ArticleCell cycle (Georgetown, Tex.)2017
Smc1β is required for activation of SAC during mouse oocyte meiosis.
Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Review
- The role of declining ataxia-telangiectasia-mutated (ATM) function in oocyte aging.Cell death discovery · 2024Article
- The Antioxidant Salidroside Ameliorates the Quality of Postovulatory Aged Oocyte and Embryo Development in Mice.Antioxidants (Basel, Switzerland) · 2024Article
- Chromosome Segregation in the Oocyte: What Goes Wrong during Aging.International journal of molecular sciences · 2022Review
- Identification of genes involved in inbreeding depression of reproduction in Langshan chickens.Animal bioscience · 2021Article
- Article
- Regulation of the meiotic divisions of mammalian oocytes and eggs.Biochemical Society transactions · 2018Review
- Postovulatory aging causes the deterioration of porcine oocytes via induction of oxidative stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Eg5 orchestrates porcine oocyte maturational progression by maintaining meiotic organelle arrangement.Cell division · 2018Article
- Age-Related Loss of Cohesion: Causes and Effects.International journal of molecular sciences · 2017Review
- Dynein promotes porcine oocyte meiotic progression by maintaining cytoskeletal structures and cortical granule arrangement.Cell cycle (Georgetown, Tex.) · 2017Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smc1β is a meiosis-specific cohesin subunit that is essential for sister chromatid cohesion and DNA recombination. Previous studies have shown that Smc1β-deficient mice in both sexes are sterile. Ablation of Smc1β during male meiosis leads to the blockage of spermatogenesis in pachytene stage, and ablation of Smc1β during female meiosis generates a highly error-prone oocyte although it could develop to metaphase II stage. However, the underlying mechanisms regarding how Smc1β maintains the correct meiotic progression in mouse oocytes have not been clearly defined. Here, we find that GFP-fused Smc1β is expressed and localized to the chromosomes from GV to MII stages during mouse oocyte meiotic maturation. Knockdown of Smc1β by microinjection of gene-specific morpholino causes the impaired spindle apparatus and chromosome alignment which are highly correlated with the defective kinetochore-microtubule attachments, consequently resulting in a prominently higher incidence of aneuploid eggs. In addition, the premature extrusion of polar bodies and escape of metaphase I arrest induced by low dose of nocodazole treatment in Smc1β-depleted oocytes indicates that Smc1β is essential for activation of spindle assembly checkpoint (SAC) activity. Collectively, we identify a novel function of Smc1β as a SAC participant beyond its role in chromosome cohesion during mouse oocyte meiosis.
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