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Journal articles on the topic 'Transcription and repair'

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Author: Grafiati

Published: 11 March 2023

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1

Svejstrup, Jesper Q. "Transcription-coupled DNA repair without the transcription-coupling repair factor." Trends in Biochemical Sciences 26, no. 3 (March 2001): 151. http://dx.doi.org/10.1016/s0968-0004(00)01766-7.

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2

Osley, Mary Ann. "Transcription RINGs in repair." Nature Cell Biology 7, no. 6 (June 2005): 553–55. http://dx.doi.org/10.1038/ncb0605-553.

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3

Sweder, K., and P. Hanawalt. "Transcription-coupled DNA repair." Science 262, no. 5132 (October 15, 1993): 439–40. http://dx.doi.org/10.1126/science.8211165.

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4

Svejstrup, Jesper Q. "Transcription Repair Coupling Factor." Molecular Cell 9, no. 6 (June 2002): 1151–52. http://dx.doi.org/10.1016/s1097-2765(02)00553-1.

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5

Bhatia, Prakash K., Zhigang Wang, and Errol C. Friedberg. "DNA repair and transcription." Current Opinion in Genetics & Development 6, no. 2 (April 1996): 146–50. http://dx.doi.org/10.1016/s0959-437x(96)80043-8.

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6

Drapkin, Ronny, Aziz Sancar, and Danny Reinberg. "Where transcription meets repair." Cell 77, no. 1 (April 1994): 9–12. http://dx.doi.org/10.1016/0092-8674(94)90228-3.

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7

Schaeffer, L., C. P. Selby, and A. Sancar. "Connecting repair and transcription." Trends in Cell Biology 3, no. 7 (July 1993): 229. http://dx.doi.org/10.1016/0962-8924(93)90121-g.

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8

Deger, Nazli, Yanyan Yang, Laura A. Lindsey-Boltz, Aziz Sancar, and Christopher P. Selby. "Drosophila, which lacks canonical transcription-coupled repair proteins, performs transcription-coupled repair." Journal of Biological Chemistry 294, no. 48 (October 17, 2019): 18092–98. http://dx.doi.org/10.1074/jbc.ac119.011448.

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9

Verhage, R. A., A. J. van Gool, N. de Groot, J. H. Hoeijmakers, P. van de Putte, and J. Brouwer. "Double mutants of Saccharomyces cerevisiae with alterations in global genome and transcription-coupled repair." Molecular and Cellular Biology 16, no. 2 (February 1996): 496–502. http://dx.doi.org/10.1128/mcb.16.2.496.

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The nucleotide excision repair (NER) pathway is thought to consist of two subpathways: transcription-coupled repair, limited to the transcribed strand of active genes, and global genome repair for nontranscribed DNA strands. Recently we cloned the RAD26 gene, the Saccharomyces cerevisiae homolog of human CSB/ERCC6, a gene involved in transcription-coupled repair and the disorder Cockayne syndrome. This paper describes the analysis of yeast double mutants selectively affected in each NER subpathway. Although rad26 disruption mutants are defective in transcription-coupled repair, they are not UV sensitive. However, double mutants of RAD26 with the global genome repair determinants RAD7 and RAD16 appeared more UV sensitive than the single rad7 or rad16 mutants but not as sensitive as completely NER-deficient mutants. These findings unmask a role of RAD26 and transcription-coupled repair in UV survival, indicate that transcription-coupled repair and global genome repair are partially overlapping, and provide evidence for a residual NER modality in the double mutants. Analysis of dimer removal from the active RPB2 gene in the rad7/16 rad26 double mutants revealed (i) a contribution of the global genome repair factors Rad7p and Rad16p to repair of the transcribed strand, confirming the partial overlap between both NER subpathways, and (ii) residual repair specifically of the transcribed strand. To investigate the transcription dependence of this repair activity, strand-specific repair of the inducible GAL7 gene was investigated. The template strand of this gene was repaired only under induced conditions, pointing to a role for transcription in the residual repair in the double mutants and suggesting that transcription-coupled repair can to some extent operate independently from Rad26p. Our findings also indicate locus heterogeneity for the dependence of transcription-coupled repair on RAD26.

