TY - JOUR
T1 - Loss of heterozygosity in yeast can occur by ultraviolet irradiation during the S phase of the cell cycle
AU - Daigaku, Yasukazu
AU - Mashiko, Satsuki
AU - Mishiba, Keiichiro
AU - Yamamura, Saburo
AU - Ui, Ayako
AU - Enomoto, Takemi
AU - Yamamoto, Kazuo
N1 - Funding Information:
This work was supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, Japan
PY - 2006/8/30
Y1 - 2006/8/30
N2 - A CAN1/can1Δ heterozygous allele that determines loss of heterozygosity (LOH) was used to study recombination in Saccharomyces cerevisiae cells exposed to ultraviolet (UV) light at different points in the cell cycle. With this allele, recombination events can be detected as canavanine-resistant mutations after exposure of cells to UV radiation, since a significant fraction of LOH events appear to arise from recombination between homologous chromosomes. The radiation caused a higher level of LOH in cells that were in the S phase of the cell cycle relative to either cells at other points in the cell cycle or unsynchronized cells. In contrast, the inactivation of nucleotide excision repair abolished the cell cycle-specific induction by UV of LOH. We hypothesize that DNA lesions, if not repaired, were converted into double-strand breaks during stalled replication and these breaks could be repaired through recombination using a non-sister chromatid and probably also the sister chromatid. We argue that LOH may be an outcome used by yeast cells to recover from stalled replication at a lesion.
AB - A CAN1/can1Δ heterozygous allele that determines loss of heterozygosity (LOH) was used to study recombination in Saccharomyces cerevisiae cells exposed to ultraviolet (UV) light at different points in the cell cycle. With this allele, recombination events can be detected as canavanine-resistant mutations after exposure of cells to UV radiation, since a significant fraction of LOH events appear to arise from recombination between homologous chromosomes. The radiation caused a higher level of LOH in cells that were in the S phase of the cell cycle relative to either cells at other points in the cell cycle or unsynchronized cells. In contrast, the inactivation of nucleotide excision repair abolished the cell cycle-specific induction by UV of LOH. We hypothesize that DNA lesions, if not repaired, were converted into double-strand breaks during stalled replication and these breaks could be repaired through recombination using a non-sister chromatid and probably also the sister chromatid. We argue that LOH may be an outcome used by yeast cells to recover from stalled replication at a lesion.
KW - Canavanine-resistance
KW - Cell cycle
KW - Loss of heterozygosity
KW - Saccharomyces cerevisiae
KW - Ultraviolet light
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U2 - 10.1016/j.mrfmmm.2006.04.001
DO - 10.1016/j.mrfmmm.2006.04.001
M3 - Article
C2 - 16737721
AN - SCOPUS:33747334306
VL - 600
SP - 177
EP - 183
JO - Mutation Research
JF - Mutation Research
SN - 0027-5107
IS - 1-2
ER -