Transcription coupled repair efficiency determines the cell cycle progression and apoptosis after UV exposure in hamster cells
- PMID: 12509253
- DOI: 10.1016/s1568-7864(01)00017-9
Transcription coupled repair efficiency determines the cell cycle progression and apoptosis after UV exposure in hamster cells
Abstract
Nucleotide excision repair (NER) is a major pathway for the removal of bulky adducts and helix distorting lesions from the genomic DNA. NER is highly heterogeneous across the genome and operates principally at different levels of hierarchy. Transcription coupled repair (TCR), a special sub-pathway of NER and base excision repair (BER), is critical for cellular resistance after UV irradiation in mammalian cells. In this study, we have investigated the effects of UV-C irradiation on cell cycle progression and apoptosis in G1 synchronised isogenic hamster cell lines that are deficient in TCR and NER pathways. Our results revealed the existence of two apoptotic modes at low UV (2-4J/m2) doses in TCR deficient (UV61) and NER deficient (UV5) cells: one occurring in the first G1 and the other in the second G1-phase following the first division. At high UV doses (8-32J/m2), UV61 and UV5 cells underwent apoptosis without entry into S-phase after a permanent arrest in the initial G1. In contrast to repair deficient cells, parental TCR proficient AA8 cells did not show a significant G1 arrest and apoptosis at doses below 8J/m2. UV61 (proficient in repair of 6-4 photoproducts (PPs)) and UV5 (deficient in 6-4 PP repair) cells showed similar patterns of cell cycle progression and apoptosis. Taken together, these results suggest that the persistence of 6-4 PP and the replication inhibition may not be critical for apoptotic response in hamster cells. Instead, the extent of transcription blockage resulting from the TCR deficiency constitutes the major determining factor for G1 arrest and apoptosis.
Similar articles
-
Transcription coupled repair deficiency results in increased chromosomal aberrations and apoptotic death in the UV61 cell line, the Chinese hamster homologue of Cockayne's syndrome B.Mutat Res. 2001 Mar 7;485(2):121-32. doi: 10.1016/s0921-8777(00)00065-3. Mutat Res. 2001. PMID: 11182543
-
Mechanisms of formation of chromosomal aberrations: insights from studies with DNA repair-deficient cells.Cytogenet Genome Res. 2004;104(1-4):95-9. doi: 10.1159/000077471. Cytogenet Genome Res. 2004. PMID: 15162020 Review.
-
Efficient PCNA complex formation is dependent upon both transcription coupled repair and genome overall repair.Mutat Res. 1998 Dec 14;409(3):135-46. doi: 10.1016/s0921-8777(98)00051-2. Mutat Res. 1998. PMID: 9875289
-
Influence of chromatin remodeling in the removal of UVC-induced damage in TCR proficient and deficient Chinese hamster cells.Mutat Res Genet Toxicol Environ Mutagen. 2018 Dec;836(Pt A):124-131. doi: 10.1016/j.mrgentox.2018.08.003. Epub 2018 Aug 28. Mutat Res Genet Toxicol Environ Mutagen. 2018. PMID: 30389155
-
The eukaryotic nucleotide excision repair pathway.Biochimie. 2003 Nov;85(11):1083-99. doi: 10.1016/j.biochi.2003.10.017. Biochimie. 2003. PMID: 14726015 Review.
Cited by
-
Effects of heat and UV radiation on the mobilization of transposon mariner-Mos1.Cell Stress Chaperones. 2015 Sep;20(5):843-51. doi: 10.1007/s12192-015-0611-2. Epub 2015 Jun 20. Cell Stress Chaperones. 2015. PMID: 26092118 Free PMC article.
-
UVB-induced cell death signaling is associated with G1-S progression and transcription inhibition in primary human fibroblasts.PLoS One. 2013 Oct 14;8(10):e76936. doi: 10.1371/journal.pone.0076936. eCollection 2013. PLoS One. 2013. PMID: 24155908 Free PMC article.
-
Ultraviolet light-emitting diode irradiation-induced cell death in HL-60 human leukemia cells in vitro.Mol Med Rep. 2016 Mar;13(3):2506-10. doi: 10.3892/mmr.2016.4812. Epub 2016 Jan 27. Mol Med Rep. 2016. PMID: 26820261 Free PMC article.
-
DNA damage and the balance between survival and death in cancer biology.Nat Rev Cancer. 2016 Jan;16(1):20-33. doi: 10.1038/nrc.2015.2. Epub 2015 Dec 18. Nat Rev Cancer. 2016. PMID: 26678314 Review.
-
Cockayne syndrome group B cellular and biochemical functions.Am J Hum Genet. 2003 Dec;73(6):1217-39. doi: 10.1086/380399. Epub 2003 Nov 24. Am J Hum Genet. 2003. PMID: 14639525 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Miscellaneous