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10

Nouspikel, Thierry P., Nevila Hyka-Nouspikel, and Philip C. Hanawalt. "Transcription Domain-Associated Repair in Human Cells." Molecular and Cellular Biology 26, no. 23 (October 2, 2006): 8722–30. http://dx.doi.org/10.1128/mcb.01263-06.

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ABSTRACT Nucleotide excision repair (NER), which is arguably the most versatile DNA repair system, is strongly attenuated in human cells of the monocytic lineage when they differentiate into macrophages. Within active genes, however, both DNA strands continue to be proficiently repaired. The proficient repair of the nontranscribed strand cannot be explained by the dedicated subpathway of transcription-coupled repair (TCR), which is targeted to the transcribed strand in expressed genes. We now report that the previously termed differentiation-associated repair (DAR) depends upon transcription, but not simply upon RNA polymerase II (RNAPII) encountering a lesion: proficient repair of both DNA strands can occur in a part of a gene that the polymerase never reaches, and even if the translocation of RNAPII is blocked with transcription inhibitors. This suggests that DAR may be a subset of global NER, restricted to the subnuclear compartments or chromatin domains within which transcription occurs. Downregulation of selected NER genes with small interfering RNA has confirmed that DAR relies upon the same genes as global genome repair, rather than upon TCR-specific genes. Our findings support the general view that the genomic domains within which transcription is active are more accessible than the bulk of the genome to the recognition and repair of lesions through the global pathway and that TCR is superimposed upon that pathway of NER.

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11

Leadon, S. A., and M. M. Snowden. "Differential repair of DNA damage in the human metallothionein gene family." Molecular and Cellular Biology 8, no. 12 (December 1988): 5331–38. http://dx.doi.org/10.1128/mcb.8.12.5331-5338.1988.

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We studied the repair of UV- and aflatoxin B1 (AFB1)-induced damage in the human metallothionein (hMT) gene family. After exposure to either UV or AFB1, DNA damage was initially repaired faster in the DNA fragments containing the transcribed hMT-IA, hMT-IE, and hMT-IIA genes than in the genome overall. By 6 h posttreatment, there was at least twice as much repair in these genes as in the rest of the genome. Repair of UV damage in the hMT-IB gene, which shows cell-type specific expression, and in the hMT-IIB gene, which is a nontranscribed processed pseudogene, was about the same as in the rest of the genome, whereas repair of AFB1-induced damage was deficient in these two genes. Inducing transcription of the three expressed hMT genes with CdCl2 or of only the hMT-IIA gene with dexamethasone increased the initial rate of repair in the induced genes another twofold over the rate observed when they were transcribed at a basal level. The rates of repair in the hMT-IB and hMT-IIB genes were not altered by these inducing treatments. Transcription of the hMT genes was transiently inhibited after UV irradiation. Inducing transcription of the genes did not shorten this UV-induced delay. Thus, the efficiency of repair of damage in a DNA sequence is dependent on the level of transcriptional activity associated with that sequence. However, an increased efficiency in repair of a gene itself is not necessarily coupled to recovery of its transcription after DNA damage.

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12

Leadon, S. A., and M. M. Snowden. "Differential repair of DNA damage in the human metallothionein gene family." Molecular and Cellular Biology 8, no. 12 (December 1988): 5331–38. http://dx.doi.org/10.1128/mcb.8.12.5331.

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We studied the repair of UV- and aflatoxin B1 (AFB1)-induced damage in the human metallothionein (hMT) gene family. After exposure to either UV or AFB1, DNA damage was initially repaired faster in the DNA fragments containing the transcribed hMT-IA, hMT-IE, and hMT-IIA genes than in the genome overall. By 6 h posttreatment, there was at least twice as much repair in these genes as in the rest of the genome. Repair of UV damage in the hMT-IB gene, which shows cell-type specific expression, and in the hMT-IIB gene, which is a nontranscribed processed pseudogene, was about the same as in the rest of the genome, whereas repair of AFB1-induced damage was deficient in these two genes. Inducing transcription of the three expressed hMT genes with CdCl2 or of only the hMT-IIA gene with dexamethasone increased the initial rate of repair in the induced genes another twofold over the rate observed when they were transcribed at a basal level. The rates of repair in the hMT-IB and hMT-IIB genes were not altered by these inducing treatments. Transcription of the hMT genes was transiently inhibited after UV irradiation. Inducing transcription of the genes did not shorten this UV-induced delay. Thus, the efficiency of repair of damage in a DNA sequence is dependent on the level of transcriptional activity associated with that sequence. However, an increased efficiency in repair of a gene itself is not necessarily coupled to recovery of its transcription after DNA damage.

