PuSH - Publication Server of Helmholtz Zentrum München

Cytoplasmic thioredoxin reductase is essential for embryogenesis but dispensable for cardiac development.

Mol. Cell. Biol. 25, 1980-1988 (2005)
Publ. Version/Full Text DOI
Free by publisher
Open Access Green as soon as Postprint is submitted to ZB.
Two distinct thioredoxin/thioredoxin reductase systems are present in the cytosol and the mitochondria of mammalian cells. Thioredoxins (Txn), the main substrates of thioredoxin reductases (Txnrd), are involved in numerous physiological processes, including cell-cell communication, redox metabolism, proliferation, and apoptosis. To investigate the individual contribution of mitochondrial (Txnrd2) and cytoplasmic (Txnrd1) thioredoxin reductases in vivo, we generated a mouse strain with a conditionally targeted deletion of Txnrd1. We show here that the ubiquitous Cre-mediated inactivation of Txnrd1 leads to early embryonic lethality. Homozygous mutant embryos display severe growth retardation and fail to turn. In accordance with the observed growth impairment in vivo, Txnrd1-deficient embryonic fibroblasts do not proliferate in vitro. In contrast, ex vivo-cultured embryonic Txnrd1-deficient cardiomyocytes are not affected, and mice with a heart-specific inactivation of Txnrd1 develop normally and appear healthy. Our results indicate that Txnrd1 plays an essential role during embryogenesis in most developing tissues except the heart.
Additional Metrics?
Edit extra informations Login
Publication type Article: Journal article
Document type Scientific Article
ISSN (print) / ISBN 0270-7306
e-ISSN 1098-5549
Quellenangaben Volume: 25, Issue: 5, Pages: 1980-1988 Article Number: , Supplement: ,
Publisher American Society for Microbiology (ASM)
Reviewing status Peer reviewed