Development 2011 Sep 01;13817:3735-44. doi: 10.1242/dev.063974.

A critical balance between Cyclin B synthesis and Myt1 activity controls meiosis entry in Xenopus oocytes.

???displayArticle.abstract???
In fully grown oocytes, meiosis is arrested at first prophase until species-specific initiation signals trigger maturation. Meiotic resumption universally involves early activation of M phase-promoting factor (Cdc2 kinase-Cyclin B complex, MPF) by dephosphorylation of the inhibitory Thr14/Tyr15 sites of Cdc2. However, underlying mechanisms vary. In Xenopus oocytes, deciphering the intervening chain of events has been hampered by a sensitive amplification loop involving Cdc2-Cyclin B, the inhibitory kinase Myt1 and the activating phosphatase Cdc25. In this study we provide evidence that the critical event in meiotic resumption is a change in the balance between inhibitory Myt1 activity and Cyclin B neosynthesis. First, we show that in fully grown oocytes Myt1 is essential for maintaining prophase I arrest. Second, we demonstrate that, upon upregulation of Cyclin B synthesis in response to progesterone, rapid inactivating phosphorylation of Myt1 occurs, mediated by Cdc2 and without any significant contribution of Mos/MAPK or Plx1. We propose a model in which the appearance of active MPF complexes following increased Cyclin B synthesis causes Myt1 inhibition, upstream of the MPF/Cdc25 amplification loop.

???displayArticle.pubmedLink??? 21795279
???displayArticle.link??? Development


Species referenced: Xenopus
Genes referenced: ccnb1.2 cdc25c cdk1 mos myt1 plk1
???displayArticle.antibodies??? Mos Ab2
???displayArticle.morpholinos??? mos MO1