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13

Daniel, Laurianne, Elena Cerutti, Lise-Marie Donnio, Julie Nonnekens, Christophe Carrat, Simona Zahova, Pierre-Olivier Mari, and Giuseppina Giglia-Mari. "Mechanistic insights in transcription-coupled nucleotide excision repair of ribosomal DNA." Proceedings of the National Academy of Sciences 115, no. 29 (July 2, 2018): E6770—E6779. http://dx.doi.org/10.1073/pnas.1716581115.

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Nucleotide excision repair (NER) guarantees genome integrity against UV light-induced DNA damage. After UV irradiation, cells have to cope with a general transcriptional block. To ensure UV lesions repair specifically on transcribed genes, NER is coupled with transcription in an extremely organized pathway known as transcription-coupled repair. In highly metabolic cells, more than 60% of total cellular transcription results from RNA polymerase I activity. Repair of the mammalian transcribed ribosomal DNA has been scarcely studied. UV lesions severely block RNA polymerase I activity and the full transcription-coupled repair machinery corrects damage on actively transcribed ribosomal DNAs. After UV irradiation, RNA polymerase I is more bound to the ribosomal DNA and both are displaced to the nucleolar periphery. Importantly, the reentry of RNA polymerase I and the ribosomal DNA is dependent on the presence of UV lesions on DNA and independent of transcription restart.

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14

Selvam, Kathiresan, Dalton A. Plummer, Peng Mao, and John J. Wyrick. "Set2 histone methyltransferase regulates transcription coupled-nucleotide excision repair in yeast." PLOS Genetics 18, no. 3 (March 9, 2022): e1010085. http://dx.doi.org/10.1371/journal.pgen.1010085.

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Helix-distorting DNA lesions, including ultraviolet (UV) light-induced damage, are repaired by the global genomic-nucleotide excision repair (GG-NER) and transcription coupled-nucleotide excision repair (TC-NER) pathways. Previous studies have shown that histone post-translational modifications (PTMs) such as histone acetylation and methylation can promote GG-NER in chromatin. Whether histone PTMs also regulate the repair of DNA lesions by the TC-NER pathway in transcribed DNA is unknown. Here, we report that histone H3 K36 methylation (H3K36me) by the Set2 histone methyltransferase in yeast regulates TC-NER. Mutations in Set2 or H3K36 result in UV sensitivity that is epistatic with Rad26, the primary TC-NER factor in yeast, and cause a defect in the repair of UV damage across the yeast genome. We further show that mutations in Set2 or H3K36 in a GG-NER deficient strain (i.e., rad16Δ) partially rescue its UV sensitivity. Our data indicate that deletion of SET2 rescues UV sensitivity in a GG-NER deficient strain by activating cryptic antisense transcription, so that the non-transcribed strand (NTS) of yeast genes is repaired by TC-NER. These findings indicate that Set2 methylation of H3K36 establishes transcriptional asymmetry in repair by promoting canonical TC-NER of the transcribed strand (TS) and suppressing cryptic TC-NER of the NTS.

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15

Sengupta, Shiladitya, Haibo Wang, Chunying Yang, Bartosz Szczesny, Muralidhar L. Hegde, and Sankar Mitra. "Ligand-induced gene activation is associated with oxidative genome damage whose repair is required for transcription." Proceedings of the National Academy of Sciences 117, no. 36 (August 21, 2020): 22183–92. http://dx.doi.org/10.1073/pnas.1919445117.

