Depletion of lipid storage droplet‐1 delays endoreplication progression and induces cell death in Drosophila salivary gland

Author:

Nguyen Yen D. H.1ORCID,Pham Tuan L. A.1ORCID,Nishihara Taisei1,Kamei Kaeko1ORCID,Tran Duy Binh1ORCID

Affiliation:

1. Department of Functional Chemistry, Kyoto Institute of Technology Kyoto Japan

Abstract

AbstractPerilipins are evolutionarily conserved from insects to mammals. Drosophila lipid storage droplet‐1 (LSD‐1) is a lipid storage droplet membrane surface‐binding protein family member and a counterpart to mammalian perilipin 1 and is known to play a role in lipolysis. However, the function of LSD‐1 during specific tissue development remains under investigation. This study demonstrated the role of LSD‐1 in salivary gland development. Knockdown of Lsd‐1 in the salivary gland was established using the GAL4/UAS system. The third‐instar larvae of knockdown flies had small salivary glands containing cells with smaller nuclei. The null mutant Drosophila also showed the same phenotype. The depletion of LSD‐1 expression induced a delay of endoreplication due to decreasing CycE expression and increasing DNA damage. Lsd‐1 genetically interacted with Myc in the third‐instar larvae. These results demonstrate that LSD‐1 is involved in cell cycle and cell death programs in the salivary gland, providing novel insight into the effects of LSD‐1 in regulating salivary gland development and the interaction between LSD‐1 and Myc.

Publisher

Wiley

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