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Molecular and Cellular Biology, December 2003, p. 8450-8461, Vol. 23, No. 23
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.23.8450-8461.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

End Resection Initiates Genomic Instability in the Absence of Telomerase

Jennifer A. Hackett1,2 and Carol W. Greider2*

Predoctoral Training Program in Human Genetics and Molecular Biology,1 Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland 212052

Received 24 July 2003/ Returned for modification 27 August 2003/ Accepted 5 September 2003

Telomere dysfunction causes genomic instability. However, the mechanism that initiates this instability when telomeres become short is unclear. We measured the mutation rate and loss of heterozygosity along a chromosome arm in diploid yeast that lacked telomerase to distinguish between mechanisms for the initiation of instability. Sequence loss was localized near chromosome ends in the absence of telomerase but not after breakage of a dicentric chromosome. In the absence of telomerase, the increase in mutation rate is dependent on the exonuclease Exo1p. Thus, exonucleolytic end resection, rather than chromosome fusion and breakage, is the primary mechanism that initiates genomic instability when telomeres become short.

* Corresponding author. Mailing address: Department of Molecular Biology and Genetics, 725 N. Wolfe St., Baltimore, MD 21205. Phone: (410) 614-6506. Fax: (410) 614-2987. E-mail: cgreider{at}jhmi.edu.

Molecular and Cellular Biology, December 2003, p. 8450-8461, Vol. 23, No. 23
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.23.8450-8461.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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