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Kinase-independent function of checkpoint kinase 1 (Chk1) in the replication of damaged DNA.

The checkpoint kinases Chk1 and ATR are broadly known for their role in the response to the accumulation of damaged DNA. Because Chk1 activation requires its phosphorylation by ATR, it is expected that ATR or Chk1 down-regulation should cause similar alterations in the signals triggered by DNA lesio... Full description

Journal Title: Proceedings of the National Academy of Sciences of the United States of America May 8, 2012, Vol.109(19), pp.7344-7349
Main Author: Speroni, Juliana
Other Authors: Federico, María Belén , Mansilla, Sabrina F , Soria, Gastón , Gottifredi, Vanesa
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1116345109
Link: http://search.proquest.com/docview/1012208160/?pq-origsite=primo
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title: Kinase-independent function of checkpoint kinase 1 (Chk1) in the replication of damaged DNA.
format: Article
creator:
  • Speroni, Juliana
  • Federico, María Belén
  • Mansilla, Sabrina F
  • Soria, Gastón
  • Gottifredi, Vanesa
subjects:
  • Binding Sites–Genetics
  • Blotting, Western–Genetics
  • Cell Line, Tumor–Metabolism
  • Checkpoint Kinase 1–Genetics
  • Chromatin Immunoprecipitation–Metabolism
  • DNA Damage–Metabolism
  • DNA Repair–Radiation Effects
  • DNA Replication–Genetics
  • DNA-Directed DNA Polymerase–Metabolism
  • Green Fluorescent Proteins–Metabolism
  • Humans–Metabolism
  • Microscopy, Confocal–Metabolism
  • Proliferating Cell Nuclear Antigen–Metabolism
  • Protein Binding–Metabolism
  • Protein Kinases–Metabolism
  • RNA Interference–Metabolism
  • Ultraviolet Rays–Metabolism
  • Proliferating Cell Nuclear Antigen
  • Green Fluorescent Proteins
  • Protein Kinases
  • Chek1 Protein, Human
  • Checkpoint Kinase 1
  • DNA-Directed DNA Polymerase
  • Rad30 Protein
ispartof: Proceedings of the National Academy of Sciences of the United States of America, May 8, 2012, Vol.109(19), pp.7344-7349
description: The checkpoint kinases Chk1 and ATR are broadly known for their role in the response to the accumulation of damaged DNA. Because Chk1 activation requires its phosphorylation by ATR, it is expected that ATR or Chk1 down-regulation should cause similar alterations in the signals triggered by DNA lesions. Intriguingly, we found that Chk1, but not ATR, promotes the progression of replication forks after UV irradiation. Strikingly, this role of Chk1 is independent of its kinase-domain and of its partnership with Claspin. Instead, we demonstrate that the ability of Chk1 to promote replication fork progression on damaged DNA templates relies on its recently identified proliferating cell nuclear antigen-interacting motif, which is required for its release from chromatin after DNA damage. Also supporting the importance of Chk1 release, a histone H2B-Chk1 chimera, which is permanently immobilized in chromatin, is unable to promote the replication of damaged DNA. Moreover, inefficient chromatin dissociation of Chk1 impairs the efficient recruitment of the specialized DNA polymerase [eta] (pol [eta]) to replication-associated foci after UV. Given the critical role of pol [eta] during translesion DNA synthesis (TLS), these findings unveil an unforeseen facet of the regulation by Chk1 of DNA replication. This kinase-independent role of Chk1 is exclusively associated to the maintenance of active replication forks after UV irradiation in a manner in which Chk1 release prompts TLS to avoid replication stalling. pol eta foci | pol iota foci | DNA fibers | Chk1 inhibitors doi/10.1073/pnas.1116345109
language: eng
source:
identifier: E-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1116345109
fulltext: fulltext
issn:
  • 10916490
  • 1091-6490
url: Link


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titleKinase-independent function of checkpoint kinase 1 (Chk1) in the replication of damaged DNA.
creatorSperoni, Juliana ; Federico, María Belén ; Mansilla, Sabrina F ; Soria, Gastón ; Gottifredi, Vanesa
contributorSperoni, Juliana (correspondence author) ; Speroni, Juliana (record owner)
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identifierE-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1116345109
subjectBinding Sites–Genetics ; Blotting, Western–Genetics ; Cell Line, Tumor–Metabolism ; Checkpoint Kinase 1–Genetics ; Chromatin Immunoprecipitation–Metabolism ; DNA Damage–Metabolism ; DNA Repair–Radiation Effects ; DNA Replication–Genetics ; DNA-Directed DNA Polymerase–Metabolism ; Green Fluorescent Proteins–Metabolism ; Humans–Metabolism ; Microscopy, Confocal–Metabolism ; Proliferating Cell Nuclear Antigen–Metabolism ; Protein Binding–Metabolism ; Protein Kinases–Metabolism ; RNA Interference–Metabolism ; Ultraviolet Rays–Metabolism ; Proliferating Cell Nuclear Antigen ; Green Fluorescent Proteins ; Protein Kinases ; Chek1 Protein, Human ; Checkpoint Kinase 1 ; DNA-Directed DNA Polymerase ; Rad30 Protein
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descriptionThe checkpoint kinases Chk1 and ATR are broadly known for their role in the response to the accumulation of damaged DNA. Because Chk1 activation requires its phosphorylation by ATR, it is expected that ATR or Chk1 down-regulation should cause similar alterations in the signals triggered by DNA lesions. Intriguingly, we found that Chk1, but not ATR, promotes the progression of replication forks after UV irradiation. Strikingly, this role of Chk1 is independent of its kinase-domain and of its partnership with Claspin. Instead, we demonstrate that the ability of Chk1 to promote replication fork progression on damaged DNA templates relies on its recently identified proliferating cell nuclear antigen-interacting motif, which is required for its release from chromatin after DNA damage. Also supporting the importance of Chk1 release, a histone H2B-Chk1 chimera, which is permanently immobilized in chromatin, is unable to promote the replication of damaged DNA. Moreover, inefficient chromatin dissociation of Chk1 impairs the efficient recruitment of the specialized DNA polymerase [eta] (pol [eta]) to replication-associated foci after UV. Given the critical role of pol [eta] during translesion DNA synthesis (TLS), these findings unveil an unforeseen facet of the regulation by Chk1 of DNA replication. This kinase-independent role of Chk1 is exclusively associated to the maintenance of active replication forks after UV irradiation in a manner in which Chk1 release prompts TLS to avoid replication stalling. pol eta foci | pol iota foci | DNA fibers | Chk1 inhibitors doi/10.1073/pnas.1116345109
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8DNA-Directed DNA Polymerase–Metabolism
9Green Fluorescent Proteins–Metabolism
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13Protein Binding–Metabolism
14Protein Kinases–Metabolism
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titleKinase-independent function of checkpoint kinase 1 (Chk1) in the replication of damaged DNA.
authorSperoni, Juliana ; Federico, María Belén ; Mansilla, Sabrina F ; Soria, Gastón ; Gottifredi, Vanesa
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5DNA Damage–Metabolism
6DNA Repair–Radiation Effects
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8DNA-Directed DNA Polymerase–Metabolism
9Green Fluorescent Proteins–Metabolism
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13Protein Binding–Metabolism
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18Green Fluorescent Proteins
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22DNA-Directed DNA Polymerase
23Rad30 Protein
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