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Among several reversible epigenetic changes occurring during transcriptional activation, only demethylation of histones and cytosine-phosphate-guanines (CpGs) in gene promoters and other regulatory regions by specific demethylase(s) generates reactive oxygen species (ROS), which oxidize DNA and other cellular components. Here, we show induction of oxidized bases and single-strand breaks (SSBs), but not direct double-strand breaks (DSBs), in the genome during gene activation by ligands of the nuclear receptor superfamily. We observed that these damages were preferentially repaired in promoters via the base excision repair (BER)/single-strand break repair (SSBR) pathway. Interestingly, BER/SSBR inhibition suppressed gene activation. Constitutive association of demethylases with BER/SSBR proteins in multiprotein complexes underscores the coordination of histone/DNA demethylation and genome repair during gene activation. However, ligand-independent transcriptional activation occurring during heat shock (HS) induction is associated with the generation of DSBs, the repair of which is likewise essential for the activation of HS-responsive genes. These observations suggest that the repair of distinct damages induced during diverse transcriptional activation is a universal prerequisite for transcription initiation. Because of limited investigation of demethylation-induced genome damage during transcription, this study suggests that the extent of oxidative genome damage resulting from various cellular processes is substantially underestimated.

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16

Guintini, Laetitia, Audrey Paillé, Marco Graf, Brian Luke, Raymund J. Wellinger, and Antonio Conconi. "Transcription of ncRNAs promotes repair of UV induced DNA lesions in Saccharomyces cerevisiae subtelomeres." PLOS Genetics 18, no. 4 (April 29, 2022): e1010167. http://dx.doi.org/10.1371/journal.pgen.1010167.

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Ultraviolet light causes DNA lesions that are removed by nucleotide excision repair (NER). The efficiency of NER is conditional to transcription and chromatin structure. UV induced photoproducts are repaired faster in the gene transcribed strands than in the non-transcribed strands or in transcriptionally inactive regions of the genome. This specificity of NER is known as transcription-coupled repair (TCR). The discovery of pervasive non-coding RNA transcription (ncRNA) advocates for ubiquitous contribution of TCR to the repair of UV photoproducts, beyond the repair of active gene-transcribed strands. Chromatin rules transcription, and telomeres form a complex structure of proteins that silences nearby engineered ectopic genes. The essential protective function of telomeres also includes preventing unwanted repair of double-strand breaks. Thus, telomeres were thought to be transcriptionally inert but more recently, ncRNA transcription was found to initiate in subtelomeric regions. On the other hand, induced DNA lesions like the UV photoproducts must be recognized and repaired also at the ends of chromosomes. In this study, repair of UV induced DNA lesions was analyzed in the subtelomeric regions of budding yeast. The T4-endonuclease V nicking-activity at cyclobutene pyrimidine dimer (CPD) sites was exploited to monitor CPD formation and repair. The presence of two photoproducts, CPDs and pyrimidine (6,4)-pyrimidones (6-4PPs), was verified by the effective and precise blockage of Taq DNA polymerase at these sites. The results indicate that UV photoproducts in silenced heterochromatin are slowly repaired, but that ncRNA transcription enhances NER throughout one subtelomeric element, called Y’, and in distinct short segments of the second, more conserved element, called X. Therefore, ncRNA-transcription dependent TCR assists global genome repair to remove CPDs and 6-4PPs from subtelomeric DNA.

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17

Tremblay, Maxime, Yumin Teng, Michel Paquette, Raymond Waters, and Antonio Conconi. "Complementary Roles of Yeast Rad4p and Rad34p in Nucleotide Excision Repair of Active and Inactive rRNA Gene Chromatin." Molecular and Cellular Biology 28, no. 24 (October 20, 2008): 7504–13. http://dx.doi.org/10.1128/mcb.00137-08.

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ABSTRACT Nucleotide excision repair (NER) removes a plethora of DNA lesions. It is performed by a large multisubunit protein complex that finds and repairs damaged DNA in different chromatin contexts and nuclear domains. The nucleolus is the most transcriptionally active domain, and in yeast, transcription-coupled NER occurs in RNA polymerase I-transcribed genes (rDNA). Here we have analyzed the roles of two members of the xeroderma pigmentosum group C family of proteins, Rad4p and Rad34p, during NER in the active and inactive rDNA. We report that Rad4p is essential for repair in the intergenic spacer, the inactive rDNA coding region, and for strand-specific repair at the transcription initiation site, whereas Rad34p is not. Rad34p is necessary for transcription-coupled NER that starts about 40 nucleotides downstream of the transcription initiation site of the active rDNA, whereas Rad4p is not. Thus, although Rad4p and Rad34p share sequence homology, their roles in NER in the rDNA locus are almost entirely distinct and complementary. These results provide evidences that transcription-coupled NER and global genome NER participate in the removal of UV-induced DNA lesions from the transcribed strand of active rDNA. Furthermore, nonnucleosome rDNA is repaired faster than nucleosome rDNA, indicating that an open chromatin structure facilitates NER in vivo.

