作者: Tamar Enoch , Paul Nurse
DOI: 10.1016/0092-8674(90)90669-6
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摘要: Entry into mitosis in fission yeast is controlled by the p34cdc2 protein kinase, which activated cdc25+ and inhibited wee1+. In "wee" mutants one or other of these controls circumvented resulting advancement mitosis. We report that dependence on DNA synthesis lost wee control either mutations cdc2+ overproduction cdc25+. contrast, maintained when wee1+ bypassed. propose activity requires completion earlier cell-cycle events such as synthesis, thus links kinase activation to events. Constitutive expression homologs could explain why not dependent replication some early embryos.