Relation of the Types of DNA Damage to Replication Stress and the Induction of Premature Chromosome Condensation

Caffeine-Induced Premature Chromosome Condensation Results in the Apoptosis-Like Programmed Cell Death in Root Meristems of Vicia faba

“…Previously we described that prolonged HU treatment led to rapid phosphorylation of histone H2A variant H2AX on S139 resulting in the formation of phospho-H2AXS139 foci along megabase chromatin domains near the sites of DSBs [ 37 ]. We also showed that the breakage of restrictive interactions of intra-S-phase checkpoints during PCC induction resulted in the accumulation of SSBs (co-locatization experiments using anti-ssDNA and anti-H2AXS139ph antibodies; [ 38 ]). Here, through quantitative immunocytochemical, tissue printing-related and biochemical analyses, we finally proved that both replication stress and PCC induction resulted in DNA damage ( Fig 1A and 1B ) and HU induced DSBs while HU/CF SSBs ( Fig 1 and Fig 2 ).…”

“…Our previous results showed that labeling cell nuclei using antibodies recognizing PARP2 gene product, i.e. poly(ADP-ribose) polymerase 2 (PARP-2), was an equally sensitive test detecting SSBs within DNA molecules [ 38 ]. Immunocytochemical analysis showed a low constitutive level of PARP-2 protein in the control cells (1.5% ± 0.3), an over 14-fold increase in PARP-2 protein after treatment with HU (21.3% ± 1.9) and specific labeling of almost half of the cells forming the root meristem (46.2% ± 2.8) in the series in which PCC was induced with CF ( Fig 1Ag , Fig 1Ag' , Fig 1Ah and Fig 1Ai ).…”

New Research Directions in DNA Repair

“…In the cells of S. pombe, Rad17 (RFC1 factor and four small subunits RFC2-5) and Rad9/Hus1/Rad1 (PCNAlike 9-1-1 complex), participate not only in the functional organization of the intra-S phase checkpoint, but also other cell cycle checkpoints whose function is to monitor the structural DNA damage [e.g. G2(Majka et al, 2006, reviewed byLin & Dutta, 2007)]. Recruitment of PCNA-like complexes to the sites of DNA damage in a molecule is, perhaps, independent of the activation of ATR and Chk1(Niimi et al, 2008;Scorah et al, 2008), but is an important element of the mechanism signaling the appearance of structural disorders.…”