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Eukaryotic Cell, February 2003, p. 134-142, Vol. 2, No. 1
1535-9778/03/$08.00+0     DOI: 10.1128/EC.2.1.134-142.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

mRNAs Encoding Telomerase Components and Regulators Are Controlled by UPF Genes in Saccharomyces cerevisiae

Jeffrey N. Dahlseid,1,{dagger} Jodi Lew-Smith,2,{ddagger} Michael J. Lelivelt,3 Shinichiro Enomoto,2 Amanda Ford,3 Michelle Desruisseaux,2 Mark McClellan,2 Neal Lue,4 Michael R. Culbertson,3 and Judith Berman2,5*

Department of Chemistry, St. Olaf College, Northfield, Minnesota 55057,1 Department of Genetics, Cell Biology and Development,2 Department of Microbiology, University of Minnesota, Minneapolis, Minnesota 55455,5 Laboratories of Genetics and Molecular Biology, University of Wisconsin, Madison, Wisconsin 53706,3 Department of Microbiology and Immunology, Weill Medical College of Cornell University, New York, New York 100214

Received 13 August 2002/ Accepted 31 October 2002

Telomeres, the chromosome ends, are maintained by a balance of activities that erode and replace the terminal DNA sequences. Furthermore, telomere-proximal genes are often silenced in an epigenetic manner. In Saccharomyces cerevisiae, average telomere length and telomeric silencing are reduced by loss of function of UPF genes required in the nonsense-mediated mRNA decay (NMD) pathway. Because NMD controls the mRNA levels of several hundred wild-type genes, we tested the hypothesis that NMD affects the expression of genes important for telomere functions. In upf mutants, high-density oligonucleotide microarrays and Northern blots revealed that the levels of mRNAs were increased for genes encoding the telomerase catalytic subunit (Est2p), in vivo regulators of telomerase (Est1p, Est3p, Stn1p, and Ten1p), and proteins that affect telomeric chromatin structure (Sas2p and Orc5p). We investigated whether overexpressing these genes could mimic the telomere length and telomeric silencing phenotypes seen previously in upf mutant strains. Increased dosage of STN1, especially in combination with increased dosage of TEN1, resulted in reduced telomere length that was indistinguishable from that in upf mutants. Increased levels of STN1 together with EST2 resulted in reduced telomeric silencing like that of upf mutants. The half-life of STN1 mRNA was not altered in upf mutant strains, suggesting that an NMD-controlled transcription factor regulates the levels of STN1 mRNA. Together, these results suggest that NMD maintains the balance of gene products that control telomere length and telomeric silencing primarily by maintaining appropriate levels of STN1, TEN1, and EST2 mRNA.

* Corresponding author. Mailing address: Department of Genetics, Cell Biology, and Development, University of Minnesota, 6-160 Jackson Hall, 321 Church St. SE, Minneapolis, MN 55455. Phone: (612) 625-1971. Fax: (612) 625-6140. E-mail: judith{at}cbs.umn.edu.

{dagger} Present address: Departments of Biology and Chemistry, Gustavus Adolphus College, Saint Peter, MN 56082.

{ddagger} Present address: Incyte Genomics, Inc., Proteome Division, Beverly, MA 01915.

Eukaryotic Cell, February 2003, p. 134-142, Vol. 2, No. 1
1535-9778/03/$08.00+0     DOI: 10.1128/EC.2.1.134-142.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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