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Tissue‐specific expression of Cre recombinase from the Tgfb3 locus
Author(s) -
Yang LiangTung,
Li WaiYee,
Kaartinen Vesa
Publication year - 2008
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.20372
Subject(s) - cre recombinase , biology , gene targeting , fate mapping , null allele , microbiology and biotechnology , exon , gene , mutant , transgene , chimera (genetics) , genetically modified mouse , embryonic stem cell , genetics
Tgfb3 , a member of the TGF‐β superfamily, is tightly regulated, both spatially and temporally, during embryogenesis. Previous mouse knockout studies have demonstrated that Tgfb3 is absolutely required for normal palatal fusion and pulmonary development. We have generated a novel tool to ablate genes in Tgfb3 ‐expressing cells by targeting the promoterless Cre‐pgk‐Neo cassette into exon 1 of the mouse Tgfb3 gene, which generates a functionally null Tgfb3 allele. Using the Rosa26 reporter assay, we demonstrate that Cre ‐induced recombination was already induced at embryonal day 10 (E10) in the ventricular myocardium, limb buds, and otic vesicles. At E14, robust recombination was detected in the prefusion palatal epithelium. Deletion of the TGF‐β type I receptor Alk5 ( Tgfbr1) specifically in Tgfb3 expressing cells using the Tgfb3‐Cre driver line lead to a cleft palate phenotype similar to that seen in conventional Tgfb3 null mutants. In addition, Alk5/ Tgfb3‐Cre mice displayed hydrocephalus, and severe intracranial bleeding due to germinal matrix hemorrhage. genesis 46:112–118, 2008. © 2008 Wiley‐Liss, Inc.