In mammals, the restoration of rRNA transcription after fertilisation is accompanied by a gradual differentiation of the nucleolar structure by a process called embryonic nucleogenesis. During cleavage, the nucleolar components appear sterically related to a class of nuclear bodies already detectable in pronuclei. These structures, due to their apparent function as centres of nucleolus formation, have been designated nucleolus precursor bodies (NPBs). It was found recently not only that the size and morphology of the NPBs differ among mammalian species, but that the pattern of embryonic nucleologenesis and even the molecular composition of different NPB compartments vary from one species to another. Accordingly we assumed that at least two definitely different types of NPBs exist, namely the mouse-type NPB and cow-type NPB. In the mouse-type NPB, the original compact material of the NPB remains detectable in the early functional nucleolus. This NPB core does not contain DNA or typical Ag-NOR nucleolar proteins. At the onset of rRNA transcription, the nucleolonema is formed at the periphery of the NPB. The cow-type NPB shows a homogeneous distribution of typical nucleolar proteins throughout its body from the pronucleolar to the early 8-cell stage. At the beginning of rRNA transcription, the cow-type NPB is penetrated by perinucleolar DNA and rRNA synthesis is detectable deep inside the nucleolus. In this case, the entire NPB is readily transformed into a typical nucleolus. These processes are recognisable using fine-structure analysis of preimplantation mammalian embryos. For this reason this approach is often used as a method of evaluating the state of experimental embryos; in such studies, the species differences must be taken into account.

The role of mitogen-activated protein (MAP) kinase in mouse egg activation induced by protein kinase inhibitors and a protein tyrosine kinase (PTK) inhibitor was investigated. Separated egg proteins were first probed with anti-Active MAP kinase antibody and then re-probed with anti-ERK2 antibody. Staurosporine and Ro-31-8220, at concentrations that normally inhibit protein kinase C, did not affect egg activation or MAP kinase activity, while higher dosages caused egg activation. Staurosporine at 2 μM induced the metaphase–interphase transition without emission of the second polar body (PB2), while Ro-31-8220 at 40 μM induced PB2 emission, first cleavage, and then the transition to interphase. Half the eggs were also activated by the PTK inhibitor genistein. In each treatment, the proportion of eggs that entered interphase was well correlated with the degree of MAP kinase inactivation. Artificial activation of this kinase by okadaic acid overcame the interphase transition. These data suggest that protein kinase inhibitors and a protein tyrosine kinase inhibitor induce the interphase transition by inactivating MAP kinase in mouse eggs.