Publication

A sharp Pif1-dependent threshold separates DNA double-strand breaks from critically short telomeres

Strecker, J., Stinus, S., Caballero, M. P., Szilard, R. K., Chang, M. & Durocher, D., 3-Aug-2017, In : eLife. 6, 59 p., e23783.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Strecker, J., Stinus, S., Caballero, M. P., Szilard, R. K., Chang, M., & Durocher, D. (2017). A sharp Pif1-dependent threshold separates DNA double-strand breaks from critically short telomeres. eLife, 6, [e23783]. https://doi.org/10.7554/eLife.23783

Author

Strecker, Jonathan ; Stinus, Sonia ; Caballero, Mariana Pliego ; Szilard, Rachel K. ; Chang, Michael ; Durocher, Daniel. / A sharp Pif1-dependent threshold separates DNA double-strand breaks from critically short telomeres. In: eLife. 2017 ; Vol. 6.

Harvard

Strecker, J, Stinus, S, Caballero, MP, Szilard, RK, Chang, M & Durocher, D 2017, 'A sharp Pif1-dependent threshold separates DNA double-strand breaks from critically short telomeres', eLife, vol. 6, e23783. https://doi.org/10.7554/eLife.23783

Standard

A sharp Pif1-dependent threshold separates DNA double-strand breaks from critically short telomeres. / Strecker, Jonathan; Stinus, Sonia; Caballero, Mariana Pliego; Szilard, Rachel K.; Chang, Michael; Durocher, Daniel.

In: eLife, Vol. 6, e23783, 03.08.2017.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Strecker J, Stinus S, Caballero MP, Szilard RK, Chang M, Durocher D. A sharp Pif1-dependent threshold separates DNA double-strand breaks from critically short telomeres. eLife. 2017 Aug 3;6. e23783. https://doi.org/10.7554/eLife.23783


BibTeX

@article{598b5217186043ac95ff78449c6bc9f6,
title = "A sharp Pif1-dependent threshold separates DNA double-strand breaks from critically short telomeres",
abstract = "DNA double-strand breaks (DSBs) and short telomeres are structurally similar, yet have diametrically opposed fates. Cells must repair DSBs while blocking the action of telomerase on these ends. Short telomeres must avoid recognition by the DNA damage response while promoting telomerase recruitment. In Saccharomyces cerevisiae, the Pif1 helicase, a telomerase inhibitor, lies at the interface of these end-fate decisions. Using Pif1 as a sensor, we uncover a transition point in which 34 bp of telomeric (TG(1-3))(n) repeat sequence renders a DNA end insensitive to Pif1 action, thereby enabling extension by telomerase. A similar transition point exists at natural chromosome ends, where telomeres shorter than similar to 40 bp are inefficiently extended by telomerase. This phenomenon is not due to known Pif1 modifications and we instead propose that Cdc13 renders TG(34+) ends insensitive to Pif1 action. We contend that the observed threshold of Pif1 activity defines a dividing line between DSBs and telomeres.",
keywords = "SACCHAROMYCES-CEREVISIAE TELOMERES, LENGTH REGULATION, REPEAT DIVERGENCE, CHROMOSOME ENDS, CDC13 PROTEIN, IN-VIVO, YEAST, BINDING, ELONGATION, SEQUENCES",
author = "Jonathan Strecker and Sonia Stinus and Caballero, {Mariana Pliego} and Szilard, {Rachel K.} and Michael Chang and Daniel Durocher",
year = "2017",
month = aug,
day = "3",
doi = "10.7554/eLife.23783",
language = "English",
volume = "6",
journal = "eLife",
issn = "2050-084X",
publisher = "ELIFE SCIENCES PUBLICATIONS LTD",

}

RIS

TY - JOUR

T1 - A sharp Pif1-dependent threshold separates DNA double-strand breaks from critically short telomeres

AU - Strecker, Jonathan

AU - Stinus, Sonia

AU - Caballero, Mariana Pliego

AU - Szilard, Rachel K.

AU - Chang, Michael

AU - Durocher, Daniel

PY - 2017/8/3

Y1 - 2017/8/3

N2 - DNA double-strand breaks (DSBs) and short telomeres are structurally similar, yet have diametrically opposed fates. Cells must repair DSBs while blocking the action of telomerase on these ends. Short telomeres must avoid recognition by the DNA damage response while promoting telomerase recruitment. In Saccharomyces cerevisiae, the Pif1 helicase, a telomerase inhibitor, lies at the interface of these end-fate decisions. Using Pif1 as a sensor, we uncover a transition point in which 34 bp of telomeric (TG(1-3))(n) repeat sequence renders a DNA end insensitive to Pif1 action, thereby enabling extension by telomerase. A similar transition point exists at natural chromosome ends, where telomeres shorter than similar to 40 bp are inefficiently extended by telomerase. This phenomenon is not due to known Pif1 modifications and we instead propose that Cdc13 renders TG(34+) ends insensitive to Pif1 action. We contend that the observed threshold of Pif1 activity defines a dividing line between DSBs and telomeres.

AB - DNA double-strand breaks (DSBs) and short telomeres are structurally similar, yet have diametrically opposed fates. Cells must repair DSBs while blocking the action of telomerase on these ends. Short telomeres must avoid recognition by the DNA damage response while promoting telomerase recruitment. In Saccharomyces cerevisiae, the Pif1 helicase, a telomerase inhibitor, lies at the interface of these end-fate decisions. Using Pif1 as a sensor, we uncover a transition point in which 34 bp of telomeric (TG(1-3))(n) repeat sequence renders a DNA end insensitive to Pif1 action, thereby enabling extension by telomerase. A similar transition point exists at natural chromosome ends, where telomeres shorter than similar to 40 bp are inefficiently extended by telomerase. This phenomenon is not due to known Pif1 modifications and we instead propose that Cdc13 renders TG(34+) ends insensitive to Pif1 action. We contend that the observed threshold of Pif1 activity defines a dividing line between DSBs and telomeres.

KW - SACCHAROMYCES-CEREVISIAE TELOMERES

KW - LENGTH REGULATION

KW - REPEAT DIVERGENCE

KW - CHROMOSOME ENDS

KW - CDC13 PROTEIN

KW - IN-VIVO

KW - YEAST

KW - BINDING

KW - ELONGATION

KW - SEQUENCES

U2 - 10.7554/eLife.23783

DO - 10.7554/eLife.23783

M3 - Article

VL - 6

JO - eLife

JF - eLife

SN - 2050-084X

M1 - e23783

ER -

ID: 47227442