunity. Mechanistically, SDE70 physically interacts with CsRUB2, a citrus ubiquitin‐related protein. Furthermore,
CsRUB2
overexpression in Wanjincheng oranges reduced resistance to HLB but enhanced resistance to citrus canker. Both SDE70 and CsRUB2 elevated salicylic acid (SA) and hydrogen peroxide (H
2
O
2
) levels in transgenic plants while lowering methyl salicylate (MeSA) levels. CsRUB2 also decreased jasmonic acid (JA). In contrast to the suppressive effect of SDE70, CsRUB2 enhanced the transcription of citrus immunity genes. Transient expression assays further demonstrated that the SDE70–CsRUB2 interaction dysregulates citrus immunity by perturbing SA, MeSA, JA, and H
2
O
2
signals. These findings provide a theoretical basis for understanding citrus–
Ca
Las interactions and breeding citrus varieties with broad‐spectrum resistance to both HLB and citrus canker.