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International journal of biological macromolecules · 2026

The BiP gene encoding endoplasmic reticulum chaperone binding immunoglobulin protein regulates survival and reproduction in Diaphorina citri.

СтатьяНазвание и аннотация: Перевод в очереди
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Li Min, Huang Yuanyuan, Zhong Ming, Zou Xiuqi, Yang Zhijie, Tu Shengfeng, Yu Lin, Sang Wen

Аннотация

The Asian citrus psyllid, Diaphorina citri, a vector of citrus Huanglongbing (HLB) disease, requires flush shoot feeding for reproduction, which induces the endoplasmic reticulum (ER) chaperone binding immunoglobulin protein (BiP). Using RNA interference (RNAi), DcBiP function was investigated. DcBiP expression decreased to 0.23-fold at 24 h and 0.35-fold at 48 h following RNAi-mediated knockdown. DcBiP knockdown resulted in 5255 differentially expressed genes (3054 upregulated and 2201 downregulated). Transcriptomic analysis combined with RT-qPCR validation demonstrated altered expression patterns in genes involved in unfolded protein response (UPR), autophagy, and apoptosis following DcBiP knockdown, suggesting a potential coordinated cellular stress response that may contribute to impaired survival and reproduction. Phenotypically, survival rates decreased to 37.78% (females) and 34.44% (males), with mortality peaking at 6-24 h post-treatment. Ovarian diameter was reduced by 32.99% (to 67.01% of the control), the proportion of mature ovaries (Stages IV-V) decreased from 45.00% to 5.00%, and fecundity dropped to 39.70%. Post-interference, DcVg expression decreased to 0.41-fold at 24 h and further to 0.38-fold at 48 h, while DcVgR expression decreased to 0.46-fold at 24 h and 0.54-fold at 48 h. Qualitative transmission electron microscopy (TEM) analysis of ovarian samples revealed ultrastructural alterations, including ER vesiculation and autophagosome formation, in dsDcBiP-treated samples. Collectively, DcBiP is essential for psyllid survival and reproduction, representing a promising target for RNAi-based pest management.

ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

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