Difference between revisions of "Li 2014 Mol Cell Biol"

Latest revision as of 13:30, 28 March 2018

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

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 {{Publication
-|title=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 [Epub ahead of print].
+|title=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.
 |info=[http://www.ncbi.nlm.nih.gov/pubmed/24732801 PMID: 24732801]
 |authors=Li S, Yao Y, Xu R, Pesenti S, Cottet-Rousselle C, Rieusset J, Tokarska-Schlattner M, Liao K, Schlattner U, Rousseau D
 |year=2014
 |journal=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.
+|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
+|mipnetlab=FR Grenoble Schlattner U
 }}
 {{Labeling
 |area=Respiration
 |organism=Mouse
-|tissues=Fat
+|tissues=Fat, Other cell lines
-|model cell lines=Other cell lines
 |preparations=Permeabilized cells
 |couplingstates=LEAK, OXPHOS
-|substratestates=CI, CII
+|pathways=N, S
 |instruments=Oxygraph-2k
 }}