Holliday junction resolution: regulation in space and time.
Holliday junction resolution: regulation in space and time.
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DOI：
10.1016/j.dnarep.2014.03.013
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发表时间：
2014-07
期刊：
影响因子：
3.8
通讯作者：
West, Stephen C.
中科院分区：
文献类型：
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作者：
Matos, Joao;West, Stephen C.
在DNA损伤的重组修复过程中，姐妹染色单体之间或同源染色体之间可形成霍利迪连接体（HJs）。多种途径作用于HJs以将其从DNA上移除，这对于染色体的正确分离至关重要。尽管已经鉴定并描述了多种参与HJ加工的酶，但调节和实现途径使用的细胞机制才刚刚开始被阐明。一个由核心细胞周期激酶和磷酸酶组成的保守网络通过对两种结构选择性核酸酶——酵母Mus81 - Mms4（人类MUS81 - EME1）和Yen1（人类GEN1）的活性进行时空控制来调节HJ代谢。这些调节周期的作用是建立HJ加工酶的顺序激活，在途径使用中形成一种层级结构，确保消除那些可能干扰染色体分离的染色体相互作用。Mus81 - Mms4/EME1和Yen1/GEN1似乎定义了一类特殊的酶，它们的进化是为了满足在染色体即将分离时保障DNA修复完成的细胞需求。
Holliday junctions (HJs) can be formed between sister chromatids or homologous chromosomes during the recombinational repair of DNA lesions. A variety of pathways act upon HJs to remove them from DNA, in events that are critical for appropriate chromosome segregation. Despite the identification and characterization of multiple enzymes involved in HJ processing, the cellular mechanisms that regulate and implement pathway usage have only just started to be delineated. A conserved network of core cell-cycle kinases and phosphatases modulate HJ metabolism by exerting spatial and temporal control over the activities of two structure-selective nucleases: yeast Mus81-Mms4 (human MUS81-EME1) and Yen1 (human GEN1). These regulatory cycles operate to establish the sequential activation of HJ processing enzymes, implementing a hierarchy in pathway usage that ensure the elimination of chromosomal interactions which would otherwise interfere with chromosome segregation. Mus81-Mms4/EME1 and Yen1/GEN1 emerge to define a special class of enzymes, evolved to satisfy the cellular need of safeguarding the completion of DNA repair when on the verge of chromosome segregation.
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影响因子：
16
作者：
Chen, XB;Melchionna, R;McGowan, CH
通讯作者：
McGowan, CH
影响因子：
10.5
作者：
Fricke, WM;Brill, SJ
通讯作者：
Brill, SJ
影响因子：
5.3
作者：
GANGLOFF, S;MCDONALD, JP;ROTHSTEIN, R
通讯作者：
ROTHSTEIN, R
SLX1和MUS81-EME1核酸酶对Holliday连接分辨率和DNA修复的合作控制。
影响因子：
16
作者：
Castor, Dennis;Nair, Nidhi;Declais, Anne-Cecile;Lachaud, Christophe;Toth, Rachel;Macartney, Thomas J.;Lilley, David M. J.;Arthur, J. Simon C.;Rouse, John
通讯作者：
Rouse, John
影响因子：
64.8
作者：
通讯作者：
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