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<p>Primers were used in this study.</p>

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NIAID Data Ecosystem2026-05-10 收录
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Citrus Huanglongbing (HLB), a devastating disease caused by the Gram-negative bacterium ‘Candidatus Liberibacter asiaticus’ (CLas), poses serious threats to global citrus production and lacks effective control strategies. Previously, SDE2470 (CLIBASIA_02470) was identified as a Sec-dependent effector that contributes to CLas pathogenesis, although its underlying molecular mechanisms were not fully elucidated. In this study, SDE2470 was found to target a citrus vascular one-zinc-finger transcription factor CsVOZ2. CsVOZ2 overexpression (CsVOZ2-OE) in transgenic citrus plants significantly suppressed CLas colonization, whereas its RNA interference (RNAi) in citrus hairy roots enhanced susceptibility to CLas. Additionally, CsVOZ2-OE significantly increased reactive oxygen species (ROS) and abscisic acid (ABA) contents accumulation and activated related genes expression. Further investigation revealed that the E3 ligase CsBTS1 directly interacts with CsVOZ2 and promotes its degradation via the 26S proteasome pathway. CsBTS1E3-OE in citrus hairy roots markedly enhanced CLas proliferation. Importantly, SDE2470 directly interacts with CsBTS1E3 and strengthen CsBTS1E3-CsVOZ2 interaction. Meanwhile, SDE2470 strengthened the E3 ligase activity of CsBTS1, promoting CsVOZ2 degradation. Taken together, these findings support a model in which SDE2470 hijacks CsBTS1 to destabilize CsVOZ2, thereby disrupting ROS- and ABA-dependent immunity and promoting CLas infection in citrus.

柑橘黄龙病(Citrus Huanglongbing, HLB)是由革兰氏阴性菌‘亚洲韧皮部杆菌(Candidatus Liberibacter asiaticus, CLas)’引发的毁灭性病害,对全球柑橘产业造成严重威胁,且目前尚无有效防控策略。此前研究已鉴定出SDE2470(CLIBASIA_02470)为Sec依赖型效应蛋白(Sec-dependent effector),其在CLas致病过程中发挥作用,但具体分子机制尚未完全阐明。本研究发现,SDE2470可靶向柑橘血管单锌指转录因子CsVOZ2。在转基因柑橘植株中过表达CsVOZ2(CsVOZ2-OE)可显著抑制CLas的定殖,而在柑橘毛状根中通过RNA干扰(RNA interference, RNAi)沉默CsVOZ2,则会增强植株对CLas的感病性。此外,CsVOZ2过表达可显著提升活性氧(reactive oxygen species, ROS)与脱落酸(abscisic acid, ABA)的积累量,并激活相关免疫基因的表达。进一步研究显示,E3泛素连接酶(E3 ligase)CsBTS1可直接与CsVOZ2相互作用,并通过26S蛋白酶体通路(26S proteasome pathway)促进CsVOZ2的降解。在柑橘毛状根中过表达CsBTS1E3(CsBTS1E3-OE)可显著促进CLas的增殖。值得注意的是,SDE2470可直接与CsBTS1E3结合,并增强CsBTS1E3与CsVOZ2之间的相互作用;同时,SDE2470还可提升CsBTS1E3的E3泛素连接酶活性,加速CsVOZ2的降解。综上,本研究结果支持如下模型:SDE2470通过劫持CsBTS1E3以削弱CsVOZ2的稳定性,进而破坏依赖ROS与ABA的免疫防御过程,最终促进CLas对柑橘的侵染。

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2025-12-19
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