Slo2 potassium channel function depends on RNA editing-regulated expression of a SCYL1 protein.
Elife
; 92020 04 21.
Article
em En
| MEDLINE
| ID: mdl-32314960
ABSTRACT
Slo2 potassium channels play important roles in neuronal function, and their mutations in humans may cause epilepsies and cognitive defects. However, it is largely unknown how Slo2 is regulated by other proteins. Here we show that the function of C. elegans Slo2 (SLO-2) depends on adr-1, a gene important to RNA editing. ADR-1 promotes SLO-2 function not by editing the transcripts of slo-2 but those of scyl-1, which encodes an orthologue of mammalian SCYL1. Transcripts of scyl-1 are greatly decreased in adr-1 mutants due to deficient RNA editing at a single adenosine in their 3'-UTR. SCYL-1 physically interacts with SLO-2 in neurons. Single-channel open probability (Po) of neuronal SLO-2 is ~50% lower in scyl-1 knockout mutant than wild type. Moreover, human Slo2.2/Slack Po is doubled by SCYL1 in a heterologous expression system. These results suggest that SCYL-1/SCYL1 is an evolutionarily conserved regulator of Slo2 channels.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Regulação da Expressão Gênica
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Proteínas Adaptadoras de Transporte Vesicular
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Proteínas de Ligação a DNA
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Canais de Potássio Ativados por Sódio
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Neurônios
Limite:
Animals
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Humans
Idioma:
En
Revista:
Elife
Ano de publicação:
2020
Tipo de documento:
Article