Activation of the anaphase-promoting complex and degradation of cyclin B is not required for progression from Meiosis I to II in Xenopus oocytes

Sister chromatid separation and cyclin degradation in mitosis depend on the association of the anaphase-promoting complex (APC) with the Fizzy protein (Cdc20), leading to the metaphase/anaphase transition and exit from mitosi s [1-3]. In Xenopus, after metaphase of the first meiotic division, only pa rtial cyclin degradation occurs, and chromosome segregation during anaphase I proceeds without sister chromatid separation [4-7], We investigated the role of xFizzy during meiosis using an antisense depletion approach. xFizzy accumulates to high levels in Meiosis I, and injection of antisense oligon ucleotides to xFizzy blocks neatly all APC-mediated cyclin B degradation an d Cdc2/cyclin B (MPF) inactivation between Meiosis I and II. However, even without APC activation, xFizzy-ablated oocytes progress to Meiosis II as sh own by cyclin E synthesis, further accumulation of cyclin B, and evolution of the metaphase I spindle to a metaphase II spindle via a disc-shaped aggr egate of microtubules known to follow anaphase I [8], Inhibition of the MAP K pathway by U0126 in antisense-injected oocytes prevents cyclin B accumula tion beyond the level that is present at metaphase I, Full synthesis and ac cumulation can be restored in the presence of U0126 by the expression of a constitutively active form of the MAPK target, p90(Rsk). Thus, p90(Rsk) is sufficient not only to partially inhibit APC activity [7], but also to stim ulate cyclin B synthesis in Meiosis II.