title: Expression of the v-Mos oncogene in male meiotic germ cells of transgenic mice results in metaphase arrest.
abstract: To explore the role of pp39mos in male germ cell meiosis, we have constructed transgenic mice carrying either the c-Mos or v-Mos genes linked to the human male germ cell-specific phosphoglycerate kinase-2 promoter. All male transgenic mice bearing the v-Mos but not the c-Mos construct were sterile due to arrest of germ cells at metaphase I. Immunocytochemistry performed on sections from control and c-Mos transgenic testes with eight different monoclonal and polyclonal antisera against either alpha-, beta- or gamma-tubulins demonstrated that all could recognize MI spermatocyte spindles from control and c-Mos transgenics, but only one monoclonal anti-microtubule sera decorated the spindles of v-Mos-arrested meiotic figures. Western blot analyses with this one serum revealed a change in proteins in the v-Mos samples. Immunocytochemistry with the MPM-2 monoclonal antibody, which is specific for epitopes phosphorylated during mitosis, demonstrated an increase in cytoplasmic and spindle-associated phosphoproteins in arrested v-Mos spermatocytes. Western analysis with MPM-2 showed an increase in a M(r) 50,000-55,000 and a M(r) 25,000-29,000 protein in Mos transgenic testes when compared to controls. An anti-MAP kinase antibody demonstrated an increase in all four MAP kinases in testes of transgenic mice. Thus, overexpression of pp39v-mos during male germ cell meiosis resulted in an alteration of various cell cycle related kinases and cytostatic factor-like arrest at MI.
authors.affiliation: Glaxo Research Institute, Department of Pharmacology, Research Triangle Park, North Carolina 27709, USA.
authors.forename: M P
authors.initials: MP
authors.lastname: Rosenberg
authors.forename: C R
authors.initials: CR
authors.lastname: Aversa
authors.forename: R
authors.initials: R
authors.lastname: Wallace
authors.forename: F
authors.initials: F
authors.lastname: Propst
mesh_terms: D000818:Animals; D001483:Base Sequence; D006801:Humans; D007248:Infertility, Male / Q000209:etiology; D008297:Male; D008540:Meiosis; D008677:Metaphase; D051379:Mice; D008822:Mice, Transgenic; D008870:Microtubules / Q000378:metabolism; D008969:Molecular Sequence Data; D017232:Oncogene Proteins v-mos / Q000096:biosynthesis* / Q000235:genetics / Q000633:toxicity; D010735:Phosphoglycerate Kinase / Q000096:biosynthesis / Q000235:genetics; D010750:Phosphoproteins / Q000096:biosynthesis; D017346:Protein Serine-Threonine Kinases / Q000096:biosynthesis; D017231:Proto-Oncogene Proteins c-mos / Q000096:biosynthesis* / Q000235:genetics; D013094:Spermatozoa / Q000166:cytology / Q000502:physiology*; D013737:Testis / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure
chemical_list: D017232:Oncogene Proteins v-mos; D010750:Phosphoproteins; D017346:Protein Serine-Threonine Kinases; D017231:Proto-Oncogene Proteins c-mos; D010735:Phosphoglycerate Kinase