EFFECTS OF THE V-MOS ONCOGENE ON XENOPUS DEVELOPMENT - MEIOTIC INDUCTION IN OOCYTES AND MITOTIC ARREST IN CLEAVING EMBRYOS

Previous work has demonstrated that the Xenopus protooncogene mos(xe) can induce the maturation of prophase-arrested Xenopus oocytes. Recently, we showed that mos(xe) can transform murine NIH3T3 fibroblasts, although it exhibited only 1-2% of the transforming activity of the v-mos oncogene. In this study we have investigated the ability of the v-mos protein to substitute for the mos(xe) protein in stimulating Xenopus oocytes to complete meiosis. Microinjection of in vitro synthesized RNAs encoding either the mos(xe) or v-mos proteins stimulates resting oocytes to undergo germinal vesicle breakdown. Microinjection of an antisense oligonucleotide spanning the initiation codon of the mos(xe) gene blocked progesterone-induced oocyte maturation. When oocytes were microinjected first with the mos(xe) antisense oligonucleotide, and subsequently with in vitro synthesized v-mos RNA, meiotic maturation was rescued as evidenced by germinal vesicle breakdown. The v-mos protein exhibited in vitro kinase activity when recovered by immunoprecipitation from either microinjected Xenopus oocytes or transfected monkey COS-1 cells; however, in parallel experiments, we were unable to detect in vitro kinase activity associated with the mos(xe) protein. Microinjection of in vitro synthesized v-mos RNA into cleaving Xenopus embryos resulted in mitotic arrest, demonstrating that the v-mos protein can function like the mos(xe) protein as a component of cytostatic factor. These results exemplify the apparently conflicting effects of the v-mos protein, namely, its ability to induce maturation of oocytes, its ability to arrest mitotic cleavage of Xenopus embryo, and its ability to transform mammalian fibroblasts.