Titin domains with reduced core hydrophobicity cause dilated cardiomyopathy

The underlying genetic defect in most cases of dilated cardiomyopathy (DCM), a common inherited heart disease, remains unknown. Intriguingly, many patients carry single missense variants of uncertain pathogenicity targeting the giant protein titin, a fundamental sarcomere component. To explore the d...

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Autores: Martínez-Martín, Inés, Crousilles, Audrey, Ochoa, Juan Pablo, Velázquez-Carreras, Diana, Mortensen, Simon A., Herrero-Galán, Elías, Delgado Blanco, Javier, Domínguez, Fernando, García-Pavía, Pablo, Sancho, David de, Wilmanns, Matthias, Alegre-Cebollada, Jorge
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2023
País:España
Institución:Universitat Pompeu Fabra
Repositorio:Repositorio Digital de la UPF
OAI Identifier:oai:repositori.upf.edu:10230/59088
Acceso en línea:http://hdl.handle.net/10230/59088
http://dx.doi.org/10.1016/j.celrep.2023.113490
Access Level:acceso abierto
Palabra clave:CP: Genomics
CP: Molecular biology
Titin
Missense variants
Dilated cardiomyopathy
Hydrophobicity
Protein stability
Mutation
Protein structure
Molecular dynamics
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spelling Titin domains with reduced core hydrophobicity cause dilated cardiomyopathyMartínez-Martín, InésCrousilles, AudreyOchoa, Juan PabloVelázquez-Carreras, DianaMortensen, Simon A.Herrero-Galán, ElíasDelgado Blanco, JavierDomínguez, FernandoGarcía-Pavía, PabloSancho, David deWilmanns, MatthiasAlegre-Cebollada, JorgeCP: GenomicsCP: Molecular biologyTitinMissense variantsDilated cardiomyopathyHydrophobicityProtein stabilityMutationProtein structureMolecular dynamicsThe underlying genetic defect in most cases of dilated cardiomyopathy (DCM), a common inherited heart disease, remains unknown. Intriguingly, many patients carry single missense variants of uncertain pathogenicity targeting the giant protein titin, a fundamental sarcomere component. To explore the deleterious potential of these variants, we first solved the wild-type and mutant crystal structures of I21, the titin domain targeted by pathogenic variant p.C3575S. Although both structures are remarkably similar, the reduced hydrophobicity of deeply buried position 3575 strongly destabilizes the mutant domain, a scenario supported by molecular dynamics simulations and by biochemical assays that show no disulfide involving C3575. Prompted by these observations, we have found that thousands of similar hydrophobicity-reducing variants associate specifically with DCM. Hence, our results imply that titin domain destabilization causes DCM, a conceptual framework that not only informs pathogenicity assessment of gene variants but also points to therapeutic strategies counterbalancing protein destabilization.J.A.-C. acknowledges funding from the Ministerio de Ciencia e Innovación (MCIN, MCIN/AEI/10.13039/501100011033) through grants BIO2017-83640-P (AEI/FEDER, EU), PID2020-120426GB-I00, and RED2022-134242-T and the Regional Government of Madrid (grant Tec4Bio S2018/NMT-4443, 50% co-financed by the European Social Fund and the European Regional Development Fund for the programming period 2014–2020). The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the MCIN, and the Pro CNIC Foundation and is a Severo Ochoa Center of Excellence (grant CEX2020-001041-S funded by MCIN). I.M.-M. holds a fellowship from 'la Caixa' Foundation (ID 100010434, fellowship code LCF/BQ/DR20/11790009) and received support from a Erasmus + Training fellowship. Financial support to D.d.S. comes from Eusko Jaurlaritza (Basque Government) through the project IT1584-22 and from the MCIN through grants PID2021-127907NB-I00 (AEI/FEDER, UE) and RYC-2016-19590 (AEI/FSE, EU). We thank Maria Rosaria Pricolo for analysis support with database analysis, Vytautas Gapsys for his assistance using the pmx software package, and the staff at the DIPC Supercomputing Center and the Sample Preparation and Characterization facility of the EMBL Hamburg Unit for technical support. The synchrotron data were collected at beamline operated by EMBL Hamburg at the PETRA III storage ring (DESY, Hamburg, Germany). We thank the Spectroscopy and Nuclear Magnetic Resonance Core Unit at CNIO for access to CD instrumentation. Biorender.com was used as a source for icons included in some of the figures of this paper.Elsevier202420242023info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfapplication/pdfhttp://hdl.handle.net/10230/59088http://dx.doi.org/10.1016/j.celrep.2023.113490reponame:Repositorio Digital de la UPFinstname:Universitat Pompeu FabraInglésCell Rep. 2023 Dec 26;42(12):113490info:eu-repo/grantAgreement/ES/2PE/BIO2017-83640-Pinfo:eu-repo/grantAgreement/ES/2PE/PID2020-120426GB-I00info:eu-repo/grantAgreement/ES/3PE/RED2022-134242-Tinfo:eu-repo/grantAgreement/ES/2PE/CEX2020-001041-Sinfo:eu-repo/grantAgreement/ES/3PE/PID2021-127907NB-I00info:eu-repo/grantAgreement/ES/1PE/RYC-2016-19590© 2023 The Authors. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).http://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:repositori.upf.edu:10230/590882026-06-12T07:21:37Z
dc.title.none.fl_str_mv Titin domains with reduced core hydrophobicity cause dilated cardiomyopathy
title Titin domains with reduced core hydrophobicity cause dilated cardiomyopathy
spellingShingle Titin domains with reduced core hydrophobicity cause dilated cardiomyopathy
Martínez-Martín, Inés
CP: Genomics
CP: Molecular biology
Titin
Missense variants
Dilated cardiomyopathy
Hydrophobicity
Protein stability
Mutation
Protein structure
Molecular dynamics
title_short Titin domains with reduced core hydrophobicity cause dilated cardiomyopathy
title_full Titin domains with reduced core hydrophobicity cause dilated cardiomyopathy
title_fullStr Titin domains with reduced core hydrophobicity cause dilated cardiomyopathy
title_full_unstemmed Titin domains with reduced core hydrophobicity cause dilated cardiomyopathy
title_sort Titin domains with reduced core hydrophobicity cause dilated cardiomyopathy
dc.creator.none.fl_str_mv Martínez-Martín, Inés
Crousilles, Audrey
Ochoa, Juan Pablo
Velázquez-Carreras, Diana
Mortensen, Simon A.
