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Alu insertion-mediated dsRNA structure formation with pre-existing Alu elements as a disease-causing mechanism.
Masson, Emmanuelle; Maestri, Sandrine; Bordeau, Valérie; Cooper, David N; Férec, Claude; Chen, Jian-Min.
Afiliación
  • Masson E; Univ Brest, Inserm, EFS, UMR 1078, GGB, 29200 Brest, France; CHRU Brest, 29200 Brest, France.
  • Maestri S; Univ Brest, Inserm, EFS, UMR 1078, GGB, 29200 Brest, France; CHRU Brest, 29200 Brest, France.
  • Bordeau V; Inserm U1230 BRM (Bacterial RNAs and Medicine), Université de Rennes, 35043 Rennes, France.
  • Cooper DN; Institute of Medical Genetics, School of Medicine, Cardiff University, Cardiff CF14 4XN, UK.
  • Férec C; Univ Brest, Inserm, EFS, UMR 1078, GGB, 29200 Brest, France.
  • Chen JM; Univ Brest, Inserm, EFS, UMR 1078, GGB, 29200 Brest, France. Electronic address: jian-min.chen@univ-brest.fr.
Am J Hum Genet ; 111(10): 2176-2189, 2024 Oct 03.
Article en En | MEDLINE | ID: mdl-39265574
ABSTRACT
We previously identified a homozygous Alu insertion variant (Alu_Ins) in the 3'-untranslated region (3'-UTR) of SPINK1 as the cause of severe infantile isolated exocrine pancreatic insufficiency. Although we established that Alu_Ins leads to the complete loss of SPINK1 mRNA expression, the precise mechanisms remained elusive. Here, we aimed to elucidate these mechanisms through a hypothesis-driven approach. Initially, we speculated that, owing to its particular location, Alu_Ins could independently disrupt mRNA 3' end formation and/or affect other post-transcriptional processes such as nuclear export and translation. However, employing a 3'-UTR luciferase reporter assay, Alu_Ins was found to result in only an ∼50% reduction in luciferase activity compared to wild type, which is insufficient to account for the severe pancreatic deficiency in the Alu_Ins homozygote. We then postulated that double-stranded RNA (dsRNA) structures formed between Alu elements, an upstream mechanism regulating gene expression, might be responsible. Using RepeatMasker, we identified two Alu elements within SPINK1's third intron, both oriented oppositely to Alu_Ins. Through RNAfold predictions and full-length gene expression assays, we investigated orientation-dependent interactions between these Alu repeats. We provide compelling evidence to link the detrimental effect of Alu_Ins to extensive dsRNA structures formed between Alu_Ins and pre-existing intronic Alu sequences, including the restoration of SPINK1 mRNA expression by aligning all three Alu elements in the same orientation. Given the widespread presence of Alu elements in the human genome and the potential for new Alu insertions at almost any locus, our findings have important implications for detecting and interpreting Alu insertions in disease genes.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: ARN Bicatenario / Regiones no Traducidas 3' / Elementos Alu Límite: Humans Idioma: En Revista: Am J Hum Genet Año: 2024 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: ARN Bicatenario / Regiones no Traducidas 3' / Elementos Alu Límite: Humans Idioma: En Revista: Am J Hum Genet Año: 2024 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Estados Unidos