Rad51C-deficient CL-V4B cells exhibit normal levels of mitomycin C-induced SCEs but reduced levels of UVC-induced SCEs.
The mechanisms of sister chromatid exchanges (SCEs) are not known. One hypothesis is that SCE is a manifestation of Rad51-dependent homologous recombination repair. In order to test this hypothesis, we have compared the frequencies of SCEs induced by mitomycin C (MMC) and 254nm ultraviolet radiation (UVC) in wt V79B and the Rad51C-deficient CL-V4B cells. SCEs were analysed in the first (M1) and second (M2) post-treatment mitoses. In M1 MMC induced the same frequencies of SCEs in CL-V4B and V79B cells, while the UVC-induced SCE frequencies were lower in CL-V4B than V79B cells. In CL-V4B cells, MMC-induced SCEs were higher in M2 than in M1, suggesting that interstrand cross-links (ICL) are either not removed completely or are transformed into another form of DNA damage that persists until the next cell cycle. We suggest that SCEs may represent a mechanism to bypass MMC-induced ICL without their removal.
Wojcik
Andrzej
A
Institute of Nuclear Chemistry and Technology, 03-195 Warszawa, Poland. awojcik@pu.kielce.pl
Stoilov
Lubomir
L
Szumiel
Irena
I
Legerski
Randy
R
Obe
Günter
G
D000818:Animals; D016466:CHO Cells; D002470:Cell Survival / Q000187:drug effects / Q000235:genetics / Q000528:radiation effects; D006224:Cricetinae; D003412:Cricetulus; D004260:DNA Repair / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D004268:DNA-Binding Proteins / Q000172:deficiency*; D004305:Dose-Response Relationship, Drug; D004307:Dose-Response Relationship, Radiation; D016685:Mitomycin / Q000494:pharmacology*; D008938:Mitosis / Q000187:drug effects* / Q000235:genetics / Q000528:radiation effects*; D051135:Rad51 Recombinase; D012854:Sister Chromatid Exchange / Q000187:drug effects* / Q000235:genetics / Q000528:radiation effects*; D014466:Ultraviolet Rays
D004268:DNA-Binding Proteins; D016685:Mitomycin; D051135:Rad51 Recombinase