National Key Laboratory of Green Pesticide, Department of Entomology, College of Plant Protection, South China Agricultural University, Guangzhou, China.
School of Biology and Agriculture, Shaoguan University, Shaoguan, China.
mBio. 2024 Nov 13;15(11):e0154124. doi: 10.1128/mbio.01541-24. Epub 2024 Oct 7.
Infection with pathogens can increase the fecundity and other fitness-related traits of insect vectors for their own advantage. Our previous research has reported the pivotal role of in the fecundity improvement of induced by the bacterium, " Liberibacter asiaticus" (Las), and the fungus, (). However, the posttranscriptional regulation of this process remains poorly understood. Given the significance of miRNAs in gene regulation, we delved into their roles in shaping phenotypes and their underlying molecular mechanisms. Our results indicated that two miRNAs, miR-2 and novel-miR-109, jointly inhibited expression by binding to its 3' untranslated region (UTR). In the Las interaction, the expression levels of miR-2 and novel-miR-109 in the ovaries of Las-positive psyllids were lower compared to Las-negative individuals. Overexpression of miR-2 or novel-miR-109 significantly decreased fecundity and Las titer in ovaries and caused reproductive defects reminiscent of knockdown. Similarly, in the interaction, the levels of miR-2 and novel-miR-109 markedly decreased in the ovaries. Upregulation of miR-2 or novel-miR-109 also resulted in reduced fecundity and ovary defects similar to those caused by silencing. Moreover, feeding antagomir-2 or antagomir-109 partially rescued the defective phenotypes caused by silencing in both model systems, and miR-2 and novel-miR-109 were repressed by juvenile hormone (JH) and regulated the genes associated with egg development. This study shows a conserved regulatory mechanism, whereby JH suppresses the expression of miR-2 and novel-miR-109 which, together with JH-induced transcription of , increases female fecundity induced by both symbiotic bacteria and pathogenic fungi.
Infection with pathogens can increase the fecundity and other fitness-related traits of insect vectors for their own advantage. Our previous research has reported that plays a critical role in the increase in fecundity of induced by the bacterium, "Candidatus Liberibacter asiaticus" (Las) and the fungus, (). However, the posttranscriptional regulation of this process remains poorly understood. Given the significance of miRNAs in gene regulation, we delved into their roles in shaping phenotypes and their underlying molecular mechanisms. Our results indicated that two miRNAs, miR-2 and novel-miR-109, jointly inhibited expression by binding to its 3' untranslated region (UTR). In both -Las and - interactions, the increased juvenile hormone (JH) titer and reduced abundance of miR-2 and novel-miR-109 ensure high levels of expression, consequently stimulating ovarian development and enhancing fecundity. These observations provide evidence that miR-2 and miR-109 are crucial players in the JH-dependent increase in fecundity in psyllids induced by infection with different pathogens.
病原体感染可以提高昆虫传播媒介的繁殖力和其他与适应度相关的特征，从而使自身受益。我们之前的研究报告表明， 在由细菌“亚洲韧皮杆菌”（Las）和真菌 （）诱导的繁殖力提高中起着关键作用。然而，这个过程的转录后调控仍知之甚少。鉴于 miRNAs 在基因调控中的重要性，我们深入研究了它们在塑造表型及其潜在分子机制中的作用。我们的结果表明，两种 miRNAs，miR-2 和新型-miR-109，通过结合其 3'非翻译区（UTR）共同抑制 的表达。在 Las 相互作用中，Las 阳性若虫卵巢中 miR-2 和新型-miR-109 的表达水平低于 Las 阴性个体。miR-2 或新型-miR-109 的过表达显著降低了卵巢中的繁殖力和 Las 滴度，并导致类似于 的敲低的生殖缺陷。同样，在 相互作用中，miR-2 和新型-miR-109 的水平在卵巢中明显降低。miR-2 或新型-miR-109 的上调也导致繁殖力降低和卵巢缺陷，类似于 的沉默引起的缺陷表型。此外，饲喂 antagomir-2 或 antagomir-109 部分挽救了两个模型系统中 沉默引起的缺陷表型，miR-2 和新型-miR-109 受保幼激素（JH）抑制，并调节与卵发育相关的基因。这项研究表明存在保守的调控机制，即 JH 抑制 miR-2 和新型-miR-109 的表达，同时 JH 诱导 的转录，增加了由两种共生细菌和致病性真菌诱导的雌性繁殖力。
病原体感染可以提高昆虫传播媒介的繁殖力和其他与适应度相关的特征，从而使自身受益。我们之前的研究报告表明， 在由细菌“亚洲韧皮杆菌”（Las）和真菌 （）诱导的繁殖力提高中起着关键作用。然而，这个过程的转录后调控仍知之甚少。鉴于 miRNAs 在基因调控中的重要性，我们深入研究了它们在塑造表型及其潜在分子机制中的作用。我们的结果表明，两种 miRNAs，miR-2 和新型-miR-109，通过结合其 3'非翻译区（UTR）共同抑制 的表达。在 Las 和 相互作用中，保幼激素（JH）浓度的增加和 miR-2 和新型-miR-109 的丰度降低确保了 的高表达水平，从而刺激卵巢发育并提高繁殖力。这些观察结果表明，miR-2 和 miR-109 是受不同病原体感染的若虫中 JH 依赖性繁殖力增加的关键因素。
