Surana U, Amon A, Dowzer C, McGrew J, Byers B, Nasmyth K
Research Institute of Molecular Pathology, Vienna, Austria.
EMBO J. 1993 May;12(5):1969-78. doi: 10.1002/j.1460-2075.1993.tb05846.x.
It is widely assumed that degradation of mitotic cyclins causes a decrease in mitotic cdc2/CDC28 kinase activity and thereby triggers the metaphase to anaphase transition. Two observations made on the budding yeast Saccharomyces cerevisiae are inconsistent with this scenario: (i) anaphase occurs in the presence of high levels of kinase in cdc15 mutants and (ii) overproduction of a B-type mitotic cyclin causes arrest not in metaphase as previously reported but in telophase. Kinase destruction is therefore implicated in the exit from mitosis rather than the entry into anaphase. The behaviour of esp1 mutants shows in addition that kinase destruction can occur in the absence of anaphase completion. The execution of anaphase and the destruction of CDC28 kinase activity therefore appear to take place independently of one another.
人们普遍认为，有丝分裂周期蛋白的降解会导致有丝分裂cdc2/CDC28激酶活性降低，从而引发中期到后期的转变。在芽殖酵母酿酒酵母中进行的两项观察结果与这种情况不一致：（i）在cdc15突变体中，后期在激酶水平较高的情况下发生；（ii）B型有丝分裂周期蛋白的过量产生导致细胞不是如先前报道的那样停滞在中期，而是停滞在末期。因此，激酶的破坏与有丝分裂的退出有关，而不是与进入后期有关。esp1突变体的行为还表明，在后期完成之前激酶就可能被破坏。因此，后期的执行和CDC28激酶活性的破坏似乎是相互独立发生的。
