QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online February 12, 2004

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Search for Related Content

Nuclear translation no nonsense

As every cell biology student knows, messenger RNA is transcribed in the nucleus but translated in the cytoplasm. The recent revelation that translation might also occur in the nucleus was therefore astounding. So, if translation is indeed active in the nucleus, what is its role there? Peter Cook and co-workers propose that it is to proofread RNA (see p. 899). They show that components of the transcriptional and translational machineries colocalize and copurify with the machinery for nonsense-mediated decay (NMD) – a proofreading mechanism that scans mRNA for inappropriate stop codons and destroys faulty messages. The authors go on to demonstrate that interactions between these different machineries are probably mediated by the RNA polymerase II (Pol II) C-terminal domain (CTD), which is implicated in maturation of mRNA transcripts. They also show that a non-nuclear protein (CD2) can be detected in nuclei – and so must be made there – and that its degradation is closely coupled to transcription. Cook and co-workers therefore argue that NMD uses the translational machinery to proofread newly transcribed mRNAs and that this is coupled to degradation of both faulty mRNAs and certain peptides produced as a consequence.

Related articles in JCS:

Molecular cross-talk between the transcription, translation, and nonsense-mediated decay machineries

Francisco J. Iborra, Alexandre E. Escargueil, Kon Y. Kwek, Alexandre Akoulitchev, and Peter R. Cook
JCS 2004 117: 899-906. [Abstract] [Full Text]  

This article has been cited by other articles:

				R. Wysocki, A. Javaheri, S. Allard, F. Sha, J. Cote, and S. J. Kron Role of Dot1-Dependent Histone H3 Methylation in G1 and S Phase DNA Damage Checkpoint Functions of Rad9 Mol. Cell. Biol., October 1, 2005; 25(19): 8430 - 8443. [Abstract] [Full Text] [PDF]

				A. S. Karumbati and T. E. Wilson Abrogation of the Chk1-Pds1 Checkpoint Leads to Tolerance of Persistent Single-Strand Breaks in Saccharomyces cerevisiae Genetics, April 1, 2005; 169(4): 1833 - 1844. [Abstract] [Full Text] [PDF]

				X. Jia, T. Weinert, and D. Lydall Mec1 and Rad53 Inhibit Formation of Single-Stranded DNA at Telomeres of Saccharomyces cerevisiae cdc13-1 Mutants Genetics, February 1, 2004; 166(2): 753 - 764. [Abstract] [Full Text] [PDF]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Search for Related Content