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Generation of a conditional mutant allele for Tab1 in mouse
Author(s) -
Inagaki Maiko,
Komatsu Yoshihiro,
Scott Greg,
Yamada Gen,
Ray Manas,
NinomiyaTsuji Jun,
Mishina Yuji
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.20418
Subject(s) - cre recombinase , biology , autophosphorylation , kinase , microbiology and biotechnology , gene targeting , protein kinase a , gene , genetics , genetically modified mouse , transgene
Abstract TAK1 binding protein 1 (TAB1) binds and induces autophosphorylation of TGF‐β activating kinase (TAK1). TAK1, a mitogen‐activated kinase kinase kinase, is involved in several distinct signaling pathways including non‐Smad pathways for TGF‐β superfamily members and inflammatory responses caused by cytokines. Conventional disruption of the murine Tab1 gene results in late gestational lethality showing intraventricular septum defects and underdeveloped lung alveoli. To gain a better understanding of the roles of TAB1 in different tissues, at different stages of development, and in pathological conditions, we generated Tab1 floxed mice in which the loxP sites flank Exons 9 and 10 to remove the C‐terminal region of TAB1 protein necessary for activation of TAK1. We demonstrate that Cre‐mediated recombination using Sox2‐Cre, a Cre line expressed in the epiblast during early embryogenesis, results in deletion of the gene and protein. These homozygous Cre‐recombined null embryos display an identical phenotype to conventional null embryos. This animal model will be useful in revealing distinct roles of TAB1 in different tissues at different stages. genesis 46:431–439, 2008. Published 2008 Wiley‐Liss, Inc.