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Plac8 belongs to an evolutionary conserved family of proteins, mostly abundant in plants where they control fruit weight through regulation of cell number. In mice,  Plac8  is expressed both in white and brown adipose tissues and we previously showed that  Plac8 −/−   mice develop late-onset obesity, with abnormal brown fat differentiation and reduced thermogenic capacity. We also showed that in brown adipocytes,  Plac8  is an upstream regulator of  C/EBPβ  expression. Here, we first assessed the role of  Plac8  in white adipogenesis in vitro. We show that  Plac8  is induced early after induction of 3T3-L1 adipocytes differentiation, a process that is prevented by  Plac8  knockdown; similarly, embryonic fibroblasts obtained from  Plac8  knockout mice failed to form adipocytes upon stimulation of differentiation. Knockdown of  Plac8  in 3T3-L1 was associated with reduced expression of  C/EBPβ ,  Krox20 , and  Klf4 , early regulators of the white adipogenic program, and we show that  Plac8  could transactivate the  C/EBPβ  promoter. In vivo, we show that absence of  Plac8  led to increased white fat mass with enlarged adipocytes but reduced total number of adipocytes. Finally, even though  Plac8 −/−   mice showed impaired thermogenesis due to brown fat dysfunction, this was not associated with changes in glycemia or plasma free fatty acid and triglyceride levels. Collectively, these data indicate that  Plac8  is an upstream regulator of  C/EBPβ  required for adipogenesis in vitro. However, in vivo,  Plac8  is dispensable for the differentiation of white adipocytes with preserved fat storage capacity but is required for normal fat cell number regulation.

Plac8 is required for White Adipocyte Differentiation in vitro and Cell Number Control in vivo