title: Mice doubly-deficient in the Arf GAPs SMAP1 and SMAP2 exhibit embryonic lethality.
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.
authors: Department of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Japan.
authors: Mami
authors: M
authors: Sumiyoshi
authors: Department of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Japan.
authors: Narumi
authors: N
authors: Masuda
authors: Division of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Miyagi, Japan.
authors: Nobuhiro
authors: N
authors: Tanuma
authors: Department of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Japan.
authors: Honami
authors: H
authors: Ogoh
authors: Department of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Japan.
authors: Eri
authors: E
authors: Imai
authors: Department of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Japan.
authors: Mizuki
authors: M
authors: Otsuka
authors: Department of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Japan.
authors: Natsuki
authors: N
authors: Hayakawa
authors: Department of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Japan.
authors: Kinuyo
authors: K
authors: Ohno
authors: Cell Resource Center for Biomedical Research, Institute of Development, Aging and Cancer, Tohoku University, Miyagi, Japan.
authors: Yasuhisa
authors: Y
authors: Matsui
authors: Department of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Japan.
authors: Kanae
authors: K
authors: Hara
authors: Department of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Japan.
authors: Risa
authors: R
authors: Gotoh
authors: Department of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Japan.
authors: Mai
authors: M
authors: Suzuki
authors: Department of Hematology and Rheumatology, Kinki University Faculty of Medicine, Osaka, Japan.
authors: Shinya
authors: S
authors: Rai
authors: Department of Hematology and Rheumatology, Kinki University Faculty of Medicine, Osaka, Japan.
authors: Hirokazu
authors: H
authors: Tanaka
authors: Department of Hematology and Rheumatology, Kinki University Faculty of Medicine, Osaka, Japan.
authors: Itaru
authors: I
authors: Matsumura
authors: Division of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Miyagi, Japan.
authors: Hiroshi
authors: H
authors: Shima
authors: Department of Biological Science, Graduate School of Humanities and Sciences, Nara Women's University, Nara, Japan. Electronic address: toshiwatana@cc.nara-wu.ac.jp.
authors: Toshio
authors: T
authors: Watanabe
mesh_terms: D000818:Animals; D017209:Apoptosis; D002460:Cell Line; D004622:Embryo, Mammalian / Q000166:cytology / Q000196:embryology*; D047108:Embryonic Development; D004705:Endocytosis; D006801:Humans; D008565:Membrane Proteins / Q000172:deficiency* / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D021381:Protein Transport; D017384:Sequence Deletion; D014168:Transferrin / Q000378:metabolism
chemical_list: D008565:Membrane Proteins; C529588:SMAP2 protein, mouse; C484577:Smap1 protein, mouse; D014168:Transferrin
keywords: Arf GAP; Embryogenesis; Genetic interaction; SMAP1; SMAP2