TY - JOUR
T1 - Studies on the substrate specificity of the T4 excision repair endonuclease
AU - Friedberg, Errol C.
N1 - Funding Information:
The expert technical assistanceo f Mr. JOHN KING and Mrs. TREA GALLO is appreciatedT. hesestudies were supportedb y grants CA 12428-Ol from the National Cancer Institute and ResearchC ontractA T(o4-3)-326f rom the U.S. Atomic Energy Commission.
PY - 1972/6
Y1 - 1972/6
N2 - Previous studies have shown that the v gene of bacteriophage T4 codes for an endonuclease that specifically attacks pyrimidine dimer sites in UV-irradiated DNA. The present studies have examined the role of this endonuclease in the repair of DNA damaged by nitrogen mustard, N-methyl-N′-nitro-N-nitrosoguanidine (NTG), mitomycin C and 4-nitroquinoline-N-oxide. The observation by Harm that the v gene product of phage T4 facilitates repair of UV damage to the host DNA of excision-repair defective strains enabled us to test whether it does the same with other cellular DNA lesions. It was shown that infection of UV-irradiated E. coli Bs-1 with UV-inactivated phage T4v+ resulted in rescue of a certain fraction of the host cells. However no v gene mediated repair E. coli Bs-1 was observed following treatment with the chemical agents mentioned. Furthermore, though phage T4v1 is more sensitive to UV-irradiation than phage T4, there was no observed difference in the sensitivity of these phages to nitrogen mustard or NTG. On the basis of these observations it was concluded that the v gene coded endonuclease of T4 is specific for the excision repair of pyrimidine dimers and does not participate in the repair of chemically damaged DNA. In vitro enzymatic degradation of DNA alkylated with nitrogen mustard was observed, but it is probable that this degradation is not part of a repair reaction in vivo.
AB - Previous studies have shown that the v gene of bacteriophage T4 codes for an endonuclease that specifically attacks pyrimidine dimer sites in UV-irradiated DNA. The present studies have examined the role of this endonuclease in the repair of DNA damaged by nitrogen mustard, N-methyl-N′-nitro-N-nitrosoguanidine (NTG), mitomycin C and 4-nitroquinoline-N-oxide. The observation by Harm that the v gene product of phage T4 facilitates repair of UV damage to the host DNA of excision-repair defective strains enabled us to test whether it does the same with other cellular DNA lesions. It was shown that infection of UV-irradiated E. coli Bs-1 with UV-inactivated phage T4v+ resulted in rescue of a certain fraction of the host cells. However no v gene mediated repair E. coli Bs-1 was observed following treatment with the chemical agents mentioned. Furthermore, though phage T4v1 is more sensitive to UV-irradiation than phage T4, there was no observed difference in the sensitivity of these phages to nitrogen mustard or NTG. On the basis of these observations it was concluded that the v gene coded endonuclease of T4 is specific for the excision repair of pyrimidine dimers and does not participate in the repair of chemically damaged DNA. In vitro enzymatic degradation of DNA alkylated with nitrogen mustard was observed, but it is probable that this degradation is not part of a repair reaction in vivo.
UR - http://www.scopus.com/inward/record.url?scp=0015355028&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0015355028&partnerID=8YFLogxK
U2 - 10.1016/0027-5107(72)90024-3
DO - 10.1016/0027-5107(72)90024-3
M3 - Article
C2 - 4559036
AN - SCOPUS:0015355028
SN - 0027-5107
VL - 15
SP - 113
EP - 123
JO - Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
JF - Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
IS - 2
ER -