• Media type: E-Article
  • Title: Mice doubly‐deficient in the Arf GAPs SMAP1 and SMAP2 exhibit embryonic lethality
  • Contributor: 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
  • imprint: Wiley, 2015
  • Published in: FEBS Letters
  • Language: English
  • DOI: 10.1016/j.febslet.2015.07.050
  • ISSN: 0014-5793; 1873-3468
  • Keywords: Cell Biology ; Genetics ; Molecular Biology ; Biochemistry ; Structural Biology ; Biophysics
  • Origination:
  • Footnote:
  • Description: <jats:p>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<jats:italic>SMAP1</jats:italic> and<jats:italic>SMAP2</jats:italic> promotes apoptosis in the distal region of E7.5 mouse embryos, likely resulting in embryonic lethality. Thus, at least one<jats:italic>SMAP</jats:italic> gene, either<jats:italic>SMAP1</jats:italic> or<jats:italic>SMAP2</jats:italic>, is required for proper embryogenesis.</jats:p>
  • Access State: Open Access