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Mice lacking Ran binding protein 1 are viable and show male infertility
Author(s) -
Nagai Masahiro,
Moriyama Tetsuji,
Mehmood Rashid,
Tokuhiro Keizo,
Ikawa Masahito,
Okabe Masaru,
Tanaka Hiromitsu,
Yoneda Yoshihiro
Publication year - 2011
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.2011.02.002
Subject(s) - spermatogenesis , ran , microbiology and biotechnology , germ cell , biology , knockout mouse , gtpase , genetics , endocrinology , gene
The small GTPase Ran plays important roles in multiple aspects of cellular function. Maximal RanGAP activity is achieved with the aid of RanBP1 and/or presumably of RanBP2. Here, we show that RanBP1‐knockout mice are unexpectedly viable, and exhibit male infertility due to a spermatogenesis arrest, presumably caused by down‐regulation of RanBP2 during spermatogenesis. Indeed, siRNA‐mediated depletion of RanBP2 caused severe cell death only in RanBP1‐deficient MEFs, indicating that simultaneous depletion of RanBP1 and RanBP2 severely affects normal cell viability. Collectively, we conclude that the dramatic decrease in “RanBP” activity impairs germ cell viability and affects spermatogenesis decisively in RanBP1‐knockout mice.