Increasing evidence indicates that miRNAs play crucial regulatory roles in various physiological processes of insects, including systemic metabolism. However, the molecular mechanisms of how specific miRNAs regulate energy metabolic homeostasis remain largely
unknown. In the present study, we found that an evolutionarily conserved miR-275/305 cluster was essential in maintaining energy metabolic homeostasis in response to dietary yeast
stimulation in Bactrocera dorsalis. Depletion of miR-275 and miR-305 by the CRISPR/Cas9
system significantly reduced triglyceride and glycogen contents, elevated total sugar levels,
and impaired flight capacity. Combined in vivo and in vitro experiments, we demonstrated
that... More
Increasing evidence indicates that miRNAs play crucial regulatory roles in various physiological processes of insects, including systemic metabolism. However, the molecular mechanisms of how specific miRNAs regulate energy metabolic homeostasis remain largely
unknown. In the present study, we found that an evolutionarily conserved miR-275/305 cluster was essential in maintaining energy metabolic homeostasis in response to dietary yeast
stimulation in Bactrocera dorsalis. Depletion of miR-275 and miR-305 by the CRISPR/Cas9
system significantly reduced triglyceride and glycogen contents, elevated total sugar levels,
and impaired flight capacity. Combined in vivo and in vitro experiments, we demonstrated
that miR-275 and miR-305 can bind to the 3’UTR regions of SLC2A1 and GLIS2 to repress
their expression, respectively. RNAi-mediated knockdown of these two genes partially rescued metabolic phenotypes caused by inhibiting miR-275 and miR-305. Furthermore, we
further illustrated that the miR-275/305 cluster acting as a regulator of the metabolic axis
was controlled by the insulin signaling pathway. In conclusion, our work combined genetic
and physiological approaches to clarify the molecular mechanism of metabolic homeostasis
in response to different dietary stimulations and provided a reference for deciphering the
potential targets of physiologically important miRNAs in a non-model organism.