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18

Hoeijmakers, JHJ, G. Weeda, W. Vermeulen, C. Troelstra, and D. Bootsma. "Nucleotide excision repair, transcription and human repair syndromes." European Journal of Cancer 29 (January 1993): S32. http://dx.doi.org/10.1016/0959-8049(93)90766-9.

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19

Vermeulen, W., and M. Fousteri. "Mammalian Transcription-Coupled Excision Repair." Cold Spring Harbor Perspectives in Biology 5, no. 8 (August 1, 2013): a012625. http://dx.doi.org/10.1101/cshperspect.a012625.

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20

Weitzman, Jonathan B. "FOXO transcription factor stimulates repair." Genome Biology 3 (2002): spotlight—20020422–02. http://dx.doi.org/10.1186/gb-spotlight-20020422-02.

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21

Kamarthapu, Venu, and Evgeny Nudler. "Rethinking transcription coupled DNA repair." Current Opinion in Microbiology 24 (April 2015): 15–20. http://dx.doi.org/10.1016/j.mib.2014.12.005.

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22

Spivak, Graciela. "Transcription-coupled repair: an update." Archives of Toxicology 90, no. 11 (August 22, 2016): 2583–94. http://dx.doi.org/10.1007/s00204-016-1820-x.

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23

Gaul, Liam, and Jesper Q. Svejstrup. "Transcription-coupled repair and the transcriptional response to UV-Irradiation." DNA Repair 107 (November 2021): 103208. http://dx.doi.org/10.1016/j.dnarep.2021.103208.

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24

Deng, W. P., and J. A. Nickoloff. "Preferential repair of UV damage in highly transcribed DNA diminishes UV-induced intrachromosomal recombination in mammalian cells." Molecular and Cellular Biology 14, no. 1 (January 1994): 391–99. http://dx.doi.org/10.1128/mcb.14.1.391-399.1994.

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The relationships among transcription, recombination, DNA damage, and repair in mammalian cells were investigated. We monitored the effects of transcription on UV-induced intrachromosomal recombination between neomycin repeats including a promoterless allele and an inducible heteroallele regulated by the mouse mammary tumor virus promoter. Although transcription and UV light separately stimulated recombination, increasing transcription levels reduced UV-induced recombination. Preferential repair of UV damage in transcribed strands was shown in highly transcribed DNA, suggesting that recombination is stimulated by unrepaired UV damage and that increased DNA repair in highly transcribed alleles removes recombinogenic lesions. This study indicates that the genetic consequences of DNA damage depend on transcriptional states and provides a basis for understanding tissue- and gene-specific responses to DNA-damaging agents.

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25

Deng, W. P., and J. A. Nickoloff. "Preferential repair of UV damage in highly transcribed DNA diminishes UV-induced intrachromosomal recombination in mammalian cells." Molecular and Cellular Biology 14, no. 1 (January 1994): 391–99. http://dx.doi.org/10.1128/mcb.14.1.391.

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The relationships among transcription, recombination, DNA damage, and repair in mammalian cells were investigated. We monitored the effects of transcription on UV-induced intrachromosomal recombination between neomycin repeats including a promoterless allele and an inducible heteroallele regulated by the mouse mammary tumor virus promoter. Although transcription and UV light separately stimulated recombination, increasing transcription levels reduced UV-induced recombination. Preferential repair of UV damage in transcribed strands was shown in highly transcribed DNA, suggesting that recombination is stimulated by unrepaired UV damage and that increased DNA repair in highly transcribed alleles removes recombinogenic lesions. This study indicates that the genetic consequences of DNA damage depend on transcriptional states and provides a basis for understanding tissue- and gene-specific responses to DNA-damaging agents.

