Open AccessTargeted disruption of the mouse Stat3 gene leads to early embryonic lethality
Author(s) -
Kiyoshi Takeda,
Koichi Noguchi,
Wei Shi,
Takashi Tanaka,
Makoto Matsumoto,
Nobuaki Yoshida,
Tadamitsu Kishimoto,
Shizuo Akira
Publication year - 1997
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.94.8.3801
Subject(s) - stat3 , stat protein , biology , embryogenesis , embryonic stem cell , heterozygote advantage , microbiology and biotechnology , transcription factor , embryo , gene , signal transduction , genetics , allele
Signal transducer and activator of transcription (STAT) proteins have been shown to mediate biological actions in response to cytokines. Stat3, a member of the STAT family, is activated by a variety of cytokines, including the interleukin 6 family of cytokines, leptin, granulocyte colony-stimulating factor, and epidermal growth factor. To address the biological function of Stat3, we generated mice deficient in Stat3 by gene targeting. No viable Stat3-deficient mice could be obtained from heterozygote intercross. Analysis of embryos at several gestation times revealed that Stat3-deficient embryos showed a rapid degeneration between embryonic days 6.5 and 7.5, although they developed into the egg cylinder stage until embryonic day 6.0. These results demonstrate that Stat3 is essential for the early development of mouse embryos.