Sgs1 helicase and two nucleases Dna2 and Exo1 resect DNA double-strand break ends.

Telomeres are the protein-DNA structures at the ends of eukaryotic chromosomes. In yeast, and probably most other eukaryotes, telomeres are essential. They allow the cell to distinguish intact from broken chromosomes, protect chromosomes from degradation, and are substrates for novel replication mechanisms. Telomeres are usually replicated by telomerase, a telomere-specific reverse transcriptase, although telomerase-independent mechanisms of telomere maintenance exist. Telomere replication is both cell cycle- and developmentally regulated, and its control is likely to be complex. Because telomere loss causes the kinds of chromosomal changes associated with cancer and aging, an understanding of telomere biology has medical relevance.

http://science.sciencemag.org/content/sci/270/5242/1601.full.pdf

Telomeres: Beginning to Understand the End

DNA Replication through G-Quadruplex Motifs Is Promoted by the Saccharomyces cerevisiae Pif1 DNA Helicase

Most human cancer cells show signs of genome instability, ranging from elevated mutation rates to gross chromosomal rearrangements and alterations in chromosome number. Little is known about the molecular mechanisms that generate this instability or how it is suppressed in normal cells. Recent studies of the yeast Saccharomyces cerevisiae have begun to uncover the extensive and redundant pathways that keep the rate of genome rearrangements at very low levels. These studies, which we review here, have implicated more than 50 genes in the suppression of genome instability, including genes that function in S-phase checkpoints, recombination pathways, and telomere maintenance. Human homologs of several of these genes have well-established roles as tumor suppressors, consistent with the hypothesis that the mechanisms preserving genome stability in yeast are the same mechanisms that go awry in cancer.

https://science.sciencemag.org/content/sci/297/5581/552.full.pdf

Maintenance of genome stability in Saccharomyces cerevisiae.

The Saccharomyces cerevisiae Pif1 helicase is the prototypical member of the Pif1 DNA helicase family, which is conserved from bacteria to humans. Here we show that exceptionally potent G-quadruplex unwinding is conserved among Pif1 helicases. Moreover, Pif1 helicases from organisms separated by more than 3 billion years of evolution suppressed DNA damage at G-quadruplex motifs in yeast. The G-quadruplex-induced damage generated in the absence of Pif1 helicases led to new genetic and epigenetic changes. Furthermore, when expressed in yeast, human PIF1 suppressed both G-quadruplex-associated DNA damage and telomere lengthening.

/pdf/pif1-family-helicases-suppress-genome-instability-at-g-g37d6vl879.pdf

Pif1 family helicases suppress genome instability at G-quadruplex motifs

https://www.cell.com/cell/pdf/0092-8674(94)90179-1.pdf

The saccharomyces PIF1 DNA helicase inhibits telomere elongation and de novo telomere formation

Method for affecting viability of a eucaryotic cell by contacting the cell with a modulator of the activity of a PIF-1-type helicase in the cell. Such contacting specifically increases or decreases the specific activity of the helicase in the cell.

Modulation of PIF-1-type helicases

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The saccharomyces PIF1 DNA helicase inhibits telomere elongation and de novo telomere formation

Modulation of PIF-1-type helicases