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Loss of mtch2 function impairs early development of liver, intestine and visceral adipocytes in zebrafish larvae
Author(s) -
Landgraf Kathrin,
Strobach Ariane,
Kiess Wieland,
Körner Antje
Publication year - 2016
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12330
Subject(s) - zebrafish , adipogenesis , biology , embryogenesis , in vivo , microbiology and biotechnology , adipocyte , embryo , endocrinology , adipose tissue , gene , genetics , mesenchymal stem cell
The mitochondrial carrier homologue 2 ( MTCH 2) has been shown to be essential for embryogenesis in mice, and variants in the MTCH 2 locus have been linked to obesity in humans. Here, we investigated the importance of mtch2 for embryogenesis and adipocyte formation in zebrafish in vivo . We show that mtch2 is conserved in zebrafish and broadly expressed during embryogenesis. Knock‐down of mtch2 results in impaired development of liver and intestine, and is associated with a reduced number of adipocytes and impaired postembryonic growth. The findings indicate an essential role for mtch2 during organ development and adipogenesis in vivo .