Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.


Journal

Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876

Informations de publication

Date de publication:
26 01 2021
Historique:
entrez: 20 1 2021
pubmed: 21 1 2021
medline: 12 6 2021
Statut: ppublish

Résumé

Epistasis refers to the dependence of a mutation on other mutation(s) and the genetic context in general. In the context of human disorders, epistasis complicates the spectrum of disease symptoms and has been proposed as a major contributor to variations in disease outcome. The nonadditive relationship between mutations and the lack of complete understanding of the underlying physiological effects limit our ability to predict phenotypic outcome. Here, we report positive epistasis between intragenic mutations in the cystic fibrosis transmembrane conductance regulator (CFTR)-the gene responsible for cystic fibrosis (CF) pathology. We identified a synonymous single-nucleotide polymorphism (sSNP) that is invariant for the CFTR amino acid sequence but inverts translation speed at the affected codon. This sSNP in

Identifiants

pubmed: 33468668
pii: 2010612118
doi: 10.1073/pnas.2010612118
pmc: PMC7848603
pii:
doi:

Substances chimiques

CFTR protein, human 0
Codon 0
RNA, Messenger 0
Cystic Fibrosis Transmembrane Conductance Regulator 126880-72-6

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NHLBI NIH HHS
ID : K99 HL151965
Pays : United States
Organisme : NHLBI NIH HHS
ID : R00 HL151965
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL136414
Pays : United States

Déclaration de conflit d'intérêts

The authors declare no competing interest.

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Auteurs

Robert Rauscher (R)

Biochemistry and Molecular Biology, Department of Chemistry, University of Hamburg, 20146 Hamburg, Germany.

Giovana B Bampi (GB)

Biochemistry and Molecular Biology, Department of Chemistry, University of Hamburg, 20146 Hamburg, Germany.

Marta Guevara-Ferrer (M)

Biochemistry and Molecular Biology, Department of Chemistry, University of Hamburg, 20146 Hamburg, Germany.

Leonardo A Santos (LA)

Biochemistry and Molecular Biology, Department of Chemistry, University of Hamburg, 20146 Hamburg, Germany.

Disha Joshi (D)

Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30322.
Children's Healthcare of Atlanta, Atlanta, GA 30322.

David Mark (D)

Biochemistry and Molecular Biology, Department of Chemistry, University of Hamburg, 20146 Hamburg, Germany.

Lisa J Strug (LJ)

Program in Genetics & Genome Biology, The Hospital for Sick Children, Toronto M5G 0A4, Canada.
Department of Statistical Sciences, Computer Science and Division of Biostatistics, University of Toronto, Toronto M5G 0A4, Canada.

Johanna M Rommens (JM)

Program in Genetics & Genome Biology, The Hospital for Sick Children, Toronto M5G 0A4, Canada.

Manfred Ballmann (M)

Pediatric Clinic, Universitätsmedizin, 18057 Rostock, Germany.

Eric J Sorscher (EJ)

Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30322.
Children's Healthcare of Atlanta, Atlanta, GA 30322.

Kathryn E Oliver (KE)

Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30322.
Children's Healthcare of Atlanta, Atlanta, GA 30322.

Zoya Ignatova (Z)

Biochemistry and Molecular Biology, Department of Chemistry, University of Hamburg, 20146 Hamburg, Germany; zoya.ignatova@uni-hamburg.de.

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Classifications MeSH