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Genetics. 2019 Oct 23. pii: genetics.302713.2019. doi: 10.1534/genetics.119.302713. [Epub ahead of print]

Tel1 Activation by the MRX Complex Is Sufficient for Telomere Length Regulation but Not for the DNA Damage Response in Saccharomyces cerevisiae.

Author information

1
Johns Hopkins University School of Medicine.
2
Johns Hopkins University School of Medicine cgreider@jhmi.edu.

Abstract

Previous models suggested that regulation of telomere length in S. 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 T--el1 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.

KEYWORDS:

DNA damage response; MRX complex; Tel1; epistasis; telomere

PMID:
31645360
DOI:
10.1534/genetics.119.302713
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