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1 Institut de Génétique Humaine (IGH); CNRS - UPR 1142; Montpellier, France.
2 INSERM UMR 1037; CNRS ERL 505294; CRCT (Cancer Research Center of Toulouse); Toulouse, France; University of Toulouse; Université Toulouse III Paul Sabatier (UPS); Toulouse, France.
1 Institut de Génétique Humaine (IGH); CNRS - UPR 1142; Montpellier, France.
2 INSERM UMR 1037; CNRS ERL 505294; CRCT (Cancer Research Center of Toulouse); Toulouse, France; University of Toulouse; Université Toulouse III Paul Sabatier (UPS); Toulouse, France.
Figure 1. Speculative model of Pol κ function in replication checkpoint. Upon replication fork stalling…
Figure 1. Speculative model of Pol κ function in replication checkpoint. Upon replication fork stalling with replicative DNA polymerases inhibitors (hydroxyurea, aphidicolin) or UV-blocking lesions, ssDNA is generated by the action of the helicase (CMG complex). Replicative DNA polymerases α and δ as well as TLS polymerase Pol κ contribute to synthesis and/or stabilization of small replication intermediates. These structures are bound by the checkpoint clamp 9-1-1 complex. DNA Pol κ may interact with the 9-1-1 complex on chromatin, thus facilitating local formation of the active ATR complex that include ATRIP and ToPBP1. Pol κ may also be implicated in replication fork restart by repriming (question mark).