RRC ID 90098
著者 Shen Y, Gupta K, Tan-Wong SM, Wen S, Fisher CA, Tamon L, Proudfoot NJ, Gibbons RJ, Higgs DR.
タイトル ATRX loss couples genome instability at a G-rich repeat to dysregulation of human alpha-globin expression.
ジャーナル Nat Commun
Abstract Germline mutations in the chromatin remodelling protein ATRX cause a severe developmental disorder associated with α-thalassemia. In addition, ATRX is amongst the twenty genes most frequently mutated in cancer. How ATRX mutations alter gene expression remains unclear. Using the α-globin locus as a model, here we show that ATRX deficiency downregulates α-globin in a subset of cells exhibiting DNA damage. A G-rich repeat at the α-globin locus serves as a potential site of G-quadruplex formation and DNA damage. ATRX binds this repeat co-transcriptionally, and its loss increases R-loop accumulation at this site, leading to local DNA damage and transcriptional disruption in cis. Deletion of this repeat abolishes this effect, while targeted DNA damage reinstates it. These findings reveal a mechanism linking ATRX's role in genome stability to transcriptional regulation and uncover a molecular basis of human genetic disease mediated via a distal G-rich repeat.
巻・号 17(1)
公開日 2026-2-14
DOI 10.1038/s41467-026-69169-7
PII 10.1038/s41467-026-69169-7
PMID 41688464
PMC PMC13018553
MeSH DNA Damage DNA Helicases* / genetics DNA Helicases* / metabolism G-Quadruplexes Gene Expression Regulation Genomic Instability* Humans Nuclear Proteins* / genetics Nuclear Proteins* / metabolism R-Loop Structures Transcription, Genetic X-linked Nuclear Protein* / genetics X-linked Nuclear Protein* / metabolism alpha-Globins* / genetics alpha-Globins* / metabolism alpha-Thalassemia / genetics
リソース情報
ヒト・動物細胞 HUDEP-2(RCB4557)