TY - JOUR
T1 - Saccharomyces cerevisiae lacking Snm1, Rev3 or Rad51 have a normal S- phase but arrest permanently in G2 after cisplatin treatment
AU - Grossmann, Kenneth F.
AU - Ward, Alex M.
AU - Moses, Robb E.
N1 - Funding Information:
We would like to thank Jessica C. Brown and Mara E. Matkovic for technical assistance. This research was supported by a grant from the National Institute of Health (GM58186).
PY - 2000/9/15
Y1 - 2000/9/15
N2 - The role of Snm1, Rev3 and Rad51 in S-phase after cisplatin (CDDP) DNA treatment has been examined. When isogenic deletion mutants snm1Δ, rev3Δ and rad51Δ were arrested in G1 and treated with doses of CDDP causing significant lethality (< 20% survival in the mutant strains), they progressed through S-phase with normal kinetics. The mutants arrested in G2 like wild- type cells, however they did not exit the arrest and reenter the cell cycle. This finding demonstrates that these genes are not required to allow DNA replication in the presence of damage. Therefore, Snm1, Rev3 and Rad51 may act after S to allow repair. At high levels of damage (< 40% survival in wild-type cells) S-phase was slowed in a MEC1-dependent fashion. The cross- link incision kinetics of snm1Δ and rev3Δ mutants were also examined; both showed no deficiencies in incision of cross-linked DNA. (C) 2000 Elsevier Science B.V.
AB - The role of Snm1, Rev3 and Rad51 in S-phase after cisplatin (CDDP) DNA treatment has been examined. When isogenic deletion mutants snm1Δ, rev3Δ and rad51Δ were arrested in G1 and treated with doses of CDDP causing significant lethality (< 20% survival in the mutant strains), they progressed through S-phase with normal kinetics. The mutants arrested in G2 like wild- type cells, however they did not exit the arrest and reenter the cell cycle. This finding demonstrates that these genes are not required to allow DNA replication in the presence of damage. Therefore, Snm1, Rev3 and Rad51 may act after S to allow repair. At high levels of damage (< 40% survival in wild-type cells) S-phase was slowed in a MEC1-dependent fashion. The cross- link incision kinetics of snm1Δ and rev3Δ mutants were also examined; both showed no deficiencies in incision of cross-linked DNA. (C) 2000 Elsevier Science B.V.
KW - 8-MOP - 8-methoxypsoralen
KW - CDDP - cisplatin
KW - Cell cycle checkpoint
KW - DNA cross-link repair
KW - Yeast Saccharomyces cerevisiae
UR - http://www.scopus.com/inward/record.url?scp=0034665799&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034665799&partnerID=8YFLogxK
U2 - 10.1016/S0921-8777(00)00035-5
DO - 10.1016/S0921-8777(00)00035-5
M3 - Article
C2 - 10980408
AN - SCOPUS:0034665799
SN - 0921-8777
VL - 461
SP - 1
EP - 13
JO - Mutation Research - DNA Repair
JF - Mutation Research - DNA Repair
IS - 1
ER -