Rescue of morphogenetic defects and of retinoic acid signaling in retinaldehyde dehydrogenase 2 (Raldh2) mouse mutants by chimerism with wild-type cells.

Date publication

décembre 2006

Auteurs

Membres identifiés du Cancéropôle Est :
Dr DOLLE Pascal

Tous les auteurs :
Vermot J, Messaddeq N, Niederreither K, Dierich A, Dolle P

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/17177861

Résumé

Retinoic acid (RA), the active vitamin A derivative, is an important developmental signaling molecule in vertebrates. In this study, we have assessed whether minimal numbers and/or specific distributions of RA-producing cells can support normal mouse embryonic development. Retinaldehyde dehydrogenase 2 (RALDH2) is the main RA-synthesizing enzyme acting during development. We have generated an embryonic stem (ES) cell line homozygous for an Raldh2 gene disruption, and have analyzed chimeric embryos with various contributions of wild-type cells. Whereas embryos almost completely derived from Raldh2(-/-) cells phenocopy the corresponding germline null mutants, the presence of even small numbers (

Référence

Differentiation. 2006 Dec;74(9-10):661-8.