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Particularly intriguing among these are multiple fragile X\u2010associated disorders (FXds), which arise from an expansion of CGG repeats in the 5\u2032 untranslated region of the\n                    <jats:italic>FMR1<\/jats:italic>\n                    gene. Despite arising from repeat expansions in the same gene, the clinical manifestations of FXds vary widely, encompassing developmental delays, parkinsonism, dementia, and an increased risk of infertility. FXds also exhibit molecular mechanisms observed in other REDs, that is, gene\u2010 and protein\u2010loss\u2010of\u2010function and RNA\u2010 and protein\u2010gain\u2010of\u2010function. The heterogeneity of phenotypes and pathomechanisms in FXds results from the different lengths of the CGG tract. As the number of repeats increases, the structures formed by RNA and DNA fragments containing CGG repeats change significantly, contributing to the diversity of FXd phenotypes and mechanisms. In this review, we discuss the role of RNA and DNA structures formed by expanded CGG repeats in driving FXd pathogenesis and how the genetic instability of CGG repeats is mediated by the complex interplay between transcription, DNA replication, and repair. We also discuss therapeutic strategies, including small molecules, antisense oligonucleotides, and CRISPR\u2010Cas systems, that target toxic RNA and DNA involved in the development of FXds.\n                  <\/jats:p>","DOI":"10.1002\/wrna.1874","type":"journal-article","created":{"date-parts":[[2024,11,10]],"date-time":"2024-11-10T23:56:03Z","timestamp":1731282963000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Contribution of\n                    <scp>DNA<\/scp>\n                    \/\n                    <scp>RNA<\/scp>\n                    Structures Formed by Expanded\n                    <scp>CGG<\/scp>\n                    \/\n                    <scp>CCG<\/scp>\n                    Repeats Within the\n                    <i>FMR1<\/i>\n                    Locus in the Pathogenesis of Fragile X\u2010Associated Disorders"],"prefix":"10.1002","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5318-8228","authenticated-orcid":false,"given":"Izabela","family":"Broniarek","sequence":"first","affiliation":[{"name":"Department of Gene Expression Institute of Molecular Biology and Biotechnology, Adam Mickiewicz University  Poznan Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7100-789X","authenticated-orcid":false,"given":"Daria","family":"Niewiadomska","sequence":"additional","affiliation":[{"name":"Department of Gene Expression Institute of Molecular Biology and Biotechnology, Adam Mickiewicz University  Poznan Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8352-9812","authenticated-orcid":false,"given":"Krzysztof","family":"Sobczak","sequence":"additional","affiliation":[{"name":"Department of Gene Expression Institute of Molecular Biology and Biotechnology, Adam 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