PUBLICATION
Loss of mtch2 function impairs early development of liver, intestine and visceral adipocytes in zebrafish larvae
- Authors
- Landgraf, K., Strobach, A., Kiess, W., Körner, A.
- ID
- ZDB-PUB-160729-2
- Date
- 2016
- Source
- FEBS letters 590(17): 2852-61 (Journal)
- Registered Authors
- Keywords
- MTCH2, adipocyte, embryogenesis, morpholino, organogenesis, zebrafish
- MeSH Terms
-
- Adipocytes/cytology
- Adipocytes/metabolism
- Adipogenesis/genetics
- Animals
- Embryonic Development/genetics*
- Gene Expression Regulation, Developmental
- Gene Knockdown Techniques
- Humans
- Intestines/growth & development
- Intestines/metabolism
- Larva/genetics
- Larva/growth & development
- Liver/growth & development
- Liver/metabolism*
- Mice
- Mitochondrial Membrane Transport Proteins/genetics*
- Zebrafish/genetics*
- Zebrafish/growth & development
- PubMed
- 27468124 Full text @ FEBS Lett.
Citation
Landgraf, K., Strobach, A., Kiess, W., Körner, A. (2016) Loss of mtch2 function impairs early development of liver, intestine and visceral adipocytes in zebrafish larvae. FEBS letters. 590(17):2852-61.
Abstract
The mitochondrial carrier homolog 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. Knockdown of mtch2 results in impaired development of liver and intestine, and is associated with a reduced number of adipocytes and impaired post-embryonic growth. The findings indicate an essential role for mtch2 during organ development and adipogenesis in vivo. This article is protected by copyright. All rights reserved.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping