Fully functional global genome repair of (6-4) photoproducts and compromised transcription-coupled repair of cyclobutane pyrimidine dimers in condensed mitotic chromatin
Journal Article
·
· Experimental Cell Research
- Department of Cell Biology, Tohoku University Graduate School of Medicine, Sendai 980-8575 (Japan)
- Radioisotope Research Center, Nara Medical University, Kashihara, Nara 634-8521 (Japan)
During mitosis, chromatin is highly condensed, and activities such as transcription and semiconservative replication do not occur. Consequently, the condensed condition of mitotic chromatin is assumed to inhibit DNA metabolism by impeding the access of DNA-transacting proteins. However, about 40 years ago, several researchers observed unscheduled DNA synthesis in UV-irradiated mitotic chromosomes, suggesting the presence of excision repair. We re-examined this subject by directly measuring the removal of UV-induced DNA lesions by an ELISA and by a Southern-based technique in HeLa cells arrested at mitosis. We observed that the removal of (6-4) photoproducts from the overall genome in mitotic cells was as efficient as in interphase cells. This suggests that global genome repair of (6-4) photoproducts is fully functional during mitosis, and that the DNA in mitotic chromatin is accessible to proteins involved in this mode of DNA repair. Nevertheless, not all modes of DNA repair seem fully functional during mitosis. We also observed that the removal of cyclobutane pyrimidine dimers from the dihydrofolate reductase and c-MYC genes in mitotic cells was very slow. This suggests that transcription-coupled repair of cyclobutane pyrimidine dimers is compromised or non-functional during mitosis, which is probably the consequence of mitotic transcriptional repression. -- Highlights: Black-Right-Pointing-Pointer Global genome repair of (6-4) photoproducts is fully active in mitotic cells. Black-Right-Pointing-Pointer DNA in condensed mitotic chromatin does not seem inaccessible or inert. Black-Right-Pointing-Pointer Mitotic transcriptional repression may impair transcription-coupled repair.
- OSTI ID:
- 22212316
- Journal Information:
- Experimental Cell Research, Journal Name: Experimental Cell Research Journal Issue: 5 Vol. 318; ISSN 0014-4827; ISSN ECREAL
- Country of Publication:
- United States
- Language:
- English
Similar Records
Ultraviolet-induced mutations in Cockayne syndrome cells are primarily caused by cyclobutane dimer photoproducts while repair of other photoproducts is normal
Mapping of UV photoproducts along the c-jun promoter in UV-irradiated human cells
UV light-induced cyclobutane pyrimidine dimers are mutagenic in mammalian cells
Journal Article
·
Sun Aug 01 00:00:00 EDT 1993
· Proceedings of the National Academy of Sciences of the United States of America; (United States)
·
OSTI ID:5923857
Mapping of UV photoproducts along the c-jun promoter in UV-irradiated human cells
Journal Article
·
Fri Dec 30 23:00:00 EST 1994
· Environmental and Molecular Mutagenesis
·
OSTI ID:88921
UV light-induced cyclobutane pyrimidine dimers are mutagenic in mammalian cells
Journal Article
·
Wed Oct 01 00:00:00 EDT 1986
· Mol. Cell. Biol.; (United States)
·
OSTI ID:7084198