Function of Lipid Storage Droplet 1 (Lsd1) in Wing Development of Drosophila melanogaster.

Tran Men,Masamitsu Yamaguchi,Tran Binh,Kaeko Kamei,Nguyen Huy

doi:10.3390/ijms17050648

Tran Men, Masamitsu Yamaguchi + Show 3 more

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https://doi.org/10.3390/ijms17050648

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Abstract

Perilipins are evolutionarily conserved from Drosophila to humans, the lipid storage droplet 1 (Lsd1) is a Drosophila homolog of human perilipin 1. The function of Lsd1 as a regulator of lipolysis in Drosophila has been demonstrated, as the Lsd1 mutant causes an increase of lipid droplet size. However, the functions of this gene during development are still under investigation. In order to determine the function of Lsd1 during development, Lsd1 was knocked down in Drosophila using the GAL4-UAS system. Selective knockdown of Lsd1 in the dorsal wing disc caused an atrophied wing phenotype. The generation of reactive oxygen species in the wing pouch compartment of the Lsd1-knockdown flies was significantly higher than in the control. Immunostaining with caspase-3 antibody revealed a greater number of apoptotic cells in Lsd1-knockdown wing discs than in the control. Cell death by autophagy was also induced in the knockdown flies. Moreover, cells deprived of Lsd1 showed mitochondrial expansion and decreased ATP levels. These results strongly suggest that knockdown of Lsd1 induces mitochondrial stress and the production of reactive oxygen species that result in cell death, via apoptosis and the autophagy pathway. These results highlight the roles of Drosophila Lsd1 during wing development.

Highlights

Triacylglycerols (TAG) in adipose tissue are the body’s major energy storage source [1]
Lipid storage droplet 1 (Lsd1) knockdown by En-Gal4 caused lethality, probably because of the reported leaky expression of GAL4 during embryogenesis [16,17]. These results indicate an essential role of the Lsd1 gene for viability and/or development of Drosophila
Lsd1 knockdown in the fat body caused a delay in growth at 25 ̋C and lethality at 28 ̋C. These results are consistent with previous studies of Lsd1 mutants and indicate that Lsd1 plays an important role in lipid metabolism [8]

Summary

Introduction

Triacylglycerols (TAG) in adipose tissue are the body’s major energy storage source [1]. Known as lipid droplets (LDs), are abundant in the adipose tissue and play a role in controlling the body fat banks of animals [2]. PAT domain proteins include ADRP and TIP47, and are collectively named perilipins [3]. The mutation of perilipin 1 in mice results in a lean phenotype, and a lack of perilipin 1 combined with a mutation in the leptin receptor gene in mice reverses obesity These phenotypes are derived from loss of the anti-lipase protective effect of perilipin 1 under normal conditions [8]. Loss of function or overexpression of Lsd in Drosophila indicated that Lsd probably facilitates lipid mobilization [8]. Other functions and genetic regulatory mechanisms of this gene are still under investigation

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