Abstract. During early development, intracellularCa 2+ mobilization is not only essential for fertilization, but has also been implicated during other meiotic and mitotic events, such as germinal vesicle breakdown (GVBD) and nuclear envelope breakdown (NEBD). In this study, the roles of intracellular and extracellular Ca 2+ were examined during meiotic maturation and reinitiation at parthenogenetic activation and during first mitosis in a single species using the same methodologies. Cumulus-free metaphase II mouse oocytes immediately resumed anaphase upon the induction of a large, transient Ca 2+ elevation. This resumption of meiosis and associated events, such as cortical granule discharge, were not sensitive to extracellular Ca 2+ removal, but were blocked by intracellular Ca 2+ chelators. In contrast, meiosis I was dependent on external Ca2+; in its absence, the formation and function of the first meiotic spindle was delayed, the first polar body did not form and an interphase-like state was induced. GVBD was not dependent on external Ca 2+ and showed no associated Ca ~+ changes. NEBD at first mitosis in fertilized eggs, on the other hand, was frequently, but not always associated with a brief Ca 2+ transient and was dependent on Ca 2 § mobilization. We conclude that GVBD is Ca 2+ independent, but that the dependence of NEBD on Ca 2+ suggests regulation by more than one pathway. As cells develop from Ca2+-independent germinal vesicle oocytes to internal Ca 2 § pronuclear eggs, internal Ca 2 § pools increase by approximately fourfold.

The p21 MDA6 gene product induces cell cycle arrest in p53-null pendent induction of p21 MDA6 has been observed in response human leukemic cells exposed to differentiation stimuli. We to both differentiating and DNA damaging agents. 3,4,[16][17][18][19] employed an HL-60 cell line stably transfected with a p21 MDA6 However, not all p53-negative cell lines express p21 MDA6 in these p53-positive cell lines in a p21 MDA6 -independent mancomplex formation. They also provide functional evidence that ner. 16 Thus, it is apparent that p21 MDA6 expression is not p21 MDA6 induction does not appear to be required for Ara-Cnecessary for apoptosis to proceed in all cell types, but its induced apoptosis, G 1 arrest, or the resulting reduction in the induction may be required in certain circumstances self-renewal capacity of HL-60 cells.