Diagenode

TLK1B mediated phosphorylation of Rad9 regulates its nuclear/cytoplasmic localization and cell cycle checkpoint


Sanket Awate and Arrigo De Benedetti

The Tousled like kinase 1B (TLK1B) is critical for DNA repair and survival of cells. Upon DNA damage, Chk1 phosphorylates TLK1B at S457 leading to its transient inhibition. Once TLK1B regains its kinase activity it phosphorylates Rad9 at S328. In this work we investigated the significance of this mechanism by overexpressing mutant TLK1B in which the inhibitory phosphorylation site was eliminated. We propose that normally, the inactivation of TLK1B following replication arrest and genotoxic stress functions to allow the retention of 9-1-1 at the sites of damage or stalled forks. Following reactivation of TLK1B, whose synthesis is concomitantly induced by genotoxins, Rad9 is hyperphosphorylated at S328, resulting in its dissociation and inactivation of the checkpoint that occurs once repair is complete.

Tags
Article alert

Share this article

Published
February, 2016

Source

Related product

  • Bioruptor-pico-next-gen-sequencing
    B01060001
    Bioruptor® Pico sonication device

Events

  • Epigenetic Mechanisms in Health and Disease 2017
    Barcelona, Spain
    Oct 25-Oct 26, 2017
  • 35ème Congrès de la Societé Française de Toxicologie Génétique
    Marseille, France
    Oct 26-Oct 27, 2017
  • 7th Australian Epigenetics Conference
    Brisbane, Australia
    Oct 29-Nov 1, 2017
  • Australian Genomic Technologies Association (AGTA 2017 Annual Conference)
    Hobart, Tasmania
    Oct 29-Nov 1, 2017
 See all events

         Site map   |   Contact us   |   Conditions of sales   |   Conditions of purchase   |   Privacy policy   |   Diagenode Diagnostics