Li 2014 Mol Cell Biol

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Li S, Yao Y, Xu R, Pesenti S, Cottet-Rousselle C, Rieusset J, Tokarska-Schlattner M, Liao K, Schlattner U, Rousseau D (2014) ATAD3 is a limiting factor in mitochondrial biogenesis and adipogenesis of white adipocyte-like 3T3-L1 cells. Mol Cell Biol 37.

» PMID: 24732801

Li S, Yao Y, Xu R, Pesenti S, Cottet-Rousselle C, Rieusset J, Tokarska-Schlattner M, Liao K, Schlattner U, Rousseau D (2014) Mol Cell Biol

Abstract: ATAD3 is a vital ATPase of the inner mitochondrial membrane of pluri-cellular eucaryotes with largely unknown functions. Invalidation of ATAD3 blocks organism development at early stages requiring mitochondrial mass increase. Since ATAD3 knock-down (KD) in C. elegans inhibits first of all the development of adipocyte-like intestinal tissue, we used mouse adipocyte model 3T3-L1 cells to analyze ATAD3 functions during adipogenesis. By stable and transient modulation of ATAD3 expression in adipogenesis-induced 3T3-L1 cells, we show that (i) an increase in ATAD3 is preceding mitochondrial biogenesis and remodelling; (ii) down-regulation of ATAD3 inhibits adipogenesis, lipogenesis, and impedes overexpression of many mitochondrial proteins; (iii) ATAD3 re-expression rescues the phenotype of ATAD3 KD, and (iv) differentiation and lipogenesis are accelerated by ATAD3 overexpression, but inhibited by expression of a dominant-negative mutant. We further show that the ATAD3 KD phenotype is not due to altered insulin signal, but involves a limitation of mitochondrial biogenesis and remodelling linked to Drp1. These results demonstrate that ATAD3 is limiting for in vitro adipogenesis and lipogenesis.

Keywords: 3T3-L1 cells, ACC, Adipocyte, AMPK, ATAD3, Drp1, Endoplasmic reticulum, Fission, Lipogenesis, Mitochondria, Mfn2

O2k-Network Lab: FR Grenoble Schlattner U


Labels: MiParea: Respiration 


Organism: Mouse  Tissue;cell: Fat, Other cell lines  Preparation: Permeabilized cells 


Coupling state: LEAK, OXPHOS  Pathway: N, S  HRR: Oxygraph-2k