AW Murray. 1991. “
Cell cycle extracts.” Methods Cell Biol, 36, Pp. 581-605.
Publisher's Version AW Murray. 1991. “
Coordinating cell cycle events.” Cold Spring Harb Symp Quant Biol, 56, Pp. 399-408.
Publisher's Version M Glotzer, AW Murray, and MW Kirschner. 1991. “
Cyclin is degraded by the ubiquitin pathway.” Nature, 349, 6305, Pp. 132-8.
Publisher's VersionAbstractCyclin degradation is the key step governing exit from mitosis and progress into the next cell cycle. When a region in the N terminus of cyclin is fused to a foreign protein, it produces a hybrid protein susceptible to proteolysis at mitosis. During the course of degradation, both cyclin and the hybrid form conjugates with ubiquitin. The kinetic properties of the conjugates indicate that cyclin is degraded by ubiquitin-dependent proteolysis. Thus anaphase may be triggered by the recognition of cyclin by the ubiquitin-conjugating system.
R Li and AW Murray. 1991. “
Feedback control of mitosis in budding yeast.” Cell, 66, 3, Pp. 519-31.
Publisher's VersionAbstractWe have investigated the feedback control that prevents cells with incompletely assembled spindles from leaving mitosis. We isolated budding yeast mutants sensitive to the anti-microtubule drug benomyl. Mitotic arrest-deficient (mad) mutants are the subclass of benomyl-sensitive mutants in which the completion of mitosis is not delayed in the presence of benomyl and that die as a consequence of their premature exit from mitosis. A number of properties of the mad mutants indicate that they are defective in the feedback control over the exit from mitosis: their killing by benomyl requires passage through mitosis; their benomyl sensitivity can be suppressed by an independent method for delaying the exit from mitosis; they have normal microtubules; and they have increased frequencies of chromosome loss. We cloned MAD2, which encodes a putative calcium-binding protein whose disruption is lethal. We discuss the role of feedback controls in coordinating events in the cell cycle.
AW Murray and MW Kirschner. 1991. “
What controls the cell cycle?” Sci Am, 264, 3, Pp. 56-63.
Publisher's Version J Minshull, A Murray, A Colman, and T Hunt. 1991. “
Xenopus oocyte maturation does not require new cyclin synthesis.” J Cell Biol, 114, 4, Pp. 767-72.
Publisher's VersionAbstractProgesterone induces fully grown, stage VI, Xenopus oocytes to pass through meiosis I and arrest in metaphase of meiosis II. Protein synthesis is required twice in this process: in order to activate maturation promoting factor (MPF) which induces meiosis I, and then again after the completion of meiosis I to reactivate MPF in order to induce meiosis II. We have used antisense oligonucleotides to destroy maternal stores of cyclin mRNAs, and demonstrate that new cyclin synthesis is not required for entry into either meiosis I or II. This finding is consistent with the demonstration that stage VI oocytes contain a store of B-type cyclin polypeptides (Kobayashi, H., J. Minshull, C. Ford, R. Golsteyn, R. Poon, and T. Hunt. 1991. J. Cell Biol. 114:755-765). Although approximately 70% of cyclin B2 is destroyed at first meiosis, the surviving fraction, together with a larger pool of surviving cyclin B1, must be sufficient to allow the reactivation of MPF and induce entry into second meiotic metaphase. Since stage VI oocytes do not contain any cyclin A, our results show that cyclin A is not required for meiosis in Xenopus. We discuss the possible nature of the proteins whose synthesis is required to induce meiosis I and II.