End Resection Initiates Genomic Instability in the Absence of Telomerase

Jennifer A. Hackett, Carol W. Greider

Research output: Contribution to journalArticlepeer-review

74 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)8450-8461
Number of pages12
JournalMolecular and cellular biology
Issue number23
StatePublished - Dec 2003

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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