Submitted on September 4, 2007
Revised on October 3, 2007
Accepted on October 4, 2007
Mammary glands of adipophilin-null mice produce an N-terminally truncated form of adipophilin that mediates milk lipid formation and secretion
Tanya D. Russell, Carol A. Palmer, David J. Orlicky, Elise S. Bales, Benny Hung-Jung Chang, Lawrence Chan, and James L. McManaman
Obstetrics and Gynecology, University of Colorado Denver Health Sciences Center, Aurora, CO 80045
Corresponding Author: jim.mcmanaman{at}uchsc.edu
Adipophilin, a member of the perilipin family of lipid droplet associated proteins, is hypothesized to mediate milk lipid formation and secretion. Unexpectedly the fat content of milk from adipophilin-null mice was only modestly lower than WT controls and neither TIP47 nor perilipin appeared to fully compensate for adipophilin loss. This prompted us to investigate the possibility that the mutated adipophilin gene, was not a genuine null mutation. Adipophilin transcripts were detected in adipophilin-null mammary tissue by QRT-PCR and C-terminal specific, but not N-terminal specific, adipophilin antibodies detected a single lower molecular weight product and immunostained cytoplasmic lipid droplets and secreted milk fat globules in adipophilin-null mammary tissue. Further, stable cell lines expressing cDNA constructs corresponding to the adipophilin-null mutation produced a product comparable in size to the one detected in adipophilin-null mammary glands and localized to cytoplasmic lipid droplets. Based on these data we conclude that adipophilin-null mice express an N-terminally truncated form of adipophilin that retains the ability to promote formation and secretion of milk lipids.
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