PDF(Pubmed)
Abstract：
Diaphorina citri serves as the primary vector for \'Candidatus Liberibacter asiaticus (CLas),\' the bacterium associated with the severe Asian form of huanglongbing. CLas-positive D. citri are more fecund than their CLas-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 (DcAKH) and its receptor (DcAKHR) were essential for increasing lipid metabolism and fecundity in response to CLas infection in D. citri. Knockdown of DcAKH and DcAKHR not only resulted in the accumulation of triacylglycerol and a decline of glycogen, but also significantly decreased fecundity and CLas titer in ovaries. Combined in vivo and in vitro experiments showed that miR-34 suppresses DcAKHR expression by binding to its 3\' untranslated region, whilst overexpression of miR-34 resulted in a decline of DcAKHR expression and CLas titer in ovaries and caused defects that mimicked DcAKHR knockdown phenotypes. Additionally, knockdown of DcAKH and DcAKHR significantly reduced juvenile hormone (JH) titer and JH signaling pathway genes in fat bodies and ovaries, including the JH receptor, methoprene-tolerant (DcMet), and the transcription factor, Krüppel homolog 1 (DcKr-h1), that acts downstream of it, as well as the egg development related genes vitellogenin 1-like (DcVg-1-like), vitellogenin A1-like (DcVg-A1-like) and the vitellogenin receptor (DcVgR). As a result, CLas hijacks AKH/AKHR-miR-34-JH signaling to improve D. citri lipid metabolism and fecundity, while simultaneously increasing the replication of CLas, suggesting a mutualistic interaction between CLas and D. citri ovaries.
摘要：
柑桔是亚洲念珠菌（CLas）的主要载体，与黄龙病的严重亚洲形式有关的细菌。CLas阳性D.citri比CLas阴性的同类动物更多，需要额外的能量消耗。因此,了解连接代谢和繁殖的分子机制是特别重要的。在这项研究中,我们发现脂肪动力学激素（DcAKH）及其受体（DcAKHR）对于增加D.citri中CLas感染的脂质代谢和繁殖力至关重要。敲除DcAKH和DcAKHR不仅导致三酰甘油的积累和糖原的下降，但也显著降低卵巢的繁殖力和CLas滴度。结合体内和体外实验表明，miR-34通过结合其3'非翻译区抑制DcAKHR表达，而miR-34的过表达导致卵巢中DcAKHR表达和CLas滴度下降,并导致模仿DcAKHR敲低表型的缺陷.此外,DcAKH和DcAKHR的敲除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,耐甲氧烯（DcMet），和转录因子，Krüppel同源物1（DcKr-h1），在它的下游起作用，以及卵发育相关基因卵黄蛋白原1样（DcVg-1样），卵黄蛋白原A1样（DcVg-A1样）和卵黄蛋白原受体（DcVgR）。因此,CLas劫持AKH/AKHR-miR-34-JH信号以改善D.citri脂质代谢和繁殖力，同时增加CLas的复制，表明CLas和D.citri卵巢之间存在相互作用。
