{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T12:04:45Z","timestamp":1788869085203,"version":"build-2803163510"},"reference-count":43,"publisher":"National Academy of Sciences","issue":"9","license":[{"start":{"date-parts":[[2023,2,21]],"date-time":"2023-02-21T00:00:00Z","timestamp":1676937600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001665","name":"Agence Nationale de la Recherche","doi-asserted-by":"publisher","award":["ANR-18CE12-0007-01"],"award-info":[{"award-number":["ANR-18CE12-0007-01"]}],"id":[{"id":"10.13039\/501100001665","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100004410","name":"European Molecular Biology Organization","doi-asserted-by":"publisher","award":["ALTF-284-2019"],"award-info":[{"award-number":["ALTF-284-2019"]}],"id":[{"id":"10.13039\/100004410","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004784","name":"Novartis Stiftung\u00a0f\u00fcr\u00a0Medizinisch-Biologische Forschung","doi-asserted-by":"publisher","award":["18B112"],"award-info":[{"award-number":["18B112"]}],"id":[{"id":"10.13039\/501100004784","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100014865","name":"Fondation Maladies Rares","doi-asserted-by":"publisher","award":["20161207"],"award-info":[{"award-number":["20161207"]}],"id":[{"id":"10.13039\/100014865","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2023,2,28]]},"abstract":"<jats:p>\n                    In the human genome, about 750 genes contain one intron excised by the minor spliceosome. This spliceosome comprises its own set of snRNAs, among which U4atac. Its noncoding gene,\n                    <jats:italic>RNU4ATAC<\/jats:italic>\n                    , has been found mutated in Taybi-Linder (TALS\/microcephalic\u00a0osteodysplastic primordial dwarfism type 1), Roifman (RFMN), and Lowry-Wood (LWS) syndromes. These rare developmental disorders, whose physiopathological mechanisms remain unsolved, associate ante- and post-natal growth retardation, microcephaly, skeletal dysplasia, intellectual disability, retinal dystrophy, and immunodeficiency. Here, we report bi-allelic\n                    <jats:italic>RNU4ATAC<\/jats:italic>\n                    mutations in five patients presenting with traits suggestive of the Joubert syndrome (JBTS), a well-characterized ciliopathy. These patients also present with traits typical of TALS\/RFMN\/LWS, thus widening the clinical spectrum of\n                    <jats:italic>RNU4ATAC<\/jats:italic>\n                    -associated disorders and indicating ciliary dysfunction as a mechanism downstream of minor splicing defects. Intriguingly, all five patients carry the n.16G&gt;A mutation, in the Stem II domain, either at the homozygous or compound heterozygous state. A gene ontology term enrichment analysis on minor intron-containing genes reveals that the cilium assembly process is over-represented, with no less than 86 cilium-related genes containing at least one minor intron, among which there are 23 ciliopathy-related genes. The link between\n                    <jats:italic>RNU4ATAC<\/jats:italic>\n                    mutations and ciliopathy traits is supported by alterations of primary cilium function in TALS and JBTS-like patient fibroblasts, as well as by\n                    <jats:italic>u4atac<\/jats:italic>\n                    zebrafish model, which exhibits ciliopathy-related phenotypes and ciliary defects. These phenotypes could be rescued by WT but not by pathogenic variants-carrying human U4atac. Altogether, our data indicate that alteration of cilium biogenesis is part of the physiopathological mechanisms of TALS\/RFMN\/LWS, secondarily to defects of minor intron splicing.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2102569120","type":"journal-article","created":{"date-parts":[[2023,2,21]],"date-time":"2023-02-21T13:58:31Z","timestamp":1676987911000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":29,"title":["Deficiency of the minor spliceosome component U4atac snRNA secondarily results in ciliary defects in human and zebrafish"],"prefix":"10.1073","volume":"120","author":[{"given":"Deepak","family":"Khatri","sequence":"first","affiliation":[{"name":"Universit\u00e9 Claude Bernard Lyon 1, INSERM, CNRS, Centre de Recherche en Neurosciences de Lyon CRNL U1028 UMR5292,Genetics of Neurodevelopment Team, 69500 Bron, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Audrey","family":"Putoux","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Claude Bernard Lyon 1, INSERM, CNRS, Centre de Recherche en Neurosciences de Lyon CRNL U1028 UMR5292,Genetics of Neurodevelopment Team, 69500 Bron, France"},{"name":"Department of Genetics, Clinical Genetics Unit, Centre de R\u00e9f\u00e9rence Maladies Rares des Anomalies du D\u00e9veloppement, Hospices Civils de Lyon, Universit\u00e9 Claude Bernard Lyon 1, 69500 Bron, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Audric","family":"Cologne","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Claude Bernard Lyon 1, INSERM, CNRS, Centre de Recherche en Neurosciences de Lyon CRNL U1028 UMR5292,Genetics of Neurodevelopment Team, 69500 Bron, France"},{"name":"Institut national de recherche en sciences et technologies du num\u00e9rique Erable, Laboratoire de Biom\u00e9trie et Biologie Evolutive, UMR5558 CNRS, Universit\u00e9 Claude Bernard Lyon 1, 69622 Villeurbanne, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sophie","family":"Kaltenbach","sequence":"additional","affiliation":[{"name":"Department of Histology Embryology and Cytogenetics, Assistance Publique - 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