Eukaryotic Cell
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Taylor, R.
Right arrow Articles by Atkin, A. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Taylor, R.
Right arrow Articles by Atkin, A. L.
Eukaryotic Cell, December 2005, p. 2066-2077, Vol. 4, No. 12
1535-9778/05/$08.00+0     doi:10.1128/EC.4.12.2066-2077.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Gene Set Coregulated by the Saccharomyces cerevisiae Nonsense-Mediated mRNA Decay Pathway

Rachel Taylor,{dagger} Bessie Wanja Kebaara,{dagger} Tara Nazarenus, Ashley Jones, Rena Yamanaka, Rachel Uhrenholdt, Jason P. Wendler, and Audrey L. Atkin*

School of Biological Sciences, University of Nebraska—Lincoln, Lincoln, Nebraska 68588-0666

Received 11 April 2005/ Accepted 27 September 2005

The nonsense-mediated mRNA decay (NMD) pathway has historically been thought of as an RNA surveillance system that degrades mRNAs with premature translation termination codons, but the NMD pathway of Saccharomyces cerevisiae has a second role regulating the decay of some wild-type mRNAs. In S. cerevisiae, a significant number of wild-type mRNAs are affected when NMD is inactivated. These mRNAs are either wild-type NMD substrates or mRNAs whose abundance increases as an indirect consequence of NMD. A current challenge is to sort the mRNAs that accumulate when NMD is inactivated into direct and indirect targets. We have developed a bioinformatics-based approach to address this challenge. Our approach involves using existing genomic and function databases to identify transcription factors whose mRNAs are elevated in NMD-deficient cells and the genes that they regulate. Using this strategy, we have investigated a coregulated set of genes. We have shown that NMD regulates accumulation of ADR1 and GAL4 mRNAs, which encode transcription activators, and that Adr1 is probably a transcription activator of ATS1. This regulation is physiologically significant because overexpression of ADR1 causes a respiratory defect that mimics the defect seen in strains with an inactive NMD pathway. This strategy is significant because it allows us to classify the genes regulated by NMD into functionally related sets, an important step toward understanding the role NMD plays in the normal functioning of yeast cells.


* Corresponding author. Mailing address: School of Biological Sciences, University of Nebraska—Lincoln, Lincoln, NE 68588-0666. Phone: (402) 472-1411. Fax: (402) 472-8722. E-mail: aatkin1{at}unl.edu.

{dagger} R.T. and B.W.K. contributed equally to this work.


Eukaryotic Cell, December 2005, p. 2066-2077, Vol. 4, No. 12
1535-9778/05/$08.00+0     doi:10.1128/EC.4.12.2066-2077.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Appl. Environ. Microbiol. Infect. Immun. J. Bacteriol.
Mol. Cell Biol. Microbiol. Mol. Biol. Rev. ALL ASM JOURNALS
Copyright © 2005 by the American Society for Microbiology.