Induction of maturation-promoting factor during Xenopus oocyte maturation uncouples Ca2+ store depletion from store-operated Ca2+ entry
نویسندگان
چکیده
During oocyte maturation, eggs acquire the ability to generate specialized Ca(2+) signals in response to sperm entry. Such Ca(2+) signals are crucial for egg activation and the initiation of embryonic development. We examined the regulation during Xenopus oocyte maturation of store-operated Ca(2+) entry (SOCE), an important Ca(2+) influx pathway in oocytes and other nonexcitable cells. We have previously shown that SOCE inactivates during Xenopus oocyte meiosis. SOCE inactivation may be important in preventing premature egg activation. In this study, we investigated the correlation between SOCE inactivation and the Mos-mitogen-activated protein kinase (MAPK)-maturation-promoting factor (MPF) kinase cascade, which drives Xenopus oocyte maturation. SOCE inactivation at germinal vesicle breakdown coincides with an increase in the levels of MAPK and MPF. By differentially inducing Mos, MAPK, and MPF, we demonstrate that the activation of MPF is necessary for SOCE inactivation during oocyte maturation. In contrast, sustained high levels of Mos kinase and the MAPK cascade have no effect on SOCE activation. We further show that preactivated SOCE is not inactivated by MPF, suggesting that MPF does not block Ca(2+) influx through SOCE channels, but rather inhibits coupling between store depletion and SOCE activation.
منابع مشابه
Downregulation of store-operated Ca2+ entry during mammalian meiosis is required for the egg-to-embryo transition.
A specialized Ca(2+) transient at fertilization represents the universal driver for the egg-to-embryo transition. Ca(2+) signaling remodels during oocyte maturation to endow the egg with the capacity to produce the specialized Ca(2+) transient at fertilization, which takes the form of a single (e.g. Xenopus) or multiple (e.g. mouse) Ca(2+) spikes depending on the species. Store-operated Ca(2+) ...
متن کاملStore-operated calcium entry inactivates at the germinal vesicle breakdown stage of Xenopus meiosis.
Store-operated calcium entry (SOCE) is the predominant Ca(2+) influx pathway in non-excitable cells and is activated in response to depletion of intracellular Ca(2+) stores. We have studied SOCE regulation during Xenopus oocyte meiosis. SOCE can be measured readily in stage VI Xenopus oocytes arrested at the G(2)-M transition of the cell cycle, either by Ca(2+) imaging or by recording the SOCE ...
متن کاملConstitutive recycling of the store-operated Ca2+ channel Orai1 and its internalization during meiosis
The egg's competency to activate at fertilization and transition to embryogenesis is dependent on its ability to generate a fertilization-specific Ca(2+) transient. To endow the egg with this capacity, Ca(2+) signals remodel during oocyte maturation, including inactivation of the primary Ca(2+) influx pathway store-operated Ca(2+) entry (SOCE). SOCE inactivation is coupled to internalization of...
متن کاملCalcium influx and sperm-evoked calcium responses during oocyte maturation and egg activation
Under the guidance and regulation of hormone signaling, large majority of mammalian oocytes go through twice cell cycle arrest-resumption prior to the fertilized egg splits: oocyte maturation and egg activation. Cytosolic free calcium elevations and endoplasmic reticulum calcium store alternations are actively involved in triggering the complex machineries and events during oogenesis. Among the...
متن کاملCa2+ influx and the store-operated Ca2+ entry pathway undergo regulation during mouse oocyte maturation
In preparation for fertilization, mammalian oocytes undergo optimization of the mechanisms that regulate calcium homeostasis. Among these changes is the increase in the content of the Ca(2+) stores ([Ca(2+)]ER), a process that requires Ca(2+) influx. Nevertheless, the mechanism(s) that mediates this influx remains obscure, although is known that [Ca(2+)]ER can regulate Ca(2+) influx via store-o...
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ورودعنوان ژورنال:
- The Journal of Cell Biology
دوره 156 شماره
صفحات -
تاریخ انتشار 2002