{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T14:38:23Z","timestamp":1788446303665,"version":"build-2803163510"},"reference-count":76,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2022,7,1]],"date-time":"2022-07-01T00:00:00Z","timestamp":1656633600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R01 NS055925"],"award-info":[{"award-number":["R01 NS055925"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000057","name":"National Institute of General Medical Sciences","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Mol. Biosci."],"abstract":"<jats:p>Humans contain two nearly identical copies of <jats:italic>Survival Motor Neuron<\/jats:italic> genes, <jats:italic>SMN1<\/jats:italic> and <jats:italic>SMN2<\/jats:italic>. Deletion or mutation of <jats:italic>SMN1<\/jats:italic> causes spinal muscular atrophy (SMA), one of the leading genetic diseases associated with infant mortality. <jats:italic>SMN2<\/jats:italic> is unable to compensate for the loss of <jats:italic>SMN1<\/jats:italic> due to predominant exon 7 skipping, leading to the production of a truncated protein. Antisense oligonucleotide and small molecule-based strategies aimed at the restoration of <jats:italic>SMN2<\/jats:italic> exon 7 inclusion are approved therapies of SMA. Many cis-elements and transacting factors have been implicated in regulation of <jats:italic>SMN<\/jats:italic> exon 7 splicing. Also, several structural elements, including those formed by a long-distance interaction, have been implicated in the modulation of <jats:italic>SMN<\/jats:italic> exon 7 splicing. Several of these structures have been confirmed by enzymatic and chemical structure-probing methods. Additional structures formed by inter-intronic interactions have been predicted by computational algorithms. <jats:italic>SMN<\/jats:italic> genes generate a vast repertoire of circular RNAs through inter-intronic secondary structures formed by inverted Alu repeats present in large number in <jats:italic>SMN<\/jats:italic> genes. Here, we review the structural context of the exonic and intronic cis-elements that promote or prevent exon 7 recognition. We discuss how structural rearrangements triggered by single nucleotide substitutions could bring drastic changes in <jats:italic>SMN2<\/jats:italic> exon 7 splicing. We also propose potential mechanisms by which inter-intronic structures might impact the splicing outcomes.<\/jats:p>","DOI":"10.3389\/fmolb.2022.928581","type":"journal-article","created":{"date-parts":[[2022,7,1]],"date-time":"2022-07-01T06:15:26Z","timestamp":1656656126000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":17,"title":["Structural Context of a Critical Exon of Spinal Muscular Atrophy Gene"],"prefix":"10.3389","volume":"9","author":[{"given":"Natalia N.","family":"Singh","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Collin A.","family":"O'Leary","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Taylor","family":"Eich","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Walter N.","family":"Moss","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ravindra N.","family":"Singh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2022,7,1]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"e6136","DOI":"10.7717\/peerj.6136","article-title":"ScanFold: an Approach for Genome-wide Discovery of Local RNA Structural Elements-Applications to Zika Virus and HIV","volume":"6","author":"Andrews","year":"2018","journal-title":"PeerJ"},{"key":"B2","doi-asserted-by":"publisher","first-page":"385","DOI":"10.1146\/annurev-neuro-070918-050501","article-title":"Antisense Oligonucleotide Therapies for Neurodegenerative Diseases","volume":"42","author":"Bennett","year":"2019","journal-title":"Annu. 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