TY - JOUR
T1 - Enhanced pyrimidine dimer removal in repair-proficient murine fibroblasts transforme with the denV gene of bacteriophage T4
AU - Kusewitt, Donna F.
AU - Ley, Ronald D.
AU - Henderson, Earl E.
N1 - Funding Information:
We wish to acknowledge the invaluable assistance of Sharon L. Ryan in the preparation of illustrations and helpful suggestions from Anthony Green during the course of the study. This study was funded by the Lovelace Medical Foundation.
PY - 1991/7
Y1 - 1991/7
N2 - The denV gene of bacteriophage T4, which encodes the pyrimidine dimer-specific repair enzyme endonuclease V, was introduced into murine fibroblasts with normal rodent pyrimidine dimer repair capabilities. Endonuclease V recognizes ultraviolet radiation (UVR)-induced pyrimidine dimers and produces single-strand breaks adjacent to the dimers. These nicks may serve as substrates to initiate excision repair fo pyrimidine dimers endogenous enzymes. In the present study, murine fibroblasts stably transfered with denV were able to remove 50-80% of UVR-induced pyramidine dimers, while control cells removed only about 20% of dimers under the same conditions of pyrimidine dimer induction and repair. For both control and denV-transfected cells, repair continued for at least 24 h after exposure. When removal of UVR-induced photoproducts was initiated by endogenous excision repair mechanisms, an average of 38 nucleotides were replaced per dimer removed, as determined by bromouracil photolysis; denV-initiated excision repair, on the other hand, resulted in removal of an average of 6 nucleotides per dimer repaired. The enhanced pyrimidine diner repair capabilities conferred by denV gene expression did not appear to improve post-UVR survival.
AB - The denV gene of bacteriophage T4, which encodes the pyrimidine dimer-specific repair enzyme endonuclease V, was introduced into murine fibroblasts with normal rodent pyrimidine dimer repair capabilities. Endonuclease V recognizes ultraviolet radiation (UVR)-induced pyrimidine dimers and produces single-strand breaks adjacent to the dimers. These nicks may serve as substrates to initiate excision repair fo pyrimidine dimers endogenous enzymes. In the present study, murine fibroblasts stably transfered with denV were able to remove 50-80% of UVR-induced pyramidine dimers, while control cells removed only about 20% of dimers under the same conditions of pyrimidine dimer induction and repair. For both control and denV-transfected cells, repair continued for at least 24 h after exposure. When removal of UVR-induced photoproducts was initiated by endogenous excision repair mechanisms, an average of 38 nucleotides were replaced per dimer removed, as determined by bromouracil photolysis; denV-initiated excision repair, on the other hand, resulted in removal of an average of 6 nucleotides per dimer repaired. The enhanced pyrimidine diner repair capabilities conferred by denV gene expression did not appear to improve post-UVR survival.
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U2 - 10.1016/0921-8777(91)90012-E
DO - 10.1016/0921-8777(91)90012-E
M3 - Article
C2 - 2067547
AN - SCOPUS:0025764364
SN - 0921-8777
VL - 255
SP - 1
EP - 9
JO - Mutation Research-DNA Repair
JF - Mutation Research-DNA Repair
IS - 1
ER -