Loss of CDC5 function in Saccharomyces cerevisiae leads to defects in Swe1p regulation and Bfa1p/Bub2p-independent cytokinesis.
Loss of CDC5 function in Saccharomyces cerevisiae leads to defects in Swe1p regulation and Bfa1p/Bub2p-independent cytokinesis.
复制标题
酿酒酵母中 CDC5 功能的丧失会导致 Swe1p 调节和 Bfa1p/Bub2p 独立的胞质分裂缺陷。
DOI：
10.1093/genetics/163.1.21
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发表时间：
2003
期刊：
影响因子：
3.3
通讯作者：
Lee,KyungS
中科院分区：
文献类型：
--
作者：
Park,ChongJin;Song,Sukgil;Lee,PhilipR;Shou,Wenying;Deshaies,RaymondJ;Lee,KyungS
在许多生物体中，波罗激酶似乎在M期进展过程中发挥多种作用。为了对芽殖酵母波罗激酶Cdc 5 p的功能提供新的认识，我们通过诱变C-末端结构域产生了新型温度敏感性Cdc 5突变体。在这里，我们发现，在半允许的温度下，突变体dc 5 - 3表现出协同芽伸长和生长缺陷与HSL 1的损失，一个组件的正常G2/M转换的重要。SWE 1的缺失会使出芽酵母Cdk 1同源物Cdc 28 p磷酸化并失活，从而抑制了dc 5 -3 hsl 1 Δ缺陷，表明Cdc 5 p在Swe 1 p上游的一个点发挥功能。另外，cdc 5 - 4和cdc 5 - 7突变体表现出链状细胞形态，连接的细胞体之间具有共享的胞浆，表明细胞动力学缺陷。仔细检查这些突变体发现延迟septin大会在初期的芽网站和松散的组织septin环的母亲芽颈。有丝分裂出口网络（MEN）中的组分在正常胞质分裂中起重要作用。然而，BFA 1或BUB 2，负调节MEN的损失，未能补救这些突变体的细胞动力学缺陷，表明Cdc 5 p促进胞质分裂独立的Bfa 1 p和Bub 2 p。因此，Cdc 5 p有助于激活Swe 1 p依赖的Cdc 28 p/Clb通路、正常的隔蛋白功能和胞质分裂。
In many organisms, polo kinases appear to play multiple roles during M-phase progression. To provide new insights into the function of budding yeast polo kinase Cdc5p, we generated novel temperature-sensitivecdc5mutants by mutagenizing the C-terminal domain. Here we show that, at a semipermissive temperature, thecdc5-3mutant exhibited a synergistic bud elongation and growth defect with loss ofHSL1, a component important for normal G2/M transition. Loss ofSWE1, which phosphorylates and inactivates the budding yeast Cdk1 homolog Cdc28p, suppressed thecdc5-3 hsl1Δ defect, suggesting that Cdc5p functions at a point upstream of Swe1p. In addition, thecdc5-4andcdc5-7mutants exhibited chained cell morphologies with shared cytoplasms between the connected cell bodies, indicating a cytokinetic defect. Close examination of these mutants revealed delayed septin assembly at the incipient bud site and loosely organized septin rings at the mother-bud neck. Components in the mitotic exit network (MEN) play important roles in normal cytokinesis. However, loss ofBFA1orBUB2, negative regulators of the MEN, failed to remedy the cytokinetic defect of these mutants, indicating that Cdc5p promotes cytokinesis independently of Bfa1p and Bub2p. Thus, Cdc5p contributes to the activation of the Swe1p-dependent Cdc28p/Clb pathway, normal septin function, and cytokinesis.