The cullin Rtt101p promotes replication fork progression through damaged DNA and natural pause sites

Publikationstyp:
Zeitschriftenaufsatz
Metadaten:
Autoren
  • B Luke
  • G Versini
  • M Jaquenoud
  • IW Zaidi
  • T Kurz
  • L Pintard
  • P Pasero
  • M Peter
Autoren-URL
https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000237047600025&DestLinkType=FullRecord&DestApp=WOS_CPL
DOI
10.1016/j.cub.2006.02.071
eISSN
1879-0445
Externe Identifier
  • Clarivate Analytics Document Solution ID: 036CD
  • PubMed Identifier: 16631586
ISSN
0960-9822
Ausgabe der Veröffentlichung
8
Zeitschrift
CURRENT BIOLOGY
Paginierung
786 - 792
Datum der Veröffentlichung
2006
Status
Published
Titel
The Cullin Rtt101p promotes replication fork progression through damaged DNA and natural pause sites
Sub types
  • Article
Ausgabe der Zeitschrift
16

Datenquelle: Web of Science (Lite)

Andere Metadatenquellen:
Autoren
  • Brian Luke
  • Gwennaelle Versini
  • Malika Jaquenoud
  • Iram Waris Zaidi
  • Thimo Kurz
  • Lionel Pintard
  • Philippe Pasero
  • Matthias Peter
DOI
10.1016/j.cub.2006.02.071
ISSN
0960-9822
Ausgabe der Veröffentlichung
8
Zeitschrift
Current Biology
Sprache
en
Paginierung
786 - 792
Datum der Veröffentlichung
2006
Status
Published
Herausgeber
Elsevier BV
Herausgeber URL
http://dx.doi.org/10.1016/j.cub.2006.02.071
Datum der Datenerfassung
2024
Titel
The Cullin Rtt101p Promotes Replication Fork Progression through Damaged DNA and Natural Pause Sites
Ausgabe der Zeitschrift
16

Datenquelle: Crossref

Abstract
Accurate and complete DNA replication is fundamental to maintain genome integrity. While the mechanisms and underlying machinery required to duplicate bulk genomic DNA are beginning to emerge, little is known about how cells replicate through damaged areas and special chromosomal regions such as telomeres, centromeres, and highly transcribed loci . Here, we have investigated the role of the yeast cullin Rtt101p in this process. We show that rtt101Delta cells accumulate spontaneous DNA damage and exhibit a G(2)/M delay, even though they are fully proficient to detect and repair chromosome breaks. Viability of rtt101Delta mutants depends on Rrm3p, a DNA helicase involved in displacing proteinaceous complexes at programmed pause sites . Moreover, rtt101Delta cells show hyperrecombination at forks arrested at replication fork barriers (RFBs) of ribosomal DNA. Finally, rtt101Delta mutants are sensitive to fork arrest induced by DNA alkylation, but not by nucleotide depletion. We therefore propose that the cullin Rtt101p promotes fork progression through obstacles such as DNA lesions or tightly bound protein-DNA complexes via a new mechanism involving ubiquitin-conjugation.
Addresses
  • Swiss Federal Institute of Technology Zurich (ETH), Institute of Biochemistry, ETH Hoenggerberg HPM G 10.0, Switzerland.
Autoren
  • Brian Luke
  • Gwennaelle Versini
  • Malika Jaquenoud
  • Iram Waris Zaidi
  • Thimo Kurz
  • Lionel Pintard
  • Philippe Pasero
  • Matthias Peter
DOI
10.1016/j.cub.2006.02.071
eISSN
1879-0445
Externe Identifier
  • PubMed Identifier: 16631586
Open access
false
ISSN
0960-9822
Ausgabe der Veröffentlichung
8
Zeitschrift
Current biology : CB
Schlüsselwörter
  • Saccharomyces cerevisiae
  • Methyl Methanesulfonate
  • Cullin Proteins
  • Saccharomyces cerevisiae Proteins
  • DNA, Fungal
  • Interphase
  • DNA Repair
  • DNA Replication
Sprache
eng
Medium
Print
Paginierung
786 - 792
Datum der Veröffentlichung
2006
Status
Published
Datum der Datenerfassung
2006
Titel
The cullin Rtt101p promotes replication fork progression through damaged DNA and natural pause sites.
Sub types
  • Research Support, Non-U.S. Gov't
  • Journal Article
Ausgabe der Zeitschrift
16

