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本文引用的文献

1
Synaptonemal complex formation and meiotic checkpoint signaling are linked to the lateral element protein Red1.联会复合体的形成和减数分裂检查点信号与侧元件蛋白 Red1 相关联。
Proc Natl Acad Sci U S A. 2010 Jun 22;107(25):11370-5. doi: 10.1073/pnas.1004248107. Epub 2010 Jun 3.
2
Yeast axial-element protein, Red1, binds SUMO chains to promote meiotic interhomologue recombination and chromosome synapsis.酵母轴向元件蛋白 Red1 结合 SUMO 链以促进减数分裂同源重组和染色体联会。
EMBO J. 2010 Feb 3;29(3):586-96. doi: 10.1038/emboj.2009.362. Epub 2009 Dec 3.
3
Regulation of meiotic recombination via Mek1-mediated Rad54 phosphorylation.通过 Mek1 介导的 Rad54 磷酸化调节减数分裂重组。
Mol Cell. 2009 Nov 13;36(3):393-404. doi: 10.1016/j.molcel.2009.09.029.
4
Separation and detection of large phosphoproteins using Phos-tag SDS-PAGE.使用Phos-tag SDS-PAGE分离和检测大型磷酸化蛋白。
Nat Protoc. 2009;4(10):1513-21. doi: 10.1038/nprot.2009.154. Epub 2009 Sep 24.
5
Ipl1/Aurora B kinase coordinates synaptonemal complex disassembly with cell cycle progression and crossover formation in budding yeast meiosis.Ipl1/Aurora B激酶在芽殖酵母减数分裂过程中协调联会复合体解体与细胞周期进程及交叉形成。
Genes Dev. 2009 Sep 15;23(18):2237-51. doi: 10.1101/gad.536109.
6
Meiosis I is established through division-specific translational control of a cyclin.减数分裂I是通过对一种细胞周期蛋白进行特定于分裂的翻译控制而建立的。
Cell. 2008 Apr 18;133(2):280-91. doi: 10.1016/j.cell.2008.02.032.
7
Hed1 regulates Rad51-mediated recombination via a novel mechanism.Hed1通过一种新机制调控Rad51介导的重组。
Genes Dev. 2008 Mar 15;22(6):786-95. doi: 10.1101/gad.1638708.
8
Phosphorylation of the axial element protein Hop1 by Mec1/Tel1 ensures meiotic interhomolog recombination.Mec1/Tel1对轴向元件蛋白Hop1的磷酸化作用确保了减数分裂中的同源重组。
Cell. 2008 Mar 7;132(5):758-70. doi: 10.1016/j.cell.2008.01.035.
9
Cdc7-dependent phosphorylation of Mer2 facilitates initiation of yeast meiotic recombination.Cdc7 依赖的 Mer2 磷酸化促进酵母减数分裂重组的起始。
Genes Dev. 2008 Feb 1;22(3):398-410. doi: 10.1101/gad.1626608.
10
Cdc28-Clb5 (CDK-S) and Cdc7-Dbf4 (DDK) collaborate to initiate meiotic recombination in yeast.Cdc28-Clb5(细胞周期蛋白依赖性激酶-细胞周期蛋白B5)和Cdc7-Dbf4(双特异性激酶)协同作用,启动酵母中的减数分裂重组。
Genes Dev. 2008 Feb 1;22(3):386-97. doi: 10.1101/gad.1626408.

酵母轴元件蛋白 Red1 的磷酸化的遗传要求和减数分裂功能。

Genetic requirements and meiotic function of phosphorylation of the yeast axial element protein Red1.

机构信息

Institute of Molecular Biology, Academia Sinica, 128 Academia Road, Taipei 115, Taiwan.

出版信息

Mol Cell Biol. 2011 Mar;31(5):912-23. doi: 10.1128/MCB.00895-10. Epub 2010 Dec 20.

DOI:10.1128/MCB.00895-10
PMID:21173162
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3067829/
Abstract

The synaptonemal complex (SC) is a meiosis-specific tripartite structure that forms between two homologous chromosomes; it consists of a central region and two parallel lateral elements. Lateral elements also are called axial elements prior to synapsis. In Saccharomyces cerevisiae, Red1, Hop1, and Mek1 are structural components of axial/lateral elements. The red1/mek1/hop1 mutants all exhibit reduced levels of interhomolog recombination and produce no viable spores. Red1 is a phosphoprotein. Several earlier reports proposed that phosphorylated Red1 plays important roles in meiosis, including in signaling meiotic DNA damage or in preventing exit from the pachytene chromosomes. We report here that the phosphorylation of Red1 is carried out in CDC28-dependent and CDC28-independent manners. In contrast to previous results, we found Red1 phosphorylation to be independent of meiotic DNA recombination, the Mec1/Tel1 DNA damage checkpoint kinases, and the Mek1 kinase. To functionally validate the phosphorylation of Red1, we mapped the phosphorylation sites on this protein. A red1(14A) mutant showing no detectable Red1 phosphorylation did not exhibit decreased sporulation efficiency, defects in viable spore production, or defects in meiotic DNA damage checkpoints. Thus, our results suggest that the phosphorylation of Red1 is not essential for its functions in meiosis.

摘要

联会复合体(SC)是一种在两个同源染色体之间形成的减数分裂特异性的三分体结构;它由一个中央区域和两个平行的侧部元件组成。在联会之前,侧部元件也称为轴部元件。在酿酒酵母中,Red1、Hop1 和 Mek1 是轴/侧部元件的结构成分。red1/mek1/hop1 突变体都表现出同源重组水平降低,并且不能产生有活力的孢子。Red1 是一种磷酸化蛋白。几个早期的报告提出,磷酸化的 Red1 在减数分裂中发挥重要作用,包括信号减数分裂 DNA 损伤或防止从粗线期染色体退出。我们在这里报告说,Red1 的磷酸化是由 CDC28 依赖和 CDC28 独立的方式进行的。与之前的结果相反,我们发现 Red1 磷酸化与减数分裂 DNA 重组、Mec1/Tel1 DNA 损伤检查点激酶和 Mek1 激酶无关。为了对 Red1 的磷酸化进行功能验证,我们对该蛋白上的磷酸化位点进行了作图。一个显示不出可检测到的 Red1 磷酸化的 red1(14A)突变体,其孢子形成效率没有降低,有活力的孢子产生缺陷或减数分裂 DNA 损伤检查点缺陷。因此,我们的结果表明,Red1 的磷酸化对其在减数分裂中的功能不是必需的。