Effect of UV light on sister-chromatid exchanges, activation of alternative sites of replicon initiation and thymidine incorporation in CHO AA8, UV61 and UV5 cells

Taft, Sharon A.; Ling, Su Y.; Griffiths, Tony

doi:10.1016/0921-8777(91)90029-o

Cited by 3 publications

(1 citation statement)

References 26 publications

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“…The shorter delays in completion of S-phase in AA8 and UV61 cells may be due to the interval required for removal of 6-4PPs and/or pausing of replication forks at CPD sites. It has been suggested that the bulk of replication inhibition in mammalian cells is caused by 6-4PPs (Cleaver et al, 1987;Taft et al, 1991), but still considerable controversy exists concerning the relative contributions of each photoproduct. Although some studies have shown that CPDs block DNA polymerases in vitro (Moore and Strauss, 1979;Moore et al, 1981) and in vivo on simian virus 40 replication forks (Berger and Edenberg, 1986), the fact that CHO cells that do not repair CPDs in nontranscribed regions can complete replication and mitosis after significant UV doses indicates that DNA polymerase complexes can synthesize past CPDs in the template.…”

Section: Discussionmentioning

confidence: 99%

Persistent DNA damage inhibits S-phase and G2 progression, and results in apoptosis.

Orren

Petersen

Bohr

1997

MBoC

141

101

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We used genetically related Chinese hamster ovary cell lines proficient or deficient in DNA repair to determine the direct role of UV-induced DNA photoproducts in inhibition of DNA replication and in induction of G2 arrest and apoptosis. UV irradiation of S-phase-synchronized cells causes delays in completion of the S-phase sometimes followed by an extended G2 arrest and apoptosis. The effects of UV irradiation during the S-phase on subsequent cell cycle progression are magnified in repair-deficient cells, indicating that these effects are initiated by persistent DNA damage and not by direct UV activation of signal transduction pathways. Moreover, among the lesions introduced by UV irradiation, persistence of (6-4) photoproducts inhibits DNA synthesis much more than persistence of cyclobutane pyrimidine dimers (which appear to be efficiently bypassed by the DNA replication apparatus). Apoptosis begins approximately 24 h after UV irradiation of S-phase-synchronized cells, occurs to a greater extent in repair-deficient cells, and correlates well with the inability to escape from an extended late S-phase-G2 arrest. We also find that nucleotide excision repair activity (including its coupling to transcription) is similar in the S-phase to what we have previously measured in G1 and G2.

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Section: Discussionmentioning

confidence: 99%

Persistent DNA damage inhibits S-phase and G2 progression, and results in apoptosis.

Orren

Petersen

Bohr

1997

MBoC

141

101

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Absence of UV-induced non-homologous recombination in repair-deficient CHO cell lines transfected with ERCC genes

Rainaldi¹,

Capecchi²,

Piras³

et al. 1996

Mutation Research/DNA Repair

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Effect of UVC Light on Growth, Incorporation of Thymidine, and DNA Chain Elongation in Cells Derived from the Indian Meal Moth and the Cabbage Looper

Styer

Griffiths²

1992

Radiation Research

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After exposure to 10 or 20 J/m2 UVC light, cells of the UMN-PIE-1181 line, an embryonic cell line derived from the Indian meal moth, Plodia interpunctella, exhibited a rapid and prolonged depression in the rate of incorporation of [3H]thymidine, whereas cells of the TN-368 line, an ovarian cell line derived from Trichoplusia ni, the cabbage looper, showed only a slight drop in incorporation and a rapid recovery after exposure to 10 or 40 J/m2 UVC light. The extent of this depression was not correlated to the amount of cell killing by UVC light in these cell lines or in IAL-PID2 cells. Blockage of fork progression was correlated to the depression in thymidine incorporation. TN-368 cells exhibited little blockage after exposure to 10 or 20 J/m2 UVC light, whereas UMN-PIE-1181 cells exhibited significant blockage at these fluences. Photoreactivation did not entirely relieve blockage, depression in thymidine incorporation, or cell killing, indicating that, although the (5-6) dimer appears to be the major lesion responsible for these effects, other lesions such as the (6-4) photoproduct may play a role.

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Effect of UV light on sister-chromatid exchanges, activation of alternative sites of replicon initiation and thymidine incorporation in CHO AA8, UV61 and UV5 cells

Cited by 3 publications

References 26 publications

Persistent DNA damage inhibits S-phase and G2 progression, and results in apoptosis.

Persistent DNA damage inhibits S-phase and G2 progression, and results in apoptosis.

Absence of UV-induced non-homologous recombination in repair-deficient CHO cell lines transfected with ERCC genes

Effect of UVC Light on Growth, Incorporation of Thymidine, and DNA Chain Elongation in Cells Derived from the Indian Meal Moth and the Cabbage Looper

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