ArticleeLife2022
Application of ATAC-Seq for genome-wide analysis of the chromatin state at single myofiber resolution.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 50 citations in OpenAlex.
- IRP1 deficiency alters mitochondrial metabolism and protects against metabolic syndrome pathologies.JCI insight · 2026Article
- Profiling the epigenomic landscape of late embryonic and adult mouse hind limb muscles.Scientific reports · 2026Article
- Neural Cues and Genomic Clues: NGS Insights into Neurogenic Sarcopenia and Muscle Atrophy.International journal of molecular sciences · 2025Review
- REST/NRSF Preserves muscle stem cell identity by repressing alternate cell fate.Nature communications · 2025Article
- Integrated single-cell multiome analysis reveals muscle fiber-type gene regulatory circuitry modulated by endurance exercise.Genome research · 2025Article
- Integrated single-cell functional-proteomic profiling reveals a shift in myofibre specificity in human nemaline myopathy: A proof-of-principle study.The Journal of physiology · 2025Article
- N-alpha-acetyltransferase 40 modulates ecdysteroid action through chromatin accessibility changes near the promoters of 20-hydroxyecdysone response genes in Tribolium Castaneum TcA cells.Insect biochemistry and molecular biology · 2025Article
- Article
- Analysis of the differential transcriptome expression profiles during prenatal muscle tissue development in Diqing Tibetan pigs.Frontiers in veterinary science · 2025Article
- ATAC-seq for Characterizing Host and Pathogen Genome Accessibility During Virus Infection.Methods in molecular biology (Clifton, N.J.) · 2025Article
- The E3 ubiquitin ligase Nedd4L preserves skeletal muscle stem cell quiescence by inhibiting their activation.iScience · 2024Article
- Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024Review
- Disease related changes in ATAC-seq of iPSC-derived motor neuron lines from ALS patients and controls.Nature communications · 2024Article
- ROCCO: a robust method for detection of open chromatin via convex optimization.Bioinformatics (Oxford, England) · 2023Article
- Improved quality metrics for association and reproducibility in chromatin accessibility data using mutual information.BMC bioinformatics · 2023Article
- ATAC-Seq of a Single Myofiber fromBio-protocol · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myofibers are the main components of skeletal muscle, which is the largest tissue in the body. Myofibers are highly adaptive and can be altered under different biological and disease conditions. Therefore, transcriptional and epigenetic studies on myofibers are crucial to discover how chromatin alterations occur in the skeletal muscle under different conditions. However, due to the heterogenous nature of skeletal muscle, studying myofibers in isolation proves to be a challenging task. Single-cell sequencing has permitted the study of the epigenome of isolated myonuclei. While this provides sequencing with high dimensionality, the sequencing depth is lacking, which makes comparisons between different biological conditions difficult. Here, we report the first implementation of single myofiber ATAC-Seq, which allows for the sequencing of an individual myofiber at a depth sufficient for peak calling and for comparative analysis of chromatin accessibility under various physiological and disease conditions. Application of this technique revealed significant differences in chromatin accessibility between resting and regenerating myofibers, as well as between myofibers from a mouse model of Duchenne Muscular Dystrophy (mdx) and wild-type (WT) counterparts. This technique can lead to a wide application in the identification of chromatin regulatory elements and epigenetic mechanisms in muscle fibers during development and in muscle-wasting diseases.
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