Independent inactivation of MPF and cytostatic factor (Mos) upon fertilization of Xenopus eggs

Abstract

IN vertebrates, mature eggs are arrested at the second meiotic metaphase by the cytostatic factor (CSF)¹, now known to be thec-mos proto-oncogene product (Mos)^{2, 3}. Fertilization or egg activaá-tion triggers a transient increase in the cytoplasmic free calcium^{4, 5} and releases the meiotic arrest by inactivating maturation/mitosis-promoting factor (MPF)^{6, 7}. CSF or Mos, which is also inactivated by the calcium transient^{8, 9}, seems to stabilize MPF in mature eggs and CSF-injected embryos^{2, 6, 10}. Thus, it was assumed that CSF inactivation is the primary cause of MPF inactivation on meiotic release^{2, 6, 8, 10–14}. We have directly compared the degradation kinetics of CSF (Mos) and MPF during meiotic release, using the same batch of Xenopus eggs. We report here that, at the molecular level, cyclin subunits of MPF are degraded before Mos is degraded and, at the physiological level, that MPF activity is inactivated before CSF activity during activation of Xenopus eggs. These results, in conjunction with circumstantial evidence, support the novel view that a calcium transient on fertilization induces a CSF-independent pathway for MPF inactivation, whereas CSF inactivation during meiotic release serves only to allow the fertilá-ized egg to enter mitosis.