Colledge WH, Carlton MB, Udy GB, Evans MJ:
Disruption of c-mos causes parthenogenetic development of
unfertilized mouse eggs.
Nature 1994 Jul 7;370(6484):65-8
ABSTRACT
The c-mos proto-oncogene encodes a 37-39K cytoplasmic
serine/threonine kinase implicated in the meiotic maturation events
during murine spermatogenesis and oogenesis. In Xenopus, ectopic
expression of pp39mos can promote both the meiotic maturation of
oocytes and also arrest the cleavage of blastomeres. To elucidate
the role of pp39mos we have generated homozygous mutant mice by gene
targeting in embryonic stem cells. These mice are viable and mutant
males are fertile, demonstrating that pp39mos is not essential for
spermatogenesis. In contrast, mutant females, have a reduced
fertility because of the failure of mature eggs to arrest during
meiosis. c-mos-/- oocytes undergo germinal vesicle breakdown and
extrusion of both polar bodies followed in some cases by progression
into cleavage. Mutant females also develop ovarian cysts. These
results demonstrate that a major role for pp39mos is to prevent the
spontaneous parthenogenetic activation of unfertilized eggs.
