Journal
JOURNAL OF CELL SCIENCE
Volume 130, Issue 18, Pages 3009-3022Publisher
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/jcs.198176
Keywords
Readthrough body; Nonsense-mediated mRNA decay; UPF protein; Cytoskeleton; P-body
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Funding
- Association Francaise contre les Myopathies
- Association Vaincre la Mucoviscidose
- Canceropole Nord Ouest
- Fondation ARC pour la Recherche sur le Cancer
- Pennsylvania Cystic Fibrosis Inc.
- Cystic Fibrosis Research Inc.
- National Institutes of Health [DK104681]
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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.
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