The conserved role of miR-2 and novel miR-109 in the increase in fecundity of <i>Diaphorina citri</i> induced by 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 <i>DcKr-h1</i> plays a critical role in the increase in fecundity of <i>Diaphorina citri</i> induced by the bacterium, "Candidatus Liberibacter asiaticus" (<i>C</i>Las) and the fungus, <i>Cordyceps fumosorosea</i> (<i>Cf</i>). 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 <i>DcKr-h1</i> expression by binding to its 3' untranslated region (UTR). In both <i>D. citri</i>-<i>C</i>Las and <i>D. citri</i>-<i>Cf</i> interactions, the increased juvenile hormone (JH) titer and reduced abundance of miR-2 and novel-miR-109 ensure high levels of <i>DcKr-h1</i> 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.