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26

Sweder, Kevin S., Richard A. Verhage, David J. Crowley, Gray F. Crouse, Jaap Brouwer, and Philip C. Hanawalt. "Mismatch Repair Mutants in Yeast Are Not Defective in Transcription-Coupled DNA Repair of UV-Induced DNA Damage." Genetics 143, no. 3 (July 1, 1996): 1127–35. http://dx.doi.org/10.1093/genetics/143.3.1127.

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Abstract Transcription-coupled repair, the targeted repair of the transcribed strands of active genes, is defective in bacteria, yeast, and human cells carrying mutations in mfd, RAD26 and ERCC6, respectively. Other factors probably are also uniquely involved in transcription-repair coupling. Recently, a defect was described in transcription-coupled repair for Escherichia coli mismatch repair mutants and human tumor cell lines with mutations in mismatch repair genes. We examined removal of UV-induced DNA damage in yeast strains mutated in mismatch repair genes in an effort to confirm a defect in transcription-coupled repair in this system. In addition, we determined the contribution of the mismatch repair gene MSH2 to transcription-coupled repair in the absence of global genomic repair using rad7Δ mutants. We also determined whether the Rad26-independent transcription-coupled repair observed in rad26Δ and rad7Δ rad26Δ mutants depends on MSH2 by examining repair deficiencies of rad26Δ msh2Δ and rad7Δ rad26Δ msh2Δ mutants. We found no defects in transcription-coupled repair caused by mutations in the mismatch repair genes MSH2, MLH1, PMS1, and MSH3. Yeast appears to differ from bacteria and human cells in the capacity for transcription-coupled repair in a mismatch repair mutant background.

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27

Ali, Rahmen B., Alvin K. C. Teo, Hue-Kian Oh, Linda S. H. Chuang, Teck-Choon Ayi, and Benjamin F. L. Li. "Implication of Localization of Human DNA Repair Enzyme O6-Methylguanine-DNA Methyltransferase at Active Transcription Sites in Transcription-Repair Coupling of the Mutagenic O6-Methylguanine Lesion." Molecular and Cellular Biology 18, no. 3 (March 1, 1998): 1660–69. http://dx.doi.org/10.1128/mcb.18.3.1660.

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ABSTRACT DNA lesions that halt RNA polymerase during transcription are preferentially repaired by the nucleotide excision repair pathway. This transcription-coupled repair is initiated by the arrested RNA polymerase at the DNA lesion. However, the mutagenicO 6-methylguanine (6MG) lesion which is bypassed by RNA polymerase is also preferentially repaired at the transcriptionally active DNA. We report here a plausible explanation for this observation: the human 6MG repair enzymeO 6-methylguanine-DNA methyltransferase (MGMT) is present as speckles concentrated at active transcription sites (as revealed by polyclonal antibodies specific for its N and C termini). Upon treatment of cells with low dosages ofN-methylnitrosourea, which produces 6MG lesions in the DNA, these speckles rapidly disappear, accompanied by the formation of active-site methylated MGMT (the repair product of 6MG by MGMT). The ability of MGMT to target itself to active transcription sites, thus providing an effective means of repairing 6MG lesions, possibly at transcriptionally active DNA, indicates its crucial role in human cancer and chemotherapy by alkylating agents.

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28

Desai, Ravi V., Xinyue Chen, Benjamin Martin, Sonali Chaturvedi, Dong Woo Hwang, Weihan Li, Chen Yu, et al. "A DNA repair pathway can regulate transcriptional noise to promote cell fate transitions." Science 373, no. 6557 (July 22, 2021): eabc6506. http://dx.doi.org/10.1126/science.abc6506.

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Stochastic fluctuations in gene expression (“noise”) are often considered detrimental, but fluctuations can also be exploited for benefit (e.g., dither). We show here that DNA base excision repair amplifies transcriptional noise to facilitate cellular reprogramming. Specifically, the DNA repair protein Apex1, which recognizes both naturally occurring and unnatural base modifications, amplifies expression noise while homeostatically maintaining mean expression levels. This amplified expression noise originates from shorter-duration, higher-intensity transcriptional bursts generated by Apex1-mediated DNA supercoiling. The remodeling of DNA topology first impedes and then accelerates transcription to maintain mean levels. This mechanism, which we refer to as “discordant transcription through repair” (“DiThR,” which is pronounced “dither”), potentiates cellular reprogramming and differentiation. Our study reveals a potential functional role for transcriptional fluctuations mediated by DNA base modifications in embryonic development and disease.

