Abstract

This EMBO workshop was organised by Angel Nebreda, Tim Hunt, Sergio Moreno and Paul Nurse and was held in Salamanaca, Spain, September 6–9, 2001. ![][1] The time‐trial stage of the annual ‘La vuelta’ cycle race was held in Salamanca in early September 2001. By coincidence, the cell cycle went on trial in Salamanca at the same time, at an EMBO workshop on G2/M progression and associated checkpoints organized by Angel Nebreda and Sergio Moreno—and by Tim Hunt and Paul Nurse in their pre‐Nobel‐laureate stage! This was a highly enjoyable and stimulating meeting that covered a wide range of topics concerning the less fashionable part of the cell cycle: p53 was hardly mentioned and Rb got very short shrift. In this report, I will try to highlight some of the novel trends and concepts that emerged during the meeting rather than review all the talks. My apologies to those speakers whose talks I have been unable to include. ### Polo‐like kinases: wresting mitosis from the cyclin–CDK family The plenary lecture was given by Stephen Elledge (Houston, TX), who introduced some of the themes that would recur during the meeting. He showed that, in budding yeast, the Bfa1/Byr4 protein, which makes up a two‐component GAP (GTPase activating protein) with Bub2, is regulated by phosphorylation. The Bfa1–Bub2 pathway regulates exit from mitosis in response to the structure and position of the mitotic spindle and in response to DNA damage. Elledge presented evidence that Cdc5, the polo‐like kinase in budding yeast, phosphorylates Bfa1 in anaphase to facilitate exit from mitosis. This phosphorylation was blocked by the spindle assembly and orientation checkpoints. In addition, DNA damage could block mitosis by two pathways: phosphorylation of the anaphase inhibitor securin to prevent its destruction; and hyperphosphorylation of Bfa1, which may help to prevent mitotic exit. During the meeting, it became apparent that the polo family … [1]: /embed/graphic-1.gif

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