Skip Navigation


Nucleic Acids Research Advance Access originally published online on November 28, 2008
Nucleic Acids Research 2009 37(1):298-308; doi:10.1093/nar/gkn925
This Article
Right arrow Full Text Freely available
Right arrow Print PDF (6519K) Freely available
Right arrow Screen PDF (404K) Freely available
Right arrowOA All Versions of this Article:
37/1/298    most recent
gkn925v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Ozanick, S. G.
Right arrow Articles by Anderson, J. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ozanick, S. G.
Right arrow Articles by Anderson, J. T.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 2009, Vol. 37, No. 1 298-308
© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

Rex1p deficiency leads to accumulation of precursor initiator tRNAMet and polyadenylation of substrate RNAs in Saccharomyces cerevisiae

Sarah G. Ozanick1, Xuying Wang1, Michael Costanzo2, Renee L. Brost2, Charles Boone2 and James T. Anderson1,*

1Department of Biological Sciences, Marquette University, Milwaukee, WI, USA and 2Banting and Best Department of Medical Research and the Department of Molecular Genetics, Donnelly CCBR, University of Toronto, Toronto, Canada

*To whom correspondence should be addressed. Tel: +1 414 288 1481; Fax: +1 414 288 7357; Email: james.anderson{at}mu.edu

Received August 5, 2008. Revised October 1, 2008. Accepted November 3, 2008.

A synthetic genetic array was used to identify lethal and slow-growth phenotypes produced when a mutation in TRM6, which encodes a tRNA modification enzyme subunit, was combined with the deletion of any non-essential gene in Saccharomyces cerevisiae. We found that deletion of the REX1 gene resulted in a slow-growth phenotype in the trm6-504 strain. Previously, REX1 was shown to be involved in processing the 3' ends of 5S rRNA and the dimeric tRNAArg-tRNAAsp. In this study, we have discovered a requirement for Rex1p in processing the 3' end of tRNAiMet precursors and show that precursor tRNAiMet accumulates in a trm6-504 rex1{Delta} strain. Loss of Rex1p results in polyadenylation of its substrates, including tRNAiMet, suggesting that defects in 3' end processing can activate the nuclear surveillance pathway. Finally, purified Rex1p displays Mg2+-dependent ribonuclease activity in vitro, and the enzyme is inactivated by mutation of two highly conserved amino acids.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.