@entity44854 ( XXXX ) suppresses premature calcium release in mouse eggs.

@entity141 @entity3451 @entity44854 @entity934
During oocyte maturation, capacity and sensitivity of @entity141 signaling machinery increases dramatically, preparing the metaphase II (MII)-arrested egg for fertilization. Upon sperm-egg fusion, @entity141 release from IP3-sensitive endoplasmic reticulum stores results in cytoplasmic @entity141 oscillations that drive egg activation and initiate early embryo development. Premature @entity141 release can cause parthenogenetic activation prior to fertilization; thus, preventing inappropriate @entity141 signaling is crucial for ensuring robust MII arrest. Here, we show that @entity44854 ( @entity44854 ) suppresses @entity141 release in MII eggs. @entity44854 mRNA was recruited for translation during oocyte maturation, resulting in    20-fold more @entity44854 protein in MII eggs than in fully grown immature oocytes. @entity44854 -siRNA-injected oocytes matured to MII; however, they had increased sensitivity to low pH and @entity934 ( @entity3451 ), which caused inappropriate @entity141 release and premature egg activation. When matured in vitro, @entity44854 -depleted eggs underwent spontaneous @entity141 increases that were sufficient to cause premature zona pellucida conversion. @entity44854 (-/-) females had reduced litter sizes, and their eggs had increased sensitivity to low pH and @entity3451 . @entity44854 (-/-) eggs also underwent premature zona pellucida conversion in vivo. These findings indicate that @entity44854 functions as a brake to suppress premature @entity141 release in eggs that are poised on the brink of development.
