SYCE2 is required for synaptonemal complex assembly, double strand break repair, and homologous recombination

被引:148
作者
Bolcun-Filas, Ewelina
Costa, Yael
Speed, Robert
Taggart, Mary
Benavente, Ricardo
De Rooij, Dirk G.
Cooke, Howard J. [1 ]
机构
[1] Western Gen Hosp, MRC, Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland
[2] Univ Wurzburg, Bioctr, Dept Cell & Dev Biol, D-97074 Wurzburg, Germany
[3] Univ Utrecht, Dept Endocrinol, NL-3508 TC Utrecht, Netherlands
[4] Univ Utrecht, Med Ctr, Dept Cell Biol, NL-3508 GA Utrecht, Netherlands
基金
英国医学研究理事会;
关键词
D O I
10.1083/jcb.200610027
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Synapsis is the process by which paired chromosome homologues closely associate in meiosis before crossover. In the synaptonemal complex (SC), axial elements of each homologue connect through molecules of SYCP1 to the central element, which contains the proteins SYCE1 and -2. We have derived mice lacking SYCE2 protein, producing males and females in which meiotic chromosomes align and axes form but do not synapse. Sex chromosomes are unaligned, not forming a sex body. Additionally, markers of DNA breakage and repair are retained on the axes, and crossover is impaired, culminating in both males and females failing to produce gametes. We show that SC formation can initiate at sites of SYCE1/SYCP1 localization but that these points of initiation cannot be extended in the absence of SYCE2. SC assembly is thus dependent on SYCP1, SYCE1, and SYCE2. We provide a model to explain this based on protein-protein interactions.
引用
收藏
页码:741 / 747
页数:7
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