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We previously identified snoRNAs that are abundant in healthy human muscle progenitor cells. In this study, we demonstrated that SNORA40 and SNORA70 loss-of-function impairs myogenic differentiation. Interestingly, gain-of-function can rescue impaired differentiation muscle progenitor cells in myotonic dystrophy type 1 (DM1). We identified cyclin D3 (CCND3) mRNA, which is partially located in the nucleolus, as a target for SNORA40 and SNORA70, which are required for its pseudouridylated status. Expression of the CCND3 protein is required for muscle progenitors to exit the cell-cycle when they are induced to differentiate. We revealed that this switch requires SNORA40\/70. Finally, we observed that DM1 cells show reduced levels of SNORA40\/70 and undetectable CCND3 protein. However, restoring normal levels of SNORA40\/70 partially restored CCND3 protein expression, coinciding with improved cell fusion capacity in DM1 muscle progenitors. Collectively, these data suggest that this effect may stem from SNORA40\/70-dependent pseudouridylation of CCND3 mRNA, emphasizing snoRNAs as key players in normal and pathological muscle differentiation.<\/jats:p>","DOI":"10.1093\/nar\/gkaf232","type":"journal-article","created":{"date-parts":[[2025,3,31]],"date-time":"2025-03-31T18:43:46Z","timestamp":1743446626000},"source":"Crossref","is-referenced-by-count":3,"title":["Small nucleolar RNAs promote the restoration of muscle differentiation defects in cells from myotonic dystrophy type 1"],"prefix":"10.1093","volume":"53","author":[{"given":"Baptiste","family":"Bogard","sequence":"first","affiliation":[{"name":"Universit\u00e9 de Paris Cit\u00e9 , CNRS, UMR7216 \u00c9pig\u00e9n\u00e9tique et Destin Cellulaire, F-75013\u00a0 Paris ,","place":["France"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H\u00e9l\u00e8ne","family":"Bonnet","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Paris Cit\u00e9 , 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