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et al., 2001
). However, it is not known whether lipid storage in nonadipose tissues,
a key pathogenic aspect of BSCL, is a result of lipid breakdown in adipose tissue
(extrinsic) or autonomous accumulation of lipids in affected tissues such as the liver
and muscle (intrinsic). Providing insights into this question, the
d
Seipin (fly homolog
of mammalian seipin) knockout decreased lipogenesis in the fat body (the adipose
tissue in flies) and increased ectopic lipid accumulation in the salivary gland in a
tissue-autonomous manner (
Tian et al., 2011
). Similarly, seipin knockdown in mam-
malian nonadipose cell lines (e.g., HeLa cells) increased TAG synthesis and induced
formation of small LDs (
Fei et al., 2011
). These findings suggest that seipin might
function to inhibit lipogenesis in adipose tissue, and that seipin could play distinct
roles in different tissues (
Fei, Du, & Yang, 2011; Payne et al., 2008
).
These selected examples illustrated the diverse, yet conserved, roles of
LD-associated proteins. When detrimental mutations occur to these proteins, various
disorders result, ranging frommetabolic disorders to neurodegeneration. The roles of
LDs and LD-associated proteins have just begun to be elucidated. With the con-
served pathways in LD regulation, the
Drosophila
model is ready to lead novel dis-
coveries as it has done for other fields for the past one hundred years.
Acknowledgments
This work is supported by a Mayo Clinic Graduate School Fellowship to Han Lee, a Mayo
Clinic New Investigator Startup Fund, and a Mayo Clinic Richard F. Emslander Career
Development Award to Yi Guo. We thank the Mayo Clinic Microscopy and Cell Analysis
Core Facility for assistance with the CARS application. We thank Kristi J. Simmons for
assistance with manuscript preparation.
References
