Clustering of double strand break-containing chromosome domains is not inhibited by inactivation of major repair proteins.
For efficient repair of DNA double strand breaks (DSBs) cells rely on a process that involves the Mre11/Rad50/Nbs1 complex, which may help to protect non-repaired DNA ends from separating until they can be rejoined by DNA repair proteins. It has been observed that as a secondary effect, this process can lead to unintended clustering of multiple, initially separate, DSB-containing chromosome domains. This work demonstrates that neither inactivation of the major repair proteins XRCC3 and the DNA-dependent protein kinase (DNA-PK) nor inhibition of DNA-PK by vanillin influences the aggregation of DSB-containing chromosome domains.
Krawczyk
P M
PM
Department of Cell Biology and Histology, Academic Medical Center, University of Amsterdam, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands.
Stap
J
J
van Oven
C
C
Hoebe
R
R
Aten
J A
JA
D000818:Animals; D002875:Chromosomes / Q000502:physiology* / Q000528:radiation effects*; D004249:DNA Damage / Q000502:physiology*; D004260:DNA Repair / Q000502:physiology* / Q000528:radiation effects; D004268:DNA-Binding Proteins / Q000378:metabolism* / Q000528:radiation effects; D004307:Dose-Response Relationship, Radiation; D006801:Humans; D008954:Models, Biological; D011829:Radiation Dosage
D004268:DNA-Binding Proteins