TY - JOUR
T1 - Involvement of DNA replication in ultraviolet-induced apoptosis of mammalian cells
AU - Batista, Luis Francisco Zirnberger
AU - Chiganças, Vanessa
AU - Brumatti, Gabriela
AU - Amarante-Mendes, Gustavo Pessini
AU - Menck, Carlos Frederico Martins
N1 - Funding Information:
This work was supported by FAPESP (São Paulo, Brazil), CNPq (Brasília, Brazil), CAPES (Brasilia, Brazil) and COFECUB (Aix en Provence, France). CFMM is a Fellow from the John Simon Guggenheim Memorial Foundation (New York, USA).
PY - 2006/7
Y1 - 2006/7
N2 - Exposure of cells to ultraviolet (UV) light damages the genome and the persistence of DNA lesions triggers apoptosis in mammalian cells. RNA transcription blockage by DNA damage is believed to be implicated in signaling for UV-induced apoptosis, but the role played by DNA replication in this process is still unclear. To address this point, we have employed the DNA polymerase inhibitor aphidicolin in UV-irradiated wild-type and XPB-mutated Chinese hamster ovary cells. The data obtained with synchronized cells indicate that induction of apoptosis by UV light is independent of the cell cycle phase. Nevertheless, cells treated with aphidicolin after UV exposure showed a significant prevention of apoptosis induction when compared to proliferating cells. These results were observed in both DNA-repair proficient and deficient cells, indicating that the prevention of apoptosis by aphidicolin is independent of the cells' ability to repair the photolesions caused by UV. Taken together, these data suggest that replication of damaged DNA also leads to critical events signaling for UV-induced cell death.
AB - Exposure of cells to ultraviolet (UV) light damages the genome and the persistence of DNA lesions triggers apoptosis in mammalian cells. RNA transcription blockage by DNA damage is believed to be implicated in signaling for UV-induced apoptosis, but the role played by DNA replication in this process is still unclear. To address this point, we have employed the DNA polymerase inhibitor aphidicolin in UV-irradiated wild-type and XPB-mutated Chinese hamster ovary cells. The data obtained with synchronized cells indicate that induction of apoptosis by UV light is independent of the cell cycle phase. Nevertheless, cells treated with aphidicolin after UV exposure showed a significant prevention of apoptosis induction when compared to proliferating cells. These results were observed in both DNA-repair proficient and deficient cells, indicating that the prevention of apoptosis by aphidicolin is independent of the cells' ability to repair the photolesions caused by UV. Taken together, these data suggest that replication of damaged DNA also leads to critical events signaling for UV-induced cell death.
KW - Aphidicolin
KW - Apoptosis
KW - DNA replication
KW - Ultraviolet
UR - http://www.scopus.com/inward/record.url?scp=33745823547&partnerID=8YFLogxK
U2 - 10.1007/s10495-006-7109-4
DO - 10.1007/s10495-006-7109-4
M3 - Article
C2 - 16703265
AN - SCOPUS:33745823547
SN - 1360-8185
VL - 11
SP - 1139
EP - 1148
JO - Apoptosis
JF - Apoptosis
IS - 7
ER -