Mice doubly-deficient in the Arf GAPs SMAP1 and SMAP2 exhibit embryonic lethality

Mami Sumiyoshi, Narumi Masuda, Nobuhiro Tanuma, Honami Ogoh, Eri Imai, Mizuki Otsuka, Natsuki Hayakawa, Kinuyo Ohno, Yasuhisa Matsui, Kanae Hara, Risa Gotoh, Mai Suzuki, Shinya Rai, Hirokazu Tanaka, Itaru Matsumura, Hiroshi Shima, Toshio Watanabe

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)2754-2762
Number of pages9
JournalFEBS Letters
Volume589
Issue number19
DOIs
Publication statusPublished - 2015 Sep 14

Keywords

  • Arf GAP
  • Embryogenesis
  • Genetic interaction
  • SMAP1
  • SMAP2

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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