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29

Oh, Juntaek, Jun Xu, Jenny Chong, and Dong Wang. "Molecular basis of transcriptional pausing, stalling, and transcription-coupled repair initiation." Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms 1864, no. 1 (January 2021): 194659. http://dx.doi.org/10.1016/j.bbagrm.2020.194659.

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30

Friedberg, Errol C. "Relationships Between DNA Repair and Transcription." Annual Review of Biochemistry 65, no. 1 (June 1996): 15–42. http://dx.doi.org/10.1146/annurev.bi.65.070196.000311.

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31

Compe, Emmanuel, and Jean-Marc Egly. "TFIIH: when transcription met DNA repair." Nature Reviews Molecular Cell Biology 13, no. 6 (May 10, 2012): 343–54. http://dx.doi.org/10.1038/nrm3350.

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32

Svejstrup, Jesper Q. "Mechanisms of transcription-coupled DNA repair." Nature Reviews Molecular Cell Biology 3, no. 1 (January 2002): 21–29. http://dx.doi.org/10.1038/nrm703.

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33

Hanawalt, P. "Transcription-coupled repair and human disease." Science 266, no. 5193 (December 23, 1994): 1957–58. http://dx.doi.org/10.1126/science.7801121.

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34

Mellon, Isabel. "Transcription-coupled repair: A complex affair." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 577, no. 1-2 (September 2005): 155–61. http://dx.doi.org/10.1016/j.mrfmmm.2005.03.016.

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35

Andressoo, J. O., and J. H. J. Hoeijmakers. "Transcription-coupled repair and premature ageing." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 577, no. 1-2 (September 2005): 179–94. http://dx.doi.org/10.1016/j.mrfmmm.2005.04.004.

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36

Hanawalt, P. C., B. A. Donahue, and K. S. Sweder. "Repair and Transcription: Collision or collusion?" Current Biology 4, no. 6 (June 1994): 518–21. http://dx.doi.org/10.1016/s0960-9822(00)00112-3.

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37

Selby, C., and A. Sancar. "Molecular mechanism of transcription-repair coupling." Science 260, no. 5104 (April 2, 1993): 53–58. http://dx.doi.org/10.1126/science.8465200.

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38

Mullenders, Leon H. F. "Transcription response and nucleotide excision repair." Mutation Research/DNA Repair 409, no. 2 (November 1998): 59–64. http://dx.doi.org/10.1016/s0921-8777(98)00048-2.

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39

Deaconescu, Alexandra M., Nigel Savery, and Seth A. Darst. "The bacterial transcription repair coupling factor." Current Opinion in Structural Biology 17, no. 1 (February 2007): 96–102. http://dx.doi.org/10.1016/j.sbi.2007.01.005.

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40

Portman, James R., and Terence R. Strick. "Transcription-Coupled Repair and Complex Biology." Journal of Molecular Biology 430, no. 22 (October 2018): 4496–512. http://dx.doi.org/10.1016/j.jmb.2018.04.033.

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41

van Gool, A. J. "Cockayne syndrome: defective repair of transcription?" EMBO Journal 16, no. 14 (July 15, 1997): 4155–62. http://dx.doi.org/10.1093/emboj/16.14.4155.

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42

Moses, Robb E., and Bert W. O'Malley. "DNA Transcription and Repair: A Confluence." Journal of Biological Chemistry 287, no. 28 (May 17, 2012): 23266–70. http://dx.doi.org/10.1074/jbc.r112.377135.

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Machado, Carlos R., João P. Vieira‐da‐Rocha, Isabela Cecilia Mendes, Matheus A. Rajão, Lucio Marcello, Mainá Bitar, Marcela G. Drummond, et al. "Nucleotide excision repair in T rypanosoma brucei : specialization of transcription‐coupled repair due to multigenic transcription." Molecular Microbiology 92, no. 4 (April 24, 2014): 756–76. http://dx.doi.org/10.1111/mmi.12589.

