<i>Candidatus</i> Liberibacter Asiaticus-Mediated Manipulation of the Host Long Noncoding RNA <i>Dclnc5</i> Enhances Fecundity in <i>Diaphorina citri</i>

<i>Candidatus</i> Liberibacter asiaticus (<i>C</i>Las) enhances the fecundity of <i>Diaphorina citri</i> by manipulating <i>D. citri</i> long noncoding RNA 5 (<i>Dclnc5</i>), revealing an lncRNA-mediated regulatory role in pathogen-vector interactions. We found that <i>C</i>Las infection significantly increased <i>D. citri</i> fecundity and markedly upregulated vitellogenin (V_g) at both the transcript and protein levels. Ovary lncRNA-seq comparing <i>C</i>Las-positive (<i>C</i>Las+) and <i>C</i>Las-negative (<i>C</i>Las-) identified differentially expressed lncRNAs whose predicted targets were enriched in cellular signaling, lipid metabolism, and fat digestion and absorption pathways. Integrated network analysis highlighted <i>Dclnc5</i>, which was highly expressed during the oviposition period and enriched in midgut and ovary of <i>D. citri</i>. Nuclear-cytoplasmic fractionation coupled with qRT-PCR showed predominant cytoplasmic localization of <i>Dclnc5</i>. RNAi-mediated silencing of <i>Dclnc5</i> markedly delayed ovarian development, significantly reduced egg production, and significantly decreased <i>DcVg</i> expression. These results indicate that <i>C</i>Las may influence ovarian development and fecundity in <i>D. citri</i> by modulating the expression of <i>Dclnc5</i>. These findings provide a new perspective for exploring pathogen-vector interactions.