ArticlePLoS genetics2015
Histone H2AFX Links Meiotic Chromosome Asynapsis to Prophase I Oocyte Loss in Mammals.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
50 citing papers in PubMed, 69 citations in OpenAlex.
- Loss of Nemp1 disrupts female meiosis and activates a conserved ATM-CHK2 checkpoint.Nature communications · 2026Article
- SYCP2 recruits HORMAD2 to chromosome axes for unsynapsed chromatin silencing and synapsis surveillance in meiosis.Nature communications · 2026Article
- Structure and function of the synaptonemal complex.The Journal of cell biology · 2026Review
- Coordinating meiotic prophase I progression and early oocyte differentiation.Development (Cambridge, England) · 2026Article
- Distinct cellular and reproductive consequences of meiotic chromosome synapsis defects in syce2 and sycp1 mutant zebrafish.PLoS genetics · 2025Article
- Searching for the 'X' factor: investigating the genetics of primary ovarian insufficiency.Journal of ovarian research · 2024Review
- The role of RAD51 regulators and variants in primary ovarian insufficiency, endometriosis, and polycystic ovary syndrome.NAR molecular medicine · 2024Review
- GWAS Enhances Genomic Prediction Accuracy of Caviar Yield, Caviar Color and Body Weight Traits in Sturgeons Using Whole-Genome Sequencing Data.International journal of molecular sciences · 2024Article
- RNF212B E3 ligase is essential for crossover designation and maturation during male and female meiosis in the mouse.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Establishment of glioma prognosis nomogram based on the function of meox1 in promoting the progression of cancer.Heliyon · 2024Article
- BRCA1 safeguards genome integrity by activating chromosome asynapsis checkpoint to eliminate recombination-defective oocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Maternal NAT10 orchestrates oocyte meiotic cell-cycle progression and maturation in mice.Nature communications · 2023Article
- Genetic control of meiosis surveillance mechanisms in mammals.Frontiers in cell and developmental biology · 2023Review
- Chromosomal synapsis defects can trigger oocyte apoptosis without elevating numbers of persistent DNA breaks above wild-type levels.Nucleic acids research · 2022Article
- The Hypothesis of the Prolonged Cell Cycle in Turner Syndrome.Journal of developmental biology · 2022Review
- High Stability of the Epigenome in Drosophila Interspecific Hybrids.Genome biology and evolution · 2022Article
- Regulation of Meiotic Prophase One in Mammalian Oocytes.Frontiers in cell and developmental biology · 2021Review
- DNA Damaged Induced Cell Death in Oocytes.Molecules (Basel, Switzerland) · 2020Review
- The DNA damage response is required for oocyte cyst breakdown and follicle formation in mice.PLoS genetics · 2020Article
- Premature ovarian insufficiency in the XO female mouse on the C57BL/6J genetic background.Molecular human reproduction · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Chromosome abnormalities are common in the human population, causing germ cell loss at meiotic prophase I and infertility. The mechanisms driving this loss are unknown, but persistent meiotic DNA damage and asynapsis may be triggers. Here we investigate the contribution of these lesions to oocyte elimination in mice with chromosome abnormalities, e.g. Turner syndrome (XO) and translocations. We show that asynapsed chromosomes trigger oocyte elimination at diplonema, which is linked to the presence of phosphorylated H2AFX (γH2AFX). We find that DNA double-strand break (DSB) foci disappear on asynapsed chromosomes during pachynema, excluding persistent DNA damage as a likely cause, and demonstrating the existence in mammalian oocytes of a repair pathway for asynapsis-associated DNA DSBs. Importantly, deletion or point mutation of H2afx restores oocyte numbers in XO females to wild type (XX) levels. Unexpectedly, we find that asynapsed supernumerary chromosomes do not elicit prophase I loss, despite being enriched for γH2AFX and other checkpoint proteins. These results suggest that oocyte loss cannot be explained simply by asynapsis checkpoint models, but is related to the gene content of asynapsed chromosomes. A similar mechanistic basis for oocyte loss may operate in humans with chromosome abnormalities.
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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 OpenQuestion graph.