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1
Synapsis-defective mutants reveal a correlation between chromosome conformation and the mode of double-strand break repair during Caenorhabditis elegans meiosis.联会缺陷突变体揭示了秀丽隐杆线虫减数分裂过程中染色体构象与双链断裂修复模式之间的相关性。
Genetics. 2007 Aug;176(4):2027-33. doi: 10.1534/genetics.107.076968. Epub 2007 Jun 11.
2
Synaptonemal Complex Central Region Proteins Promote Localization of Pro-crossover Factors to Recombination Events During Meiosis.联会复合体中央区域蛋白在减数分裂过程中促进前交叉因子向重组事件的本地化。
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3
Synapsis-dependent and -independent mechanisms stabilize homolog pairing during meiotic prophase in C. elegans.在秀丽隐杆线虫减数分裂前期,依赖联会和不依赖联会的机制稳定同源染色体配对。
Genes Dev. 2002 Sep 15;16(18):2428-42. doi: 10.1101/gad.1011602.
4
ATM/ATR kinases link the synaptonemal complex and DNA double-strand break repair pathway choice.ATM/ATR 激酶连接联会复合体和 DNA 双链断裂修复途径选择。
Curr Biol. 2022 Nov 7;32(21):4719-4726.e4. doi: 10.1016/j.cub.2022.08.081. Epub 2022 Sep 21.
5
CRA-1 uncovers a double-strand break-dependent pathway promoting the assembly of central region proteins on chromosome axes during C. elegans meiosis.CRA-1揭示了一种依赖双链断裂的途径,该途径在秀丽隐杆线虫减数分裂期间促进中央区域蛋白在染色体轴上的组装。
PLoS Genet. 2008 Jun 6;4(6):e1000088. doi: 10.1371/journal.pgen.1000088.
6
Meiotic recombination in C. elegans initiates by a conserved mechanism and is dispensable for homologous chromosome synapsis.秀丽隐杆线虫中的减数分裂重组通过一种保守机制启动,并且对于同源染色体联会是可有可无的。
Cell. 1998 Aug 7;94(3):387-98. doi: 10.1016/s0092-8674(00)81481-6.
7
CRL4 regulates recombination and synaptonemal complex aggregation in the Caenorhabditis elegans germline.CRL4 调控秀丽隐杆线虫生殖细胞中的重组和联会复合体聚集。
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8
HTP-3 links DSB formation with homolog pairing and crossing over during C. elegans meiosis.HTP-3在秀丽隐杆线虫减数分裂过程中将双链断裂的形成与同源配对及交叉联系起来。
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9
SYP-3 restricts synaptonemal complex assembly to bridge paired chromosome axes during meiosis in Caenorhabditis elegans.在秀丽隐杆线虫减数分裂过程中,SYP-3限制联会复合体组装以连接配对的染色体轴。
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10
Matefin/SUN-1 phosphorylation is part of a surveillance mechanism to coordinate chromosome synapsis and recombination with meiotic progression and chromosome movement.Matefin/SUN-1 的磷酸化是一个监控机制的一部分,该机制协调染色体联会和重组与减数分裂进程和染色体运动。
PLoS Genet. 2013;9(3):e1003335. doi: 10.1371/journal.pgen.1003335. Epub 2013 Mar 7.

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1
The synaptonemal complex central element SCEP3 interlinks synapsis initiation and crossover formation in Arabidopsis thaliana.联会复合体中央元件SCEP3将拟南芥中的联会起始与交叉形成相互联系起来。
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The synaptonemal complex aligns meiotic chromosomes by wetting.联会复合体通过湿润作用使减数分裂染色体排列整齐。
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Kinetic analysis of strand invasion during meiosis reveals similar rates of sister- and homolog-directed repair.减数分裂过程中链入侵的动力学分析揭示了姐妹染色单体和同源染色体定向修复的相似速率。
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NuRD chromatin remodeling is required to repair exogenous DSBs in the germline.在生殖细胞系中修复外源性双链断裂需要核小体重塑去乙酰化酶(NuRD)染色质重塑。
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7
Oogenesis in Caenorhabditis elegans.秀丽隐杆线虫中的卵子发生。
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Male-specific roles of lincRNA in fertility.长链非编码RNA在生育力中的男性特异性作用。
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9
GRAS-1 is a novel regulator of early meiotic chromosome dynamics in C. elegans.GRAS-1 是线虫早期减数分裂染色体动力学的新型调节因子。
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10
Chromatin landscape, DSB levels, and cKU-70/80 contribute to patterning of meiotic DSB processing along chromosomes in C. elegans.染色质景观、DSB 水平以及 cKU-70/80 有助于线虫减数分裂 DSB 沿着染色体进行加工。
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本文引用的文献

