Regulation of the kinetochore-microtuble interface
着丝粒-微管界面的调节
基本信息
- 批准号:6930424
- 负责人:
- 金额:$ 4.99万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2004
- 资助国家:美国
- 起止时间:2004-08-01 至 2007-07-31
- 项目状态:已结题
- 来源:
- 关键词:XenopusXenopus oocytecell component structure /functioncell cyclecell cycle proteinscell free systemcentromerechromosome movementconfocal scanning microscopygene mutationintermolecular interactionmicrotubule associated proteinmicrotubulesmolecular assembly /self assemblyphase contrast microscopyphosphorylationpostdoctoral investigatorprotein kinaseprotein localizationprotein structure functionsite directed mutagenesistime resolved datatissue /cell culture
项目摘要
DESCRIPTION (provided by applicant):
In mitosis, proper microtubule (MT) attachment to kinetochores is critical for faithful chromosome segregation. Our lab has shown that errors in kinetochore attachment occur at a high frequency in human tissue culture cells and these have to be corrected for accurate segregation. Budding yeast studies indicate a role for mitotic kinase Ipl1 (human Aurora B ortholog) in correcting MT misattachments at kinetochores. These studies show that Ipl1 phosphorylates the highly conserved outer kinetochore component Ndc80 (human Hec1 ortholog) and a MT-associated protein Dam1 (no known human ortholog). Genetic and mutagenesis studies indicate that Aurora B phosphorylation of these substrates weakens kinetochore interactions with kinetochore MTs (kMTs). Preliminary data from my yeast studies suggest Aurora B regulates another MT-associated protein Dim1 (human EB1). EB1 proteins are known to bind and promote stability of plus-end kMTs. I propose to investigate how human Hec1 and EB1 function are regulated by aurora B at the vertebrate kMT interface. I will examine the consequences of presence or absence of Aurora B phosphorylation of these k-MT substrates in mammalian cells.
描述(由申请人提供):
在有丝分裂中,适当的微管(MT)附着在着丝点上是保证染色体正确分离的关键。我们的实验室已经证明,在人类组织培养细胞中,动粒附着的错误发生的频率很高,这些错误必须得到纠正,以实现准确的分离。发芽酵母研究表明,有丝分裂激酶Ipl1(人Aurora B同源基因)在纠正MT在动粒上的错误附着中起到了作用。这些研究表明,Ipl1磷酸化高度保守的外部动粒成分Ndc80(人类Hec1同源基因)和MT相关蛋白Dam1(未发现人类同源基因)。遗传和突变研究表明,这些底物的Aurora B磷酸化减弱了动粒与动粒MTS(KMTs)的相互作用。我的酵母研究的初步数据表明,Aurora B调节另一种MT相关蛋白Dim1(人EB1)。已知EB1蛋白结合并促进正端kMT的稳定性。我建议研究人类Hec1和EB1功能是如何受极光B在脊椎动物KMT界面上调节的。我将研究哺乳动物细胞中这些k-MT底物是否存在Aurora B磷酸化的后果。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
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WALTER E GALL其他文献
WALTER E GALL的其他文献
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{{ truncateString('WALTER E GALL', 18)}}的其他基金
Regulation of the kinetochore-microtuble interface
着丝粒-微管界面的调节
- 批准号:
7097458 - 财政年份:2004
- 资助金额:
$ 4.99万 - 项目类别:
Regulation of the kinetochore-microtuble interface
着丝粒-微管界面的调节
- 批准号:
6836576 - 财政年份:2004
- 资助金额:
$ 4.99万 - 项目类别:
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