Tel1 activation by the MRX complex is sufficient for telomere length regulation but not for the DNA damage response in saccharomyces cerevisiae

Rebecca Keener, Carla J. Connelly, Carol W. Greider

Research output: Contribution to journalArticlepeer-review

Abstract

Previous models suggested that regulation of telomere length in Saccharomyces cerevisiae by Tel1(ATM) and Mec1(ATR) would parallel the established pathways regulating the DNA damage response. Here, we provide evidence that telomere length regulation differs from the DNA damage response in both the Tel1 and Mec1 pathways. We found that Rad53 mediates a Mec1 telomere length regulation pathway but is dispensable for Tel1 telomere length regulation, whereas in the DNA damage response, Rad53 is regulated by both Mec1 and Tel1. Using epistasis analysis with a Tel1 hypermorphic allele, Tel1-hy909, we found that the MRX complex is not required downstream of Tel1 for telomere elongation but is required downstream of Tel1 for the DNA damage response. Our data suggest that nucleolytic telomere end processing is not a required step for telomerase to elongate telomeres.

Original languageEnglish (US)
Pages (from-to)1271-1288
Number of pages18
JournalGenetics
Volume213
Issue number4
DOIs
StatePublished - 2019

Keywords

  • DNA damage response
  • Epistasis
  • MRX complex
  • Tel1
  • Telomere

ASJC Scopus subject areas

  • Genetics

Fingerprint Dive into the research topics of 'Tel1 activation by the MRX complex is sufficient for telomere length regulation but not for the DNA damage response in saccharomyces cerevisiae'. Together they form a unique fingerprint.

Cite this