Loss of mtch2 function impairs early development of liver, intestine and visceral adipocytes in zebrafish larvae

FEBS Lett. 2016 Sep;590(17):2852-61. doi: 10.1002/1873-3468.12330. Epub 2016 Aug 9.

Abstract

The mitochondrial carrier homologue 2 (MTCH2) has been shown to be essential for embryogenesis in mice, and variants in the MTCH2 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.

Keywords: MTCH2; adipocyte; embryogenesis; morpholino; organogenesis; zebrafish.

Publication types

  • Letter

MeSH terms

  • Adipocytes / cytology
  • Adipocytes / metabolism
  • Adipogenesis / genetics
  • Animals
  • Embryonic Development / genetics*
  • Gene Expression Regulation, Developmental
  • Gene Knockdown Techniques
  • Humans
  • Intestinal Mucosa / metabolism
  • Intestines / growth & development
  • Larva / genetics
  • Larva / growth & development
  • Liver / growth & development
  • Liver / metabolism*
  • Mice
  • Mitochondrial Membrane Transport Proteins / genetics*
  • Zebrafish / genetics*
  • Zebrafish / growth & development

Substances

  • Mitochondrial Membrane Transport Proteins
  • Mtch2 protein, mouse