Progesterone initiates the resumption of the meiotic divisions in the amphibian oocyte. Depolarization of the Rama pipiens oocyte plasma membrane begins 6-10 hr after exposure to progesterone (1-2 hr before nuclear breakdown). The oocyte cytoplasm becomes essentially isopotential with the medium by the end of the first meiotic division (20-22 hr). Voltage-clamp studies indicate that the depolarization coincides with the disappearance of an electrogenic Na+, K+-pump, and other electrophysiological studies indicate a decrease in both K+ and Cl- conductances of the oocyte plasma membrane. Measurement of [3H]-ouabain binding to the plasma-vitelline membrane complex indicates that there are high-affinity (Kd = 4.2 x 10-8M), K+-sensitive ouabain-binding sites on the unstimulated (prophase-arrest) oocyte and that ouabain binding virtually disappears during membrane depolarization. [3H]-Leucine incorporation into the plasma-vitelline membrane complex increased ninefold during depolarization with no significant change in uptake or incorporation into cytoplasmic proteins or acid soluble pool(s). This together with previous findings suggest that progesterone acts at a translational level to produce a cytoplasmic factor(s) that down-regulates the membrane Na+, K+-ATPase and alters the ion permeability and transport properties of both nuclear and plasma membranes.

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We studied the effects of actinomycin D, ct-amanitin, puromycin, and cycloheximide on the cytoplasmic activity of maturing Rana pipiens oocytes that induces chromosome condensation in transplanted brain nuclei. Treatment of oocytes with each inhibitor suppressed the chromosome condensation induced by metaphase I oocytes to varying degrees depending upon the dose of inhibitor, despite the fact that untreated metaphase I oocytes already possessed chromosome condensation activity (CCA). Treatment of brain nuclei before injection completely suppressed condensation at all doses used. Chromosome condensation induced by metaphase II oocyte cytoplasm, however, was insensitive to all tile inhibitors, even when the brain nuclei were pretreated. Oocytes treated with ot-amanitin throughout maturation induced chromosome condensation when tested at metaphase II. Removal of the oocyte chromosomes after the germinal vesicle (GV) broke down did not prevent the development of CCA, whereas removal of the entire GV before initiation of maturation deprived oocytes of CCA. The results suggest that metaphase I oocyte cytoplasm stimulates synthesis of brain nuclear RNAs that are translated into proteins necessary for chromosome condensation, whereas rectaphase II oocytes possess all the factors for chromosome condensation. In both cases, GV nucleoplasm appears indispensable for the development of CCA, whereas immediate activity of the oocyte genome is not required.Chromosome condensation is induced in interphase nuclei exposed to the cytoplasm of cells undergoing mitosis or meiosis. Such premature chromosome condensation was induced in interphase cells fused to colchicine-arrested mitotic cells in culture (13). In amphibian oocytes, BatailIon (2) and Bataillon and Tchou-Su (3) observed metaphase-like condensation of sperm chromosomes when Hyla or Triton metaphase I oocytes were inseminated. Gurdon (II,12) found that chromosomes of isolated interphase nuclei of somatic cells condensed to metaphase when injected into Xenopus laevis oocytes shortly after germinal vesicle breakdown (GVBD). The results of these

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