Herrero-Galán, Elías
Delgado Blanco, Javier
Domínguez, Fernando
García-Pavía, Pablo
Sancho, David de
Wilmanns, Matthias
Alegre-Cebollada, Jorge
author Martínez-Martín, Inés
author_facet Martínez-Martín, Inés
Crousilles, Audrey
Ochoa, Juan Pablo
Velázquez-Carreras, Diana
Mortensen, Simon A.
Herrero-Galán, Elías
Delgado Blanco, Javier
Domínguez, Fernando
García-Pavía, Pablo
Sancho, David de
Wilmanns, Matthias
Alegre-Cebollada, Jorge
author_role author
author2 Crousilles, Audrey
Ochoa, Juan Pablo
Velázquez-Carreras, Diana
Mortensen, Simon A.
Herrero-Galán, Elías
Delgado Blanco, Javier
Domínguez, Fernando
García-Pavía, Pablo
Sancho, David de
Wilmanns, Matthias
Alegre-Cebollada, Jorge
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv CP: Genomics
CP: Molecular biology
Titin
Missense variants
Dilated cardiomyopathy
Hydrophobicity
Protein stability
Mutation
Protein structure
Molecular dynamics
topic CP: Genomics
CP: Molecular biology
Titin
Missense variants
Dilated cardiomyopathy
Hydrophobicity
Protein stability
Mutation
Protein structure
Molecular dynamics
description The underlying genetic defect in most cases of dilated cardiomyopathy (DCM), a common inherited heart disease, remains unknown. Intriguingly, many patients carry single missense variants of uncertain pathogenicity targeting the giant protein titin, a fundamental sarcomere component. To explore the deleterious potential of these variants, we first solved the wild-type and mutant crystal structures of I21, the titin domain targeted by pathogenic variant p.C3575S. Although both structures are remarkably similar, the reduced hydrophobicity of deeply buried position 3575 strongly destabilizes the mutant domain, a scenario supported by molecular dynamics simulations and by biochemical assays that show no disulfide involving C3575. Prompted by these observations, we have found that thousands of similar hydrophobicity-reducing variants associate specifically with DCM. Hence, our results imply that titin domain destabilization causes DCM, a conceptual framework that not only informs pathogenicity assessment of gene variants but also points to therapeutic strategies counterbalancing protein destabilization.
publishDate 2023
dc.date.none.fl_str_mv 2023
2024
2024
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/10230/59088
http://dx.doi.org/10.1016/j.celrep.2023.113490
url http://hdl.handle.net/10230/59088
http://dx.doi.org/10.1016/j.celrep.2023.113490
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Cell Rep. 2023 Dec 26;42(12):113490
info:eu-repo/grantAgreement/ES/2PE/BIO2017-83640-P
info:eu-repo/grantAgreement/ES/2PE/PID2020-120426GB-I00
info:eu-repo/grantAgreement/ES/3PE/RED2022-134242-T
info:eu-repo/grantAgreement/ES/2PE/CEX2020-001041-S
info:eu-repo/grantAgreement/ES/3PE/PID2021-127907NB-I00
info:eu-repo/grantAgreement/ES/1PE/RYC-2016-19590
dc.rights.none.fl_str_mv http://creativecommons.org/licenses/by/4.0/
info:eu-repo/semantics/openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:Repositorio Digital de la UPF
instname:Universitat Pompeu Fabra
instname_str Universitat Pompeu Fabra
reponame_str Repositorio Digital de la UPF
collection Repositorio Digital de la UPF
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repository.mail.fl_str_mv
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