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Meiotic cohesin STAG 3 is required for chromosome axis formation and sister chromatid cohesion
Author(s) -
Winters Tristan,
McNicoll Francois,
Jessberger Rolf
Publication year - 2014
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/embj.201387330
Subject(s) - cohesin , establishment of sister chromatid cohesion , biology , meiosis , centromere , chromatid , chromosome segregation , sister chromatids , genetics , meiosis ii , homologous chromosome , microbiology and biotechnology , chromatin , synapsis , chromosome , dna , gene
The cohesin complex is essential for mitosis and meiosis. The specific meiotic roles of individual cohesin proteins are incompletely understood. We report in vivo functions of the only meiosis‐specific STAG component of cohesin, STAG 3. Newly generated STAG 3‐deficient mice of both sexes are sterile with meiotic arrest. In these mice, meiotic chromosome architecture is severely disrupted as no bona fide axial elements ( AE ) form and homologous chromosomes do not synapse. Axial element protein SYCP 3 forms dot‐like structures, many partially overlapping with centromeres. Asynapsis marker HORMAD 1 is diffusely distributed throughout the chromatin, and SYCP 1, which normally marks synapsed axes, is largely absent. Centromeric and telomeric sister chromatid cohesion are impaired. Centromere and telomere clustering occurs in the absence of STAG 3, and telomere structure is not severely affected. Other cohesin proteins are present, localize throughout the STAG 3‐devoid chromatin, and form complexes with cohesin SMC 1β. No other deficiency in a single meiosis‐specific cohesin causes a phenotype as drastic as STAG 3 deficiency. STAG 3 emerges as the key STAG cohesin involved in major functions of meiotic cohesin.