ArticleThe Journal of clinical investigation2012
Compromised genomic integrity impedes muscle growth after Atrx inactivation.
Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it.
- ATR-X syndrome: genetics, clinical spectrum, and management.Human genetics · 2021Pooled it
- The ATRXt Protein Represses rDNA Transcription While Mirroring ATRX Interactions and Heterochromatin Localization.International journal of molecular sciences · 2026Article
- Repeat-rich RNA guides repetitive genomic elements into biomolecular condensates for heterochromatin organization and muscle integrity.Nucleic acids research · 2026Article
- ATRX loss couples genome instability at a G-rich repeat to dysregulation of human alpha-globin expression.Nature communications · 2026Article
- Alternative Lengthening of Telomeres: The Need forInternational journal of molecular sciences · 2025Article
- Construction of the porcine genome mobile element variations and investigation of its role in population diversity and gene expression.Journal of animal science and biotechnology · 2024Article
- Knockout tales: the versatile roles of histone H3.3 in development and disease.Epigenetics & chromatin · 2023Review
- A new mouse model of ATR-X syndrome carrying a common patient mutation exhibits neurological and morphological defects.Human molecular genetics · 2023Article
- Mutations inhibiting KDM4B drive ALT activation in ATRX-mutated glioblastomas.Nature communications · 2021Article
- ATRX limits the accessibility of histone H3-occupied HSV genomes during lytic infection.PLoS pathogens · 2021Article
- Histone variants in skeletal myogenesis.Epigenetics · 2021Review
- Epigenomic Reprogramming as a Driver of Malignant Glioma.Cancer cell · 2020Review
- MYCN amplification and ATRX mutations are incompatible in neuroblastoma.Nature communications · 2020Article
- Neurodevelopmental Disorders Caused by Defective Chromatin Remodeling: Phenotypic Complexity Is Highlighted by a Review of ATRX Function.Frontiers in genetics · 2020Review
- ATRX affects the repair of telomeric DSBs by promoting cohesion and a DAXX-dependent activity.PLoS biology · 2020Article
- Mechanisms of DNA Replication and Repair: Insights from the Study of G-Quadruplexes.Molecules (Basel, Switzerland) · 2019Review
- C3aR signaling and gliosis in response to neurodevelopmental damage in the cerebellum.Journal of neuroinflammation · 2019Article
- PML is recruited to heterochromatin during S phase and represses DAXX-mediated histone H3.3 chromatin assembly.Journal of cell science · 2019Article
- The macroH2A1.2 histone variant links ATRX loss to alternative telomere lengthening.Nature structural & molecular biology · 2019Article
- Snf2h Drives Chromatin Remodeling to Prime Upper Layer Cortical Neuron Development.Frontiers in molecular neuroscience · 2019Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
ATR-X syndrome is a severe intellectual disability disorder caused by mutations in the ATRX gene. Many ancillary clinical features are attributed to CNS deficiencies, yet most patients have muscle hypotonia, delayed ambulation, or kyphosis, pointing to an underlying skeletal muscle defect. Here, we identified a cell-intrinsic requirement for Atrx in postnatal muscle growth and regeneration in mice. Mice with skeletal muscle-specific Atrx conditional knockout (Atrx cKO mice) were viable, but by 3 weeks of age presented hallmarks of underdeveloped musculature, including kyphosis, 20% reduction in body mass, and 34% reduction in muscle fiber caliber. Atrx cKO mice also demonstrated a marked regeneration deficit that was not due to fewer resident satellite cells or their inability to terminally differentiate. However, activation of Atrx-null satellite cells from isolated muscle fibers resulted in a 9-fold reduction in myoblast expansion, caused by delayed progression through mid to late S phase. While in S phase, Atrx colocalized specifically to late-replicating chromatin, and its loss resulted in rampant signs of genomic instability. These observations support a model in which Atrx maintains chromatin integrity during the rapid developmental growth of a tissue.
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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.