A monitor for bud emergence in the yeast morphogenesis checkpoint
A monitor for bud emergence in the yeast morphogenesis checkpoint
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DOI：
10.1091/mbc.e03-03-0154
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发表时间：
2003-08-01
影响因子：
3.3
通讯作者：
Lew, DJ
中科院分区：
文献类型：
--
作者：
Theesfeld, CL;Zyla, TR;Lew, DJ
细胞周期转换受到外部信号和内部检查点的调节，内部检查点监控关键细胞周期事件令人满意的进展。在萌芽酵母中，形态发生检查点阻止细胞周期，以响应影响肌动蛋白细胞骨架和芽形成的扰动。在这里，我们确定了这个检查点途径中的一个步骤，它似乎直接对芽的出现做出反应。激酶Hsl1p的激活依赖于它被募集到由Septins组织的皮质区域，Septins是一类保守的细丝形成蛋白家族。在延迟或阻止出芽的条件下，Hsl1p仍被募集到隔膜皮质，但Hsl1p的过度磷酸化和Hsl1p结合蛋白Hsl7p的募集仅在芽萌发后发生。此时，隔膜皮质在母亲和花蕾之间展开形成一个衣领，Hsl1p和Hsl7p被限制在隔膜衣领的芽侧。我们讨论了将细胞几何形状(在这种情况下，芽的出现)转换为调节细胞增殖的生化信号的模型。
Cell cycle transitions are subject to regulation by both external signals and internal checkpoints that monitor satisfactory progression of key cell cycle events. In budding yeast, the morphogenesis checkpoint arrests the cell cycle in response to perturbations that affect the actin cytoskeleton and bud formation. Herein, we identify a step in this checkpoint pathway that seems to be directly responsive to bud emergence. Activation of the kinase Hsl1p is dependent upon its recruitment to a cortical domain organized by the septins, a family of conserved filament-forming proteins. Under conditions that delayed or blocked bud emergence, Hsl1p recruitment to the septin cortex still took place, but hyperphosphorylation of Hsl1p and recruitment of the Hsl1p-binding protein Hsl7p to the septin cortex only occurred after bud emergence. At this time, the septin cortex spread to form a collar between mother and bud, and Hsl1p and Hsl7p were restricted to the bud side of the septin collar. We discuss models for translating cellular geometry (in this case, the emergence of a bud) into biochemical signals regulating cell proliferation.