Premature termination codon readthrough in human cells occurs in novel cytoplasmic foci and requires UPF proteins.
J Cell Sci
; 130(18): 3009-3022, 2017 Sep 15.
Article
en En
| MEDLINE
| ID: mdl-28743738
ABSTRACT
Nonsense-mutation-containing messenger ribonucleoprotein particles (mRNPs) transit through cytoplasmic foci called P-bodies before undergoing nonsense-mediated mRNA decay (NMD), a cytoplasmic mRNA surveillance mechanism. This study shows that the cytoskeleton modulates transport of nonsense-mutation-containing mRNPs to and from P-bodies. Impairing the integrity of cytoskeleton causes inhibition of NMD. The cytoskeleton thus plays a crucial role in NMD. Interestingly, disruption of actin filaments results in both inhibition of NMD and activation of premature termination codon (PTC) readthrough, while disruption of microtubules causes only NMD inhibition. Activation of PTC readthrough occurs concomitantly with the appearance of cytoplasmic foci containing UPF proteins and mRNAs with nonsense mutations but lacking the P-body marker DCP1a. These findings demonstrate that in human cells, PTC readthrough occurs in novel 'readthrough bodies' and requires the presence of UPF proteins.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Codón sin Sentido
/
ARN Helicasas
/
Citoplasma
Límite:
Humans
Idioma:
En
Revista:
J Cell Sci
Año:
2017
Tipo del documento:
Article
País de afiliación:
Francia