ArticleDevelopment (Cambridge, England)2015
ATRX contributes to epigenetic asymmetry and silencing of major satellite transcripts in the maternal genome of the mouse embryo.
Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 59 citations in OpenAlex.
- ATRX: From Chromatin Remodeling to Disease.Genesis (New York, N.Y. : 2000) · 2025Review
- A parent-of-origin effect on embryonic telomere elongation determines telomere length inheritance.Current biology : CB · 2025Article
- Telomere Elongation During Pre-Implantation Embryo Development.Advances in anatomy, embryology, and cell biology · 2024Review
- Nuclear Distribution of the Chromatin-Remodeling Protein ATRX in Mouse Early Embryos during Normal Development and Developmental Arrest In Vitro.Life (Basel, Switzerland) · 2023Article
- Acute irradiation induces a senescence-like chromatin structure in mammalian oocytes.Communications biology · 2023Article
- Pericentric major satellite transcription is essential for meiotic chromosome stability and spindle pole organization.Open biology · 2023Article
- Inhibition of p53 and ATRX increases telomeric recombination in primary fibroblasts.FEBS open bio · 2023Article
- A change in biophysical properties accompanies heterochromatin formation in mouse embryos.Genes & development · 2023Article
- LSM1-mediated Major Satellite RNA decay is required for nonequilibrium histone H3.3 incorporation into parental pronuclei.Nature communications · 2023Article
- Mitotic Antipairing of Homologous Chromosomes.Results and problems in cell differentiation · 2022Article
- METTL3-mediated mRNA NCell death & disease · 2021Article
- The Multiple Facets of ATRX Protein.Cancers · 2021Review
- DAXX Is a Crucial Factor for Proper Development of Mammalian Oocytes and Early Embryos.International journal of molecular sciences · 2021Review
- RNA-Binding RING E3-Ligase DZIP3/hRUL138 Stabilizes Cyclin D1 to Drive Cell-Cycle and Cancer Progression.Cancer research · 2021Article
- Epigenomic Reprogramming as a Driver of Malignant Glioma.Cancer cell · 2020Review
- Loss of CBX2 induces genome instability and senescence-associated chromosomal rearrangements.The Journal of cell biology · 2020Article
- MIWI prevents aneuploidy during meiosis by cleaving excess satellite RNA.The EMBO journal · 2020Article
- H3K9me3 maintenance on a human artificial chromosome is required for segregation but not centromere epigenetic memory.Journal of cell science · 2020Article
- Review
- SUMOylated PRC1 controls histone H3.3 deposition and genome integrity of embryonic heterochromatin.The EMBO journal · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A striking proportion of human cleavage-stage embryos exhibit chromosome instability (CIN). Notably, until now, no experimental model has been described to determine the origin and mechanisms of complex chromosomal rearrangements. Here, we examined mouse embryos deficient for the chromatin remodeling protein ATRX to determine the cellular mechanisms activated in response to CIN. We demonstrate that ATRX is required for silencing of major satellite transcripts in the maternal genome, where it confers epigenetic asymmetry to pericentric heterochromatin during the transition to the first mitosis. This stage is also characterized by a striking kinetochore size asymmetry established by differences in CENP-C protein between the parental genomes. Loss of ATRX results in increased centromeric mitotic recombination, a high frequency of sister chromatid exchanges and double strand DNA breaks, indicating the formation of mitotic recombination break points. ATRX-deficient embryos exhibit a twofold increase in transcripts for aurora kinase B, the centromeric cohesin ESCO2, DNMT1, the ubiquitin-ligase (DZIP3) and the histone methyl transferase (EHMT1). Thus, loss of ATRX activates a pathway that integrates epigenetic modifications and DNA repair in response to chromosome breaks. These results reveal the cellular response of the cleavage-stage embryo to CIN and uncover a mechanism by which centromeric fission induces the formation of large-scale chromosomal rearrangements. Our results have important implications to determine the epigenetic origins of CIN that lead to congenital birth defects and early pregnancy loss, as well as the mechanisms involved in the oocyte to embryo transition.
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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.