CLSTN3B promotes lipid droplet maturation and lipid storage in mouse adipocytes

Chuanhai Zhang, Mengchen Ye, Kamran Melikov, Dengbao Yang, Goncalo Dias do Vale, Jeffrey McDonald, Kaitlyn Eckert, Mei-Jung Lin and Xing Zeng ()
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Chuanhai Zhang: UT Southwestern Medical Center
Mengchen Ye: University of California Berkeley
Kamran Melikov: National Institutes of Health
Dengbao Yang: UT Southwestern Medical Center
Goncalo Dias do Vale: UT Southwestern Medical Center
Jeffrey McDonald: UT Southwestern Medical Center
Kaitlyn Eckert: UT Southwestern Medical Center
Mei-Jung Lin: UT Southwestern Medical Center
Xing Zeng: UT Southwestern Medical Center

Nature Communications, 2024, vol. 15, issue 1, 1-18

Abstract: Abstract Interorganelle contacts facilitate material exchanges and sustain the structural and functional integrity of organelles. Lipid droplets (LDs) of adipocytes are responsible for energy storage and mobilization responding to body needs. LD biogenesis defects compromise the lipid-storing capacity of adipocytes, resulting in ectopic lipid deposition and metabolic disorders, yet how the uniquely large LDs in adipocytes attain structural and functional maturation is incompletely understood. Here we show that the mammalian adipocyte-specific protein CLSTN3B is crucial for adipocyte LD maturation. CLSTN3B employs an arginine-rich segment to promote extensive contact and hemifusion-like structure formation between the endoplasmic reticulum (ER) and LD, allowing ER-to-LD phospholipid diffusion during LD expansion. CLSTN3B ablation results in reduced LD surface phospholipid density, increased turnover of LD-surface proteins, and impaired LD functions. Our results establish the central role of CLSTN3B in the adipocyte-specific LD maturation pathway that enhances lipid storage and maintenance of metabolic health under caloric overload in mice of both sexes.

Date: 2024
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DOI: 10.1038/s41467-024-53750-z

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