TY - JOUR
T1 - Intermediate (6-4) photoproduct repair in Chinese hamster V79 mutant V-H1 correlates with intermediate levels of DNA incision and repair replication
AU - Mitchell, David L.
AU - Zdzienicka, Małgorzata Z.
AU - van Zeeland, Albert A.
AU - Nairn, Rodney S.
N1 - Funding Information:
We wisht o thankJo e Vaughana ndR onaldF ilon for technicaal ssistanceJo, hn Riley and Judy Ing for art work, and Carol Hildmanf or assistancine manuscripptr eparationT.h is work was supported by U.S.P.H.S.g rantsC A24540a ndC A36361f rom the NationalC ancerI nstituteb, y the Foundation of BasicM edicalR esearc(hM EDIGON) grantN o. 501-091,t he Associationo f the EuropeanC om-
PY - 1989/5
Y1 - 1989/5
N2 - A DNA-repair mutant isolated from Chinese hamster V79 cells, V-H1, has been characterized as having only slightly reduced unscheduled DNA synthesis (UDS) and intermediate levels of DNA incision and repair replication after UV exposure. This observation was unexpected, since V-H1 has been shown by genetic complementation analysis to belong to the UV5 complementation class (i.e., class 2), exhibiting equivalent UV hypersensitivity and hypermutability as UV5 cells, which are defective in incision, UDS and repair replication. We have examined the repair of cyclobutane dimers and (6-4) photoproducts in V-H1 and V79 cells and shown that V-H1 cells are deficient in cyclobutane dimer repair, but exhibit intermediate (6-4) photoproduct repair, unlike UV5 cells which are completely deficient in (6-4) photoproduct repair. Our results confirm observations made in other UV-hypersensitive Chinese hamster cell mutants in CHO complementation class 2, and suggest that the gene affected in these mutants (ERCC2) may be involved in at least two distinct repair pathways in hamster cells.
AB - A DNA-repair mutant isolated from Chinese hamster V79 cells, V-H1, has been characterized as having only slightly reduced unscheduled DNA synthesis (UDS) and intermediate levels of DNA incision and repair replication after UV exposure. This observation was unexpected, since V-H1 has been shown by genetic complementation analysis to belong to the UV5 complementation class (i.e., class 2), exhibiting equivalent UV hypersensitivity and hypermutability as UV5 cells, which are defective in incision, UDS and repair replication. We have examined the repair of cyclobutane dimers and (6-4) photoproducts in V-H1 and V79 cells and shown that V-H1 cells are deficient in cyclobutane dimer repair, but exhibit intermediate (6-4) photoproduct repair, unlike UV5 cells which are completely deficient in (6-4) photoproduct repair. Our results confirm observations made in other UV-hypersensitive Chinese hamster cell mutants in CHO complementation class 2, and suggest that the gene affected in these mutants (ERCC2) may be involved in at least two distinct repair pathways in hamster cells.
KW - (6-4) Photoproducts
KW - DNA repair
KW - Repair replication
KW - UV-hypersensitive hamster cells
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U2 - 10.1016/0165-7992(89)90091-2
DO - 10.1016/0165-7992(89)90091-2
M3 - Article
C2 - 2716768
AN - SCOPUS:0024565014
SN - 0165-7992
VL - 226
SP - 43
EP - 47
JO - Mutation Research Letters
JF - Mutation Research Letters
IS - 1
ER -