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To address this issue, we investigated the consequences of loss of 3D-genome architecture in skeletal muscles by generating myofiber-specific\n                  <jats:italic>Ctcf-<\/jats:italic>\n                  deficient (\n                  <jats:italic>Ctcf<\/jats:italic>\n                  <jats:sup>mKO<\/jats:sup>\n                  ) mice.\n                  <jats:italic>Ctcf<\/jats:italic>\n                  <jats:sup>mKO<\/jats:sup>\n                  mice did not exhibit muscular phenotype at birth but spontaneously developed a severe myopathy. Integrated analysis of snRNAseq, ATACseq and promoter-capture Hi-C revealed both common and fiber-type specific patterns of dysregulated gene expression associated with alterations in chromatin accessibility and promoter-based interactions in Ctcf-deficient myonuclei at distinct stages of myopathy development. Decreased chromatin accessibility at promoters and changes in their connectivity with distal elements were observed across all myonuclei as a direct consequence of\n                  <jats:italic>Ctcf<\/jats:italic>\n                  deficiency at early stages and associated with downregulation of genes implicated in myofiber contraction and anabolism, metabolism, adhesion and neuromuscular transmission. Conversely, at later stages, upregulation of genes leading to persistent activation of ER stress\/UPR and catabolism resulted from global reconfiguration of chromatin structure and connectivity, partly as indirect consequence of\n                  <jats:italic>Ctcf<\/jats:italic>\n                  deficiency. Notably, type-IIB myonuclei exhibited specific alterations in gene expression that culminated in loss of fiber-type identity and ectopic expression of inflammatory genes. These results reveal a requirement of Ctcf for maintenance of fiber-type identity and transcriptional adaptation\n                  <jats:italic>in vivo<\/jats:italic>\n                  , through multilayered control of 3D genome integrity. They also indicate an unprecedented association between\n                  <jats:italic>Ctcf<\/jats:italic>\n                  deficiency in myofibers and susceptibility to develop myopathies, whereby\n                  <jats:italic>Ctcf<\/jats:italic>\n                  dispensability for developmental myogenesis confers vulnerability to develop myopathic syndromes.\n                <\/jats:p>","DOI":"10.64898\/2026.09.28.754564","type":"posted-content","created":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T16:15:28Z","timestamp":1790698528000},"source":"Crossref","is-referenced-by-count":0,"title":["Ctcf deficiency in myofibers induces pathological genome reprogramming toward the spontaneous development of myopathy"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9699-5580","authenticated-orcid":false,"given":"Jimmy","family":"Massenet","sequence":"first","affiliation":[{"name":"Sanford Burnham Prebys Medical Discovery, Center for Cardiovascular and Muscular Diseases, La Jolla, CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0872-6506","authenticated-orcid":false,"given":"Chiara","family":"Nicoletti","sequence":"additional","affiliation":[{"name":"Sanford Burnham Prebys Medical Discovery, Center for Cardiovascular and Muscular Diseases, La Jolla, CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1697-9968","authenticated-orcid":false,"given":"Luca","family":"Caputo","sequence":"additional","affiliation":[{"name":"Sanford Burnham Prebys Medical Discovery, Center for Cardiovascular and Muscular Diseases, La Jolla, CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5054-0027","authenticated-orcid":false,"given":"S\u00f6ren S.","family":"H\u00fcttner","sequence":"additional","affiliation":[{"name":"Department of Human Genetics, McGill University, 3640 University St., Montr\u00e9al, Canada, H3A 0C7"},{"name":"Lady Davis Institute for Medical Research, Jewish General Hospital, 3755 chemin de la Cote Ste. 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