High nutrient levels and TORC1 activity reduce cell viability following prolonged telomere dysfunction and cell cycle arrest
- Publication type:
- Journal article
- Metadata:
-
- Autoren
- Julia Klermund
- Katharina Bender
- Brian Luke
- Autoren-URL
- https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000344468100028&DestLinkType=FullRecord&DestApp=WOS_CPL
- DOI
- 10.1016/j.celrep.2014.08.053
- Externe Identifier
- Clarivate Analytics Document Solution ID: AS7YP
- PubMed Identifier: 25263563
- ISSN
- 2211-1247
- Ausgabe der Veröffentlichung
- 1
- Zeitschrift
- CELL REPORTS
- Paginierung
- 324 - 335
- Datum der Veröffentlichung
- 2014
- Status
- Published
- Titel
- High Nutrient Levels and TORC1 Activity Reduce Cell Viability following Prolonged Telomere Dysfunction and Cell Cycle Arrest
- Sub types
- Article
- Ausgabe der Zeitschrift
- 9
Data source: Web of Science (Lite)
- Other metadata sources:
-
- Autoren
- Julia Klermund
- Katharina Bender
- Brian Luke
- DOI
- 10.1016/j.celrep.2014.08.053
- ISSN
- 2211-1247
- Ausgabe der Veröffentlichung
- 1
- Zeitschrift
- Cell Reports
- Sprache
- en
- Paginierung
- 324 - 335
- Datum der Veröffentlichung
- 2014
- Status
- Published
- Herausgeber
- Elsevier BV
- Herausgeber URL
- http://dx.doi.org/10.1016/j.celrep.2014.08.053
- Datum der Datenerfassung
- 2022
- Titel
- High Nutrient Levels and TORC1 Activity Reduce Cell Viability following Prolonged Telomere Dysfunction and Cell Cycle Arrest
- Ausgabe der Zeitschrift
- 9
Data source: Crossref
- Abstract
- Cells challenged with DNA damage activate checkpoints to arrest the cell cycle and allow time for repair. Successful repair coupled to subsequent checkpoint inactivation is referred to as recovery. When DNA damage cannot be repaired, a choice between permanent arrest and cycling in the presence of damage (checkpoint adaptation) must be made. While permanent arrest jeopardizes future lineages, continued proliferation is associated with the risk of genome instability. We demonstrate that nutritional signaling through target of rapamycin complex 1 (TORC1) influences the outcome of this decision. Rapamycin-mediated TORC1 inhibition prevents checkpoint adaptation via both Cdc5 inactivation and autophagy induction. Preventing adaptation results in increased cell viability and hence proliferative potential. In accordance, the ability of rapamycin to increase longevity is dependent upon the DNA damage checkpoint. The crosstalk between TORC1 and the DNA damage checkpoint may have important implications in terms of therapeutic alternatives for diseases associated with genome instability.
- Addresses
- Zentrum für Molekulare Biologie der Universität Heidelberg (ZMBH), DKFZ-ZMBH Alliance, 69120 Heidelberg, Germany.
- Autoren
- Julia Klermund
- Katharina Bender
- Brian Luke
- DOI
- 10.1016/j.celrep.2014.08.053
- eISSN
- 2211-1247
- Externe Identifier
- PubMed Identifier: 25263563
- Open access
- false
- ISSN
- 2211-1247
- Ausgabe der Veröffentlichung
- 1
- Zeitschrift
- Cell reports
- Schlüsselwörter
- Telomere
- Yeasts
- DNA Damage
- Multiprotein Complexes
- Signal Transduction
- Cell Survival
- DNA Repair
- TOR Serine-Threonine Kinases
- Cell Cycle Checkpoints
- Mechanistic Target of Rapamycin Complex 1
- Sprache
- eng
- Medium
- Print-Electronic
- Online publication date
- 2014
- Paginierung
- 324 - 335
- Datum der Veröffentlichung
- 2014
- Status
- Published
- Publisher licence
- CC BY-NC-ND
- Datum der Datenerfassung
- 2014
- Titel
- High nutrient levels and TORC1 activity reduce cell viability following prolonged telomere dysfunction and cell cycle arrest.
