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脂动激素信号转导介导了 '亚洲韧皮杆菌' 感染的生殖力增强。

Adipokinetic hormone signaling mediates the enhanced fecundity of infected by ' Liberibacter asiaticus'.

机构信息

National Key Laboratory of Green Pesticide, Department of Entomology, College of Plant Protection, South China Agricultural University, Guangzhou, China.

School of Science, Western Sydney University, Penrith, Australia.

出版信息

Elife. 2024 Jul 10;13:RP93450. doi: 10.7554/eLife.93450.

Abstract

serves as the primary vector for ' Liberibacter asiaticus (Las),' the bacterium associated with the severe Asian form of huanglongbing. Las-positive are more fecund than their Las-negative counterparts and require extra energy expenditure. Therefore, understanding the molecular mechanisms linking metabolism and reproduction is of particular importance. In this study, we found adipokinetic hormone () and its receptor () were essential for increasing lipid metabolism and fecundity in response to Las infection in . Knockdown of and not only resulted in the accumulation of triacylglycerol and a decline of glycogen, but also significantly decreased fecundity and Las titer in ovaries. Combined in vivo and in vitro experiments showed that miR-34 suppresses expression by binding to its 3' untranslated region, whilst overexpression of miR-34 resulted in a decline of expression and Las titer in ovaries and caused defects that mimicked knockdown phenotypes. Additionally, knockdown of and significantly reduced juvenile hormone (JH) titer and JH signaling pathway genes in fat bodies and ovaries, including the JH receptor, (), and the transcription factor, ), that acts downstream of it, as well as the egg development related genes (), () and the vitellogenin receptor (). As a result, Las hijacks AKH/AKHR-miR-34-JH signaling to improve lipid metabolism and fecundity, while simultaneously increasing the replication of Las, suggesting a mutualistic interaction between Las and ovaries.

摘要

作为“亚洲韧皮杆菌(Las)”的主要载体,这种细菌与严重的亚洲黄龙病有关。Las 阳性的比 Las 阴性的更具繁殖力,需要额外的能量消耗。因此,了解代谢和繁殖之间的分子机制尤为重要。在这项研究中,我们发现,激素和其受体对于增加脂肪代谢和繁殖力以应对 Las 感染至关重要。和的敲低不仅导致甘油三酯的积累和糖原的减少,而且还显著降低了卵巢中的繁殖力和 Las 滴度。体内和体外实验相结合表明,miR-34 通过与其 3'非翻译区结合来抑制的表达,而过表达 miR-34 导致卵巢中表达和 Las 滴度下降,并导致类似于敲低表型的缺陷。此外,和的敲低显著降低了脂肪体和卵巢中的保幼激素(JH)滴度和 JH 信号通路基因,包括 JH 受体、()和其下游的转录因子,以及与卵子发育相关的基因()、()和卵黄蛋白原受体()。因此,Las 劫持 AKH/AKHR-miR-34-JH 信号来改善的脂肪代谢和繁殖力,同时增加 Las 的复制,表明 Las 和的卵巢之间存在互利的相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c29/11236419/f4fabaf57f8b/elife-93450-fig1.jpg

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