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

Author:

Bolcun-Filas Ewelina1,Costa Yael1,Speed Robert1,Taggart Mary1,Benavente Ricardo2,De Rooij Dirk G34,Cooke Howard J1

Affiliation:

1. Medical Research Council Human Genetics Unit, Western General Hospital, Edinburgh EH4 2XU, Scotland, UK

2. Department of Cell and Developmental Biology, Biocenter of the University of Würzburg, D-97074 Würzburg, Germany

3. Department of Endocrinology, Utrecht University, 3508 TC Utrecht, Netherlands

4. Department of Cell Biology, Universitair Medisch Centrum Utrecht, 3508 GA Utrecht, Netherlands

Abstract

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.

Publisher

Rockefeller University Press

Subject

Cell Biology

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