- Sub types
- Research Support, Non-U.S. Gov't
- Journal Article
- Ausgabe der Zeitschrift
- 9
Data source: Europe PubMed Central
- Abstract
- Cells challenged with DNA damage activate checkpoints to arrest the cell cycle and allow time for repair. Successful repair coupled to subsequent checkpoint inactivation is referred to as recovery. When DNA damage cannot be repaired, a choice between permanent arrest and cycling in the presence of damage (checkpoint adaptation) must be made. While permanent arrest jeopardizes future lineages, continued proliferation is associated with the risk of genome instability. We demonstrate that nutritional signaling through target of rapamycin complex 1 (TORC1) influences the outcome of this decision. Rapamycin-mediated TORC1 inhibition prevents checkpoint adaptation via both Cdc5 inactivation and autophagy induction. Preventing adaptation results in increased cell viability and hence proliferative potential. In accordance, the ability of rapamycin to increase longevity is dependent upon the DNA damage checkpoint. The crosstalk between TORC1 and the DNA damage checkpoint may have important implications in terms of therapeutic alternatives for diseases associated with genome instability.
- Date of acceptance
- 2014
- Autoren
- Julia Klermund
- Katharina Bender
- Brian Luke
- Autoren-URL
- https://www.ncbi.nlm.nih.gov/pubmed/25263563
- DOI
- 10.1016/j.celrep.2014.08.053
- eISSN
- 2211-1247
- Ausgabe der Veröffentlichung
- 1
- Zeitschrift
- Cell Rep
- Schlüsselwörter
- Cell Cycle Checkpoints
- Cell Survival
- DNA Damage
- DNA Repair
- Mechanistic Target of Rapamycin Complex 1
- Multiprotein Complexes
- Signal Transduction
- TOR Serine-Threonine Kinases
- Telomere
- Yeasts
- Sprache
- eng
- Country
- United States
- Paginierung
- 324 - 335
- PII
- S2211-1247(14)00729-3
- Datum der Veröffentlichung
- 2014
- Status
- Published
- Datum, an dem der Datensatz öffentlich gemacht wurde
- 2015
- Titel
- High nutrient levels and TORC1 activity reduce cell viability following prolonged telomere dysfunction and cell cycle arrest.
- Sub types
- Journal Article
- Research Support, Non-U.S. Gov't
- Ausgabe der Zeitschrift
- 9
Data source: PubMed
- Abstract
- Cells challenged with DNA damage activate checkpoints to arrest the cell cycle and allow time for repair. Successful repair coupled to subsequent checkpoint inactivation is referred to as recovery. When DNA damage cannot be repaired, a choice between permanent arrest and cycling in the presence of damage (checkpoint adaptation) must be made. While permanent arrest jeopardizes future lineages, continued proliferation is associated with the risk of genome instability. We demonstrate that nutritional signaling through target of rapamycin complex 1 (TORC1) influences the outcome of this decision. Rapamycin-mediated TORC1 inhibition prevents checkpoint adaptation via both Cdc5 inactivation and autophagy induction. Preventing adaptation results in increased cell viability and hence proliferative potential. In accordance, the ability of rapamycin to increase longevity is dependent upon the DNA damage checkpoint. The crosstalk between TORC1 and the DNA damage checkpoint may have important implications in terms of therapeutic alternatives for diseases associated with genome instability.
- Autoren
- Julia Klermund
- Katharina Bender
- Brian Luke
- DOI
- 10.1016/j.celrep.2014.08.053
- Zeitschrift
- Cell reports
- Notes
- keywords: Cell Cycle Checkpoints/genetics/physiology;Cell Survival/physiology;DNA Damage;DNA Repair;Mechanistic Target of Rapamycin Complex 1;Multiprotein Complexes/genetics/metabolism;Signal Transduction;Telomere/genetics/metabolism;TOR Serine-Threonine Kinases/genetics/metabolism;Yeasts
- Artikelnummer
- 1
- Paginierung
- 324 - 335
- Datum der Veröffentlichung
- 2014
- Datum der Datenerfassung
- 2023
- Titel
- High nutrient levels and TORC1 activity reduce cell viability following prolonged telomere dysfunction and cell cycle arrest
- Sub types
- article
- Ausgabe der Zeitschrift
- 9
Data source: Manual
- Beziehungen:
- Property of