Datenquelle: Europe PubMed Central

Abstract
Accurate and complete DNA replication is fundamental to maintain genome integrity. While the mechanisms and underlying machinery required to duplicate bulk genomic DNA are beginning to emerge, little is known about how cells replicate through damaged areas and special chromosomal regions such as telomeres, centromeres, and highly transcribed loci . Here, we have investigated the role of the yeast cullin Rtt101p in this process. We show that rtt101Delta cells accumulate spontaneous DNA damage and exhibit a G(2)/M delay, even though they are fully proficient to detect and repair chromosome breaks. Viability of rtt101Delta mutants depends on Rrm3p, a DNA helicase involved in displacing proteinaceous complexes at programmed pause sites . Moreover, rtt101Delta cells show hyperrecombination at forks arrested at replication fork barriers (RFBs) of ribosomal DNA. Finally, rtt101Delta mutants are sensitive to fork arrest induced by DNA alkylation, but not by nucleotide depletion. We therefore propose that the cullin Rtt101p promotes fork progression through obstacles such as DNA lesions or tightly bound protein-DNA complexes via a new mechanism involving ubiquitin-conjugation.
Date of acceptance
2006
Autoren
  • Brian Luke
  • Gwennaelle Versini
  • Malika Jaquenoud
  • Iram Waris Zaidi
  • Thimo Kurz
  • Lionel Pintard
  • Philippe Pasero
  • Matthias Peter
Autoren-URL
https://www.ncbi.nlm.nih.gov/pubmed/16631586
DOI
10.1016/j.cub.2006.02.071
ISSN
0960-9822
Ausgabe der Veröffentlichung
8
Zeitschrift
Curr Biol
Schlüsselwörter
  • Cullin Proteins
  • DNA Repair
  • DNA Replication
  • DNA, Fungal
  • Interphase
  • Methyl Methanesulfonate
  • Saccharomyces cerevisiae
  • Saccharomyces cerevisiae Proteins
Sprache
eng
Country
England
Paginierung
786 - 792
PII
S0960-9822(06)01279-6
Datum der Veröffentlichung
2006
Status
Published
Datum, an dem der Datensatz öffentlich gemacht wurde
2006
Titel
The cullin Rtt101p promotes replication fork progression through damaged DNA and natural pause sites.
Sub types
  • Journal Article
  • Research Support, Non-U.S. Gov't
Ausgabe der Zeitschrift
16

Datenquelle: PubMed

Abstract
Accurate and complete DNA replication is fundamental to maintain genome integrity. While the mechanisms and underlying machinery required to duplicate bulk genomic DNA are beginning to emerge, little is known about how cells replicate through damaged areas and special chromosomal regions such as telomeres, centromeres, and highly transcribed loci . Here, we have investigated the role of the yeast cullin Rtt101p in this process. We show that rtt101Delta cells accumulate spontaneous DNA damage and exhibit a G(2)/M delay, even though they are fully proficient to detect and repair chromosome breaks. Viability of rtt101Delta mutants depends on Rrm3p, a DNA helicase involved in displacing proteinaceous complexes at programmed pause sites . Moreover, rtt101Delta cells show hyperrecombination at forks arrested at replication fork barriers (RFBs) of ribosomal DNA. Finally, rtt101Delta mutants are sensitive to fork arrest induced by DNA alkylation, but not by nucleotide depletion. We therefore propose that the cullin Rtt101p promotes fork progression through obstacles such as DNA lesions or tightly bound protein-DNA complexes via a new mechanism involving ubiquitin-conjugation.
Autoren
  • Brian Luke
  • Gwennaelle Versini
  • Malika Jaquenoud
  • Iram Waris Zaidi
  • Thimo Kurz
  • Lionel Pintard
  • Philippe Pasero
  • Matthias Peter
DOI
10.1016/j.cub.2006.02.071
ISSN
0960-9822
Zeitschrift
Current biology : CB
Notes
keywords: Cullin Proteins/physiology;DNA Repair/physiology;DNA Replication/physiology;DNA, Fungal/biosynthesis;Interphase/physiology;Methyl Methanesulfonate;Saccharomyces cerevisiae Proteins/physiology;Saccharomyces cerevisiae/cytology/physiology
Artikelnummer
8
Paginierung
786 - 792
Datum der Veröffentlichung
2006
Datum der Datenerfassung
2023
Titel
The cullin Rtt101p promotes replication fork progression through damaged DNA and natural pause sites
Sub types
  • article
Ausgabe der Zeitschrift
16

Datenquelle: Manual

Beziehungen:
Eigentum von

Werkzeuge