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pubmed:abstractText |
Poly ADP-ribosylation and DNA strand breakage in response to treatment with the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were studied on SV40 minichromosomes in SV40-infected, permeabilized CV-1 monkey cells. After an initial sharp increase in poly ADP-ribosylation, strand breakage and poly ADPR increased proportionately with increasing dose of MNNG. This suggests a cause-effect relationship between the two reactions. The major poly ADP-ribose acceptor of minichromosomes was core histone H2B. In contrast, H2B, H2A, H1 and protein A24 were poly ADP-ribosylated in the nuclear chromatin of the same cells.
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