Evolutionary analyses reveal independent origins of gene repertoires and structural motifs associated to fast inactivation in calcium-selective TRPV channels.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
26 05 2020
Historique:
received: 21 01 2020
accepted: 23 04 2020
entrez: 28 5 2020
pubmed: 28 5 2020
medline: 28 11 2020
Statut: epublish

Résumé

Essential for calcium homeostasis, TRPV5 and TRPV6 are calcium-selective channels belonging to the transient receptor potential (TRP) gene family. In this study, we investigated the evolutionary history of these channels to add an evolutionary context to the already available physiological information. Phylogenetic analyses revealed that paralogs found in mammals, sauropsids, amphibians, and chondrichthyes, are the product of independent duplication events in the ancestor of each group. Within amniotes, we identified a traceable signature of three amino acids located at the amino-terminal intracellular region. The signature correlates with both the duplication events and the phenotype of fast inactivation observed in mammalian TRPV6 channels. Electrophysiological recordings and mutagenesis revealed that the signature sequence modulates the phenotype of fast inactivation in all clades of vertebrates but reptiles. A transcriptome analysis showed a change in tissue expression from gills, in marine vertebrates, to kidneys in terrestrial vertebrates. Our results highlight a cytoplasmatic structural triad composed by the Helix-Loop-Helix domain, the S2-S3 linker, and the TRP domain helix that is important on modulating the activity of calcium-selective TRPV channels.

Identifiants

pubmed: 32457384
doi: 10.1038/s41598-020-65679-6
pii: 10.1038/s41598-020-65679-6
pmc: PMC7250927
doi:

Substances chimiques

TRPV Cation Channels 0
Calcium SY7Q814VUP

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

8684

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Auteurs

Lisandra Flores-Aldama (L)

Instituto de Fisiología, Facultad de Medicina, Universidad Austral de Chile, Valdivia, Chile.
Programa de Doctorado en Ciencias mención Biología Celular y Molecular, Escuela de Graduados, Facultad de Ciencias, Universidad Austral de Chile, Valdivia, Chile.
Millennium Nucleus of Ion Channels-Associated Diseases (MiNICAD), Valdivia, Chile.

Michael W Vandewege (MW)

Department of Biology, Eastern New Mexico University, Portales, New Mexico, USA.

Kattina Zavala (K)

Instituto de Ciencias Ambientales y Evolutivas, Facultad de Ciencias, Universidad Austral de Chile, Valdivia, Chile.

Charlotte K Colenso (CK)

Instituto de Fisiología, Facultad de Medicina, Universidad Austral de Chile, Valdivia, Chile.

Wendy Gonzalez (W)

Millennium Nucleus of Ion Channels-Associated Diseases (MiNICAD), Valdivia, Chile.
Center for Bioinformatics and Molecular Simulations (CBSM) University of Talca, Talca, Chile.

Sebastian E Brauchi (SE)

Instituto de Fisiología, Facultad de Medicina, Universidad Austral de Chile, Valdivia, Chile. sbrauchi@uach.cl.
Millennium Nucleus of Ion Channels-Associated Diseases (MiNICAD), Valdivia, Chile. sbrauchi@uach.cl.

Juan C Opazo (JC)

Millennium Nucleus of Ion Channels-Associated Diseases (MiNICAD), Valdivia, Chile. jopazo@gmail.com.
Instituto de Ciencias Ambientales y Evolutivas, Facultad de Ciencias, Universidad Austral de Chile, Valdivia, Chile. jopazo@gmail.com.

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