Abstract
Ovulated eggs possess maternal apoptotic execution machinery that is inhibited for a limited time. The fertilized eggs switch off this time bomb whereas aged unfertilized eggs and parthenogenetically activated eggs fail to stop the timer and die. To investigate the nature of the molecular clock that triggers the egg decision of committing suicide, we introduce here Xenopus eggs as an in vivo system for studying the death of unfertilized eggs. We report that after ovulation, a number of eggs remains in the female body where they die by apoptosis. Similarly, ovulated unfertilized eggs recovered in the external medium die within 72 h. We showed that the death process depends on both cytochrome c release and caspase activation. The apoptotic machinery is turned on during meiotic maturation, before fertilization. The death pathway is independent of ERK but relies on activating Bad phosphorylation through the control of both kinases Cdk1 and JNK. In conclusion, the default fate of an unfertilized Xenopus egg is to die by a mitochondrial dependent apoptosis activated during meiotic maturation.
Highlights
Apoptosis is critically important in various developmental processes where it re-equilibrates the overproduction of cells occuring in several tissues [1]
We demonstrate that Xenopus eggs synchronously die within 72 h by mitochondrial and caspase-dependent apoptosis
Contribution of mitochondria and various caspases to the unfertilized egg apoptotic process We addressed the question of the implication of a mitochondrial phase in the processing of egg apoptosis
Summary
Apoptosis is critically important in various developmental processes where it re-equilibrates the overproduction of cells occuring in several tissues [1]. Meiotic maturation depends on the activation of the master regulator of M-phase, MPF (M-phase promoting factor, or Cdk kinase) that promotes the transition from the prophase I arrest to the metaphase arrest of the second meiotic division [2] From this point on, ovulated cells are called eggs and remain arrested in metaphase II because of high levels of CSF (cytostatic factor) activity that stabilizes MPF until fertilization [3]. A MEK kinase, is an integral component of CSF activity and is responsible for activating the MAP kinase pathway in maturing oocytes and eggs It has been shown in several species that ovulated eggs possess a maternal machinery of apoptotic execution that is inhibited for limited time. There is great interest in understanding unfertilized egg apoptosis in relation to failed conception and birth defects that dramatically increase with post-ovulatory age
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