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Generation of a floxed allele of Smad5 for cre‐mediated conditional knockout in the mouse
Author(s) -
Umans Lieve,
Vermeire Liesbeth,
Francis Annick,
Chang Hua,
Huylebroeck Danny,
Zwijsen An
Publication year - 2003
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/gene.10219
Subject(s) - conditional gene knockout , phenocopy , embryonic stem cell , smad , biology , genetics , allele , cre recombinase , knockout mouse , microbiology and biotechnology , phenotype , transgene , genetically modified mouse , signal transduction , gene
Summary: Smad5 is a member of the Smad family of intracellular mediators of BMP signals and in endothelial cells of TGF‐β signals. We and others previously showed that loss of Smad5 in the mouse results in embryonic lethality (between E9.5–E11.5) due to multiple embryonic and extraembryonic defects. To circumvent the early embryonic lethality and to allow tissue‐ and time‐specific Smad5 inactivation, we created a conditional Smad5 allele in the mouse. Floxed Smad5 ( Smad5 flE2,Neo / flE2,Neo ) mice were generated in which both exon2 and the Neo ‐cassette were flanked by loxP sites. Here we demonstrate that embryos with ubiquitous Cre‐mediated deletion of Smad5 ( Smad5 flΔE2 / flΔE2 ) phenocopy the conventional Smad5 knockout mice. Smad5 flE2 / flE2 mice are now available and will be a valuable tool to analyze the role of Smad5 beyond its crucial early embryonic function throughout development and postnatal life. genesis 37:5–11, 2003. © 2003 Wiley‐Liss, Inc.