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Molecular mechanisms for the final step of dissolving sister chromatid cohesion at anaphase onset

Molecular mechanisms for the final step of dissolving sister chromatid cohesion at anaphase onset
后期开始时溶解姐妹染色单体凝聚力最后一步的分子机制
批准号:
BB/S007768/1
负责人:
Tomoyuki Tanaka
金额:
$54.94万
依托单位:
依托单位国家:
英国
项目类别:
Research Grant
财政年份:
2019
资助国家:
英国
项目状态:
已结题
起止时间:
2019 至 --

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中文摘要
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英文摘要
To make a human body from a single cell (a fertilized egg), an enormous number of cell divisions must take place. Each cell division produces two daughter cells, which equally inherit genetic information from their mother cell. Human cells store their genetic information within 46 structures called chromosomes. To maintain this genetic information, all chromosomes must be precisely copied and each daughter cell must receive one copy of each chromosome when cell division takes place. Failure in this process may cause cancers and genetic abnormalities. The aim of our research is to clarify the fundamental mechanisms by which all chromosomes are properly inherited by daughter cells.In this research project, we focus on the special glue between copied chromosomes. As mentioned above, all chromosomes must be copied and each copy must be given to newly born daughter cells. It is crucial that copied chromosomes are held together with the special glue. However, at right timing, the glue must be quickly removed so that each chromosome copy is given to each daughter cell. If the glue is lost too early, chromosomes are mixed up and not correctly given to daughter cells. On the other hand, if removal of the glue is delayed, chromosome copies do not separately at right time, and both copies could be given to one daughter cell (rather than each copy to each daughter). We will study how cells regulate removal of the glue between copied chromosomes and what mechanisms ensure efficient removal of the glue. We will use both yeast and human cells in our study since they have many similarities in regulation of the chromosome glue. Use of yeast often allows us to reach conclusion more quickly. We will then address if the glue is regulated in the same way in human cells.
期刊论文(2)
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会议论文
Smc3 Deacetylation by Hos1 Facilitates Efficient Dissolution of Sister Chromatid Cohesion during Early Anaphase.
Hos1 对 Smc3 的去乙酰化促进早期后期姐妹染色单体凝聚力的有效溶解。
DOI: 10.1016/j.molcel.2020.04.036
发表时间: 2020
期刊: Molecular cell
影响因子: 16
作者: [Li S]
通讯作者: Li S
Understanding error correction for chromosome bi-orientation using in vitro reconstitution
  • 批准号:
    BB/X014517/1
  • 项目类别:
    Research Grant
  • 资助金额:
    $78.3万
  • 财政年份:
    2023
  • 负责人:
    Tomoyuki Tanaka
  • 依托单位:
Dynamic regulation of chromatin loops by cohesins and CTCF in real time: physiology and pathology
  • 批准号:
    MR/T046880/1
  • 项目类别:
    Research Grant
  • 资助金额:
    $63.24万
  • 财政年份:
    2021
  • 负责人:
    Tomoyuki Tanaka
  • 依托单位:
Mechanisms ensuring sister kinetochore bi-orientation on the mitotic spindle
  • 批准号:
    G0701147/1
  • 项目类别:
    Research Grant
  • 资助金额:
    $154.07万
  • 财政年份:
    2008
  • 负责人:
    Tomoyuki Tanaka
  • 依托单位:
国内基金
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Exploring the Intrinsic Mechanisms of CEO Turnover and Market
  • 批准号:
    --
  • 项目类别:
    外国学者研究基金
  • 资助金额:
    --
  • 批准年份:
    2024
  • 负责人:
    HAOFEI Z
  • 依托单位:
Exploring the Intrinsic Mechanisms of CEO Turnover and Market Reaction: An Explanation Based on Information Asymmetry
  • 批准号:
    W2433169
  • 项目类别:
    外国学者研究基金项目
  • 资助金额:
    --
  • 批准年份:
    2024
  • 负责人:
    HAOFEI ZHANG
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Erk1/2/CREB/BDNF通路在CSF1R相关性白质脑病致病机制中的作用研究
  • 批准号:
    82371255
  • 项目类别:
    面上项目
  • 资助金额:
    49.00万元
  • 批准年份:
    2023
  • 负责人:
    曹立
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Foxc2介导Syap1/Akt信号通路调控破骨/成骨细胞分化促进颞下颌关节骨关节炎的机制研究
  • 批准号:
    82370979
  • 项目类别:
    面上项目
  • 资助金额:
    48.00万元
  • 批准年份:
    2023
  • 负责人:
    张善勇
  • 依托单位: