A hypothesis on p34cdc2 sequestration based on the existence of Ca2+‐coordinated changes in H+ and MPF activities during pus egg activation

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Abstract
Summary— The entry into, and exit from, mitosis are controlled by a universal M‐phase promoting factor (MPF) composed of at least p34cdc2 and a cyclin. Embryonic systems are convenient for studying the association and dissociation of the active MPF complex because oocytes and eggs are naturally arrested at a specific point of the cell cycle until progression to the next point is triggered by a hormonal signal or sperm. In amphibians, eggs prior to fertilization are arrested at metaphase 2 of meiosis due to the presence of a stabilized MPF complex. Fertilization (egg activation) produces a transient increase in intracellular free Ca2+, a propagating Ca2+ wave, that specifically triggers the destruction of cyclin, leading to MPF inactivation and entry into the first embryonic interphase. We have recently shown that intracellular pH (pHi) variations in amphibian eggs, a large increase at fertilization and small oscillations during the embryonic cell cycle, were temporally and functionally related to the corresponding changes in MPF activity. In addition, the recent finding that the pHi increase at fertilization in Xenopus eggs is a propagating, Ca2+‐dependent pH wave which closely follows the Ca2+ wave, together with the absence in the egg plasma membrane of pHi‐regulating systems responsible for that pHi increase, suggest the existence of cortical or subcortical vesicles acidifying in the wake of the Ca2+ wave, thus producing the pH wave. Given the known functions of intracellular acidic compartments in various systems and the existence of acidic vesicles in marine invertebrate eggs, we propose that these hypothetic acidic vesicles in Xenopus eggs might serve as a storage for the p34cdc2 released in the cytoplasm following egg activation, both the pHi increase and MPF inactivation being triggered and synchronized by the same signal, the Ca2+ wave.

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