ArticleThe Journal of cell biology2020
Oocytes mount a noncanonical DNA damage response involving APC-Cdh1-mediated proteolysis.
Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- DNMT/TET Imbalance and Network-Level DNA Methylation Remodeling in Ovarian Aging: Mechanistic Perspectives.Biology · 2026Review
- The impact of developmental stage, tissue type, and sex on DNA double-strand break repair in Drosophila melanogaster.PLoS genetics · 2024Article
- The diverging role of CDC14B: from mitotic exit in yeast to cell fate control in humans.The EMBO journal · 2023Review
- Xrcc5/Ku80 is required for the repair of DNA damage in fully grown meiotically arrested mammalian oocytes.Cell death & disease · 2023Article
- Selective utilization of non-homologous end-joining and homologous recombination for DNA repair during meiotic maturation in mouse oocytes.Cell proliferation · 2023Article
- PAK2 is essential for chromosome alignment in metaphase I oocytes.Cell death & disease · 2023Article
- Two-step nuclear centring by competing microtubule- and actin-based mechanisms in 2-cell mouse embryos.EMBO reports · 2022Article
- MDC1 is essential for G2/M transition and spindle assembly in mouse oocytes.Cellular and molecular life sciences : CMLS · 2022Article
- Decrease in ovarian reserve through the inhibition of SIRT1-mediated oxidative phosphorylation.Aging · 2022Article
- Review
- Isolation andBio-protocol · 2021Article
- Double-strand breaks induce short-scale DNA replication and damage amplification in the fully grown mouse oocytes.Genetics · 2021Article
- Senataxin: A New Guardian of the Female Germline Important for Delaying Ovarian Aging.Frontiers in genetics · 2021Review
- Sirt1 sustains female fertility by slowing age-related decline in oocyte quality required for post-fertilization embryo development.Aging cell · 2020Article
- AMPK Activity Contributes to G2 Arrest and DNA Damage Decrease via p53/p21 Pathways in Oxidatively Damaged Mouse Zygotes.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mitotic cells, DNA damage induces temporary G2 arrest via inhibitory Cdk1 phosphorylation. In contrast, fully grown G2-stage oocytes readily enter M phase immediately following chemical induction of DNA damage in vitro, indicating that the canonical immediate-response G2/M DNA damage response (DDR) may be deficient. Senataxin (Setx) is involved in RNA/DNA processing and maintaining genome integrity. Here we find that mouse oocytes deleted of Setx accumulate DNA damage when exposed to oxidative stress in vitro and during aging in vivo, after which, surprisingly, they undergo G2 arrest. Moreover, fully grown wild-type oocytes undergo G2 arrest after chemotherapy-induced in vitro damage if an overnight delay is imposed following damage induction. Unexpectedly, this slow-evolving DDR is not mediated by inhibitory Cdk1 phosphorylation but by APC-Cdh1-mediated proteolysis of the Cdk1 activator, cyclin B1, secondary to increased Cdc14B-dependent APC-Cdh1 activation and reduced Emi1-dependent inhibition. Thus, oocytes are unable to respond immediately to DNA damage, but instead mount a G2/M DDR that evolves slowly and involves a phosphorylation-independent proteolytic pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.