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Mice doubly‐deficient in the Arf GAPs SMAP1 and SMAP2 exhibit embryonic lethality
Author(s) -
Sumiyoshi Mami,
Masuda Narumi,
Tanuma Nobuhiro,
Ogoh Honami,
Imai Eri,
Otsuka Mizuki,
Hayakawa Natsuki,
Ohno Kinuyo,
Matsui Yasuhisa,
Hara Kanae,
Gotoh Risa,
Suzuki Mai,
Rai Shinya,
Tanaka Hirokazu,
Matsumura Itaru,
Shima Hiroshi,
Watanabe Toshio
Publication year - 2015
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2015.07.050
Subject(s) - lethality , microbiology and biotechnology , embryonic stem cell , biology , phenotype , gtpase , embryo , subfamily , embryogenesis , knockout mouse , small gtpase , gene , genetics , signal transduction
In mammals, the small Arf GTPase‐activating protein (SMAP) subfamily of Arf GTPase‐activating proteins consists of closely related members, SMAP1 and SMAP2. These factors reportedly exert distinct functions in membrane trafficking, as manifested by different phenotypes seen in single knockout mice. The present study investigated whether SMAP proteins interact genetically. We report for the first time that simultaneous loss of SMAP1 and SMAP2 promotes apoptosis in the distal region of E7.5 mouse embryos, likely resulting in embryonic lethality. Thus, at least one SMAP gene, either SMAP1 or SMAP2 , is required for proper embryogenesis.