Mp. Rosenberg et al., EXPRESSION OF THE V-MOS ONCOGENE IN MALE MEIOTIC GERM-CELLS OF TRANSGENIC MICE RESULTS IN METAPHASE ARREST, Cell growth & differentiation, 6(3), 1995, pp. 325-336
To explore the role of pp39(mos) in male germ cell meiosis, we have co
nstructed transgenic mice carrying either the c-Mos or v-Mof genes lin
ked to the human male germ cell-specific phosphoglycerate kinase-2 pro
moter. All male transgenic mice bearing the v-Mos but not the c-Mos co
nstruct were sterile due to arrest of germ cells at metaphase I. Immun
ocytochemistry performed on sections from control and c-Mos transgenic
testes with eight different monoclonal and polyclonal antisera agains
t either alpha-, beta- or gamma-tubulins demonstrated that all could r
ecognize ML spermatocyte spindles from control and c-Mos transgenics,
but only one monoclonal anti-microtubule sera decorated the spindles o
f v-Mos-arrested meiotic figures. Western blot analyses with this one
serum revealed a change in proteins in the v-Mos samples. Immunocytoch
emistry with the MPM-2 monoclonal antibody, which is specific for epit
opes phosphorylated during mitosis, demonstrated an increase in cytopl
asmic and spindle-associated phosphoproteins in arrested v-Mos spermat
ocytes. Western analysis with MPM-2 showed an increase in a M(r) 50,00
0-55,000 and a M(r) 25,000-29,000 protein in Mos transgenic testes whe
n compared to controls. An anti-MAP kinase antibody demonstrated an in
crease in all four MAP kinases in testes of transgenic mice. Thus, ove
rexpression of pp39(v-mos) during male germ cell meiosis resulted in a
n alteration of various cell cycle related kinases and cytostatic fact
or-like arrest at MI.