1
SYP-3 restricts synaptonemal complex assembly to bridge paired chromosome axes during meiosis in Caenorhabditis elegans.在秀丽隐杆线虫减数分裂过程中,SYP-3限制联会复合体组装以连接配对的染色体轴。
Genetics. 2007 Aug;176(4):2015-25. doi: 10.1534/genetics.107.072413. Epub 2007 Jun 11.
2
Developmental modulation of nonhomologous end joining in Caenorhabditis elegans.秀丽隐杆线虫中非同源末端连接的发育调控
Genetics. 2006 Jul;173(3):1301-17. doi: 10.1534/genetics.106.058628. Epub 2006 May 15.
3
A link between meiotic prophase progression and crossover control.减数分裂前期进程与交叉控制之间的联系。
PLoS Genet. 2006 Feb;2(2):e12. doi: 10.1371/journal.pgen.0020012. Epub 2006 Feb 3.
4
Partner choice during meiosis is regulated by Hop1-promoted dimerization of Mek1.减数分裂过程中的配偶选择由Hop1促进的Mek1二聚化调控。
Mol Biol Cell. 2005 Dec;16(12):5804-18. doi: 10.1091/mbc.e05-05-0465. Epub 2005 Oct 12.
5
RAD-51-dependent and -independent roles of a Caenorhabditis elegans BRCA2-related protein during DNA double-strand break repair.秀丽隐杆线虫BRCA2相关蛋白在DNA双链断裂修复过程中依赖RAD-51和不依赖RAD-51的作用
Mol Cell Biol. 2005 Apr;25(8):3127-39. doi: 10.1128/MCB.25.8.3127-3139.2005.
6
The genetics and molecular biology of the synaptonemal complex.联会复合体的遗传学与分子生物学
Annu Rev Cell Dev Biol. 2004;20:525-58. doi: 10.1146/annurev.cellbio.19.111301.155141.
7
The cohesion protein ORD is required for homologue bias during meiotic recombination.在减数分裂重组过程中,同源偏好需要黏连蛋白ORD。
J Cell Biol. 2004 Mar 15;164(6):819-29. doi: 10.1083/jcb.200310077. Epub 2004 Mar 8.
8
Mek1 kinase activity functions downstream of RED1 in the regulation of meiotic double strand break repair in budding yeast.在芽殖酵母减数分裂双链断裂修复的调控中,Mek1激酶活性在RED1下游发挥作用。
Mol Biol Cell. 2004 Jan;15(1):11-23. doi: 10.1091/mbc.e03-07-0499. Epub 2003 Oct 31.
9
Meiotic double-strand breaks at the interface of chromosome movement, chromosome remodeling, and reductional division.减数分裂双链断裂发生在染色体运动、染色体重塑和减数分裂的界面处。
Genes Dev. 2003 Nov 1;17(21):2675-87. doi: 10.1101/gad.275203. Epub 2003 Oct 16.
10
Synaptonemal complex assembly in C. elegans is dispensable for loading strand-exchange proteins but critical for proper completion of recombination.秀丽隐杆线虫中突触复合体的组装对于加载链交换蛋白而言并非必需,但对于重组的正确完成至关重要。
Dev Cell. 2003 Sep;5(3):463-74. doi: 10.1016/s1534-5807(03)00232-6.

联会缺陷突变体揭示了秀丽隐杆线虫减数分裂过程中染色体构象与双链断裂修复模式之间的相关性。

Synapsis-defective mutants reveal a correlation between chromosome conformation and the mode of double-strand break repair during Caenorhabditis elegans meiosis.

作者信息

Smolikov Sarit, Eizinger Andreas, Hurlburt Allison, Rogers Eric, Villeneuve Anne M, Colaiácovo Mónica P

机构信息

Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.

出版信息

Genetics. 2007 Aug;176(4):2027-33. doi: 10.1534/genetics.107.076968. Epub 2007 Jun 11.

DOI:10.1534/genetics.107.076968
PMID:17565963
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1950611/
Abstract

SYP-3 is a new structural component of the synaptonemal complex (SC) required for the regulation of chromosome synapsis. Both chromosome morphogenesis and nuclear organization are altered throughout the germlines of syp-3 mutants. Here, our analysis of syp-3 mutants provides insights into the relationship between chromosome conformation and the repair of meiotic double-strand breaks (DSBs). Although crossover recombination is severely reduced in syp-3 mutants, the production of viable offspring accompanied by the disappearance of RAD-51 foci suggests that DSBs are being repaired in these synapsis-defective mutants. Our studies indicate that once interhomolog recombination is impaired, both intersister recombination and nonhomologous end-joining pathways may contribute to repair during germline meiosis. Moreover, our studies suggest that the conformation of chromosomes may influence the mode of DSB repair employed during meiosis.

摘要

SYP-3是联会复合体(SC)的一种新结构成分,是调节染色体联会所必需的。在syp-3突变体的整个生殖系中,染色体形态发生和核组织都会发生改变。在这里,我们对syp-3突变体的分析为染色体构象与减数分裂双链断裂(DSB)修复之间的关系提供了见解。虽然在syp-3突变体中交叉重组严重减少,但伴随着RAD-51焦点消失的活后代的产生表明这些联会缺陷突变体中的DSB正在被修复。我们的研究表明,一旦同源重组受损,姐妹染色单体间重组和非同源末端连接途径都可能在生殖系减数分裂期间参与修复。此外,我们的研究表明染色体的构象可能会影响减数分裂期间使用的DSB修复模式。