Lipids are indispensable to life. They serve as fundamental structural components of cellular membranes and the primary energy depot. In addition, they act as signaling molecules for cellular homeostasis. Although much is known about how lipids are synthesized and modified within a cell, open questions remain regarding how extracellular lipids are incorporated into the intracellular lipid pool. Disorder and deficiency in lipid metabolism can lead to a variety of diseases, some of which have been modeled using the nematode C. elegans. Mutations that inactivate peroxisomal thiolase DAF-22 cause excess fat storage in abnormally enlarged lipid droplets (LDs) in C. elegans. In a genetic screen, tmem-120 mutant alleles were found to suppress LDs expansion in daf-22 mutant worms. This...[ Read more ]

Lipids are indispensable to life. They serve as fundamental structural components of cellular membranes and the primary energy depot. In addition, they act as signaling molecules for cellular homeostasis. Although much is known about how lipids are synthesized and modified within a cell, open questions remain regarding how extracellular lipids are incorporated into the intracellular lipid pool. Disorder and deficiency in lipid metabolism can lead to a variety of diseases, some of which have been modeled using the nematode C. elegans. Mutations that inactivate peroxisomal thiolase DAF-22 cause excess fat storage in abnormally enlarged lipid droplets (LDs) in C. elegans. In a genetic screen, tmem-120 mutant alleles were found to suppress LDs expansion in daf-22 mutant worms. This finding indicates the critical role of TMEM-120 in regulating fat storage. Here, I present evidence on the role of vesicular trafficking in TMEM-120 localization. I also generated several tissue-specific tmem-120 deletion strains and investigated the possible function of TMEM-120 in different tissues.