ERp44/CG9911 promotes fat storage in Drosophila adipocytes by regulating ER Ca2+ homeostasis

Fat storage is one of the important strategies employed in regulating energy homeostasis. Impaired lipid storage causes metabolic disorders in both mammals and Drosophila. In this study, we report CG9911, the Drosophila homolog of ERp44 (endoplasmic reticulum protein 44) plays a role in regulating adipose tissue fat storage. Using the CRISPR/Cas9 system, we generated a CG9911 mutant line deleting 5 bp of the coding sequence. The mutant flies exhibit phenotypes of lower bodyweight, fewer lipid droplets, reduced TAG level and increased expression of lipolysis related genes. The increased lipolysis phenotype is enhanced in the presence of ER stresses and suppressed by a reduction of the ER Ca2+. Moreover, loss of CG9911 per se results in a decrease of ER Ca2+ in the fat body. Together, our results reveal a novel function of CG9911 in promoting fat storage via regulating ER Ca2+ signal in Drosophila.

Automated summary

This study reveals a novel function of CG9911 in promoting fat storage by regulating ER Ca2+ signal in Drosophila. Mutant flies with deleted CG9911 show decreased lipid storage, increased lipolysis, and altered expression of lipolysis related genes, indicating the importance of CG9911 in lipid metabolism and energy homeostasis. Additionally, the phenotype is enhanced under ER stresses and suppressed by a reduction in ER Ca2+, suggesting the intricate regulatory mechanisms involved in fat storage in Drosophila.