ArticleChromosoma2016
Functions of the MRE11 complex in the development and maintenance of oocytes.
Article in Chromosoma, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed.
- Regulatory risk loci link disrupted androgen response to the pathophysiology of polycystic ovary syndrome.Journal of the Endocrine Society · 2026Article
- Evaluation of the DNA Repair Mechanism Following In Vitro Maturation of Mouse Oocytes.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Primary ovarian insufficiency: update on clinical and genetic findings.Frontiers in endocrinology · 2024Review
- Genes in loci genetically associated with polycystic ovary syndrome are dynamically expressed in human fetal gonadal, metabolic and brain tissues.Frontiers in endocrinology · 2023Article
- Causal and Candidate Gene Variants in a Large Cohort of Women With Primary Ovarian Insufficiency.The Journal of clinical endocrinology and metabolism · 2022Observational
- Colocalization analysis of polycystic ovary syndrome to identify potential disease-mediating genes and proteins.European journal of human genetics : EJHG · 2021Article
- Meiotic Recombination Defects and Premature Ovarian Insufficiency.Frontiers in cell and developmental biology · 2021Review
- NBS1 is required for SPO11-linked DNA double-strand break repair in male meiosis.Cell death and differentiation · 2020Article
- CHTF18 ensures the quantity and quality of the ovarian reserve†.Biology of reproduction · 2020Article
- Oocytes can efficiently repair DNA double-strand breaks to restore genetic integrity and protect offspring health.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- DNA damage in aging, the stem cell perspective.Human genetics · 2020Review
- Review
- The capacity of oocytes for DNA repair.Cellular and molecular life sciences : CMLS · 2018Review
- High glucose induces the proliferation of prostatic cells via downregulating MRE11.International journal of molecular medicine · 2018Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The MRE11 complex (MRE11, RAD50, and NBS1) is a central component of the DNA damage response, governing both double-strand break repair and DNA damage response signaling. To determine the functions of the MRE11 complex in the development and maintenance of oocytes, we analyzed ovarian phenotypes of mice harboring the hypomorphic Mre11 (ATLD1) allele. Mre11 (ATLD1/ATLD1) females exhibited premature oocyte elimination attributable to defects in homologous chromosome pairing and double-strand break repair during meiotic prophase. Other aspects of meiotic progression, including attachment of telomeres to the nuclear envelope and recruitment of RAD21L, a component of the meiotic cohesin complex to the synaptonemal complex, were normal. Unlike Dmc1 (-/-) and Trp13 (Gt/Gt) mice which exhibit comparable defects in double-strand break repair and oocyte depletion by 5 days post-partum, we found that oocyte attrition occurred by 12 weeks in Mre11 (ATLD1/ATLD1) . Disruption of the oocyte checkpoint pathway governed by Chk2 gene further enhanced the survival of Mre11 (ATLD1/ATLD1) follicles. Together our data suggest that the MRE11 complex influences the elimination of oocytes with unrepaired meiotic double-strand breaks post-natally, in addition to its previously described role in double-strand break repair and homologous synapsis during female meiosis.
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Registered trials
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