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

FEBS Lett. 2015 Sep 14;589(19 Pt B):2754-62. doi: 10.1016/j.febslet.2015.07.050. Epub 2015 Aug 18.

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.

Keywords: Arf GAP; Embryogenesis; Genetic interaction; SMAP1; SMAP2.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Cell Line
  • Embryo, Mammalian / cytology
  • Embryo, Mammalian / embryology*
  • Embryonic Development
  • Endocytosis
  • Humans
  • Membrane Proteins / deficiency*
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Mice
  • Protein Transport
  • Sequence Deletion
  • Transferrin / metabolism

Substances

  • Membrane Proteins
  • SMAP2 protein, mouse
  • Smap1 protein, mouse
  • Transferrin