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44

Nadkarni, Aditi, John A. Burns, Alberto Gandolfi, Moinuddin A. Chowdhury, Laura Cartularo, Christian Berens, Nicholas E. Geacintov, and David A. Scicchitano. "Nucleotide Excision Repair and Transcription-coupled DNA Repair Abrogate the Impact of DNA Damage on Transcription." Journal of Biological Chemistry 291, no. 2 (November 11, 2015): 848–61. http://dx.doi.org/10.1074/jbc.m115.685271.

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45

Tan, Xin Yi, and Michael S. Y. Huen. "Perfecting DNA double-strand break repair on transcribed chromatin." Essays in Biochemistry 64, no. 5 (April 20, 2020): 705–19. http://dx.doi.org/10.1042/ebc20190094.

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Abstract Timely repair of DNA double-strand break (DSB) entails coordination with the local higher order chromatin structure and its transaction activities, including transcription. Recent studies are uncovering how DSBs trigger transient suppression of nearby transcription to permit faithful DNA repair, failing of which leads to elevated chromosomal aberrations and cell hypersensitivity to DNA damage. Here, we summarize the molecular bases for transcriptional control during DSB metabolism, and discuss how the exquisite coordination between the two DNA-templated processes may underlie maintenance of genome stability and cell homeostasis.

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46

Adar, Sheera, Jinchuan Hu, Jason D. Lieb, and Aziz Sancar. "Genome-wide kinetics of DNA excision repair in relation to chromatin state and mutagenesis." Proceedings of the National Academy of Sciences 113, no. 15 (March 28, 2016): E2124—E2133. http://dx.doi.org/10.1073/pnas.1603388113.

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We recently developed a high-resolution genome-wide assay for mapping DNA excision repair named eXcision Repair-sequencing (XR-seq) and have now used XR-seq to determine which regions of the genome are subject to repair very soon after UV exposure and which regions are repaired later. Over a time course, we measured repair of the UV-induced damage of cyclobutane pyrimidine dimers (CPDs) (at 1, 4, 8, 16, 24, and 48 h) and (6-4)pyrimidine-pyrimidone photoproducts [(6-4)PPs] (at 5 and 20 min and 1, 2, and 4 h) in normal human skin fibroblasts. Each type of damage has distinct repair kinetics. The (6-4)PPs are detected as early as 5 min after UV treatment, with the bulk of repair completed by 4 h. Repair of CPDs, which we previously showed is intimately coupled to transcription, is slower and in certain regions persists even 2 d after UV irradiation. We compared our results to the Encyclopedia of DNA Elements data regarding histone modifications, chromatin state, and transcription. For both damage types, and for both transcription-coupled and general excision repair, the earliest repair occurred preferentially in active and open chromatin states. Conversely, repair in regions classified as “heterochromatic” and “repressed” was relatively low at early time points, with repair persisting into the late time points. Damage that remains during DNA replication increases the risk for mutagenesis. Indeed, late-repaired regions are associated with a higher level of cancer-linked mutations. In summary, we show that XR-seq is a powerful approach for studying relationships among chromatin state, DNA repair, genome stability, mutagenesis, and carcinogenesis.

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Ross, Christian, Christine Pybus, Mario Pedraza-Reyes, Huang-Mo Sung, Ronald E. Yasbin, and Eduardo Robleto. "Novel Role of mfd: Effects on Stationary-Phase Mutagenesis in Bacillus subtilis." Journal of Bacteriology 188, no. 21 (September 1, 2006): 7512–20. http://dx.doi.org/10.1128/jb.00980-06.

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ABSTRACT Previously, using a chromosomal reversion assay system, we established that an adaptive mutagenic process occurs in nongrowing Bacillus subtilis cells under stress, and we demonstrated that multiple mechanisms are involved in generating these mutations (41, 43). In an attempt to delineate how these mutations are generated, we began an investigation into whether or not transcription and transcription-associated proteins influence adaptive mutagenesis. In B. subtilis, the Mfd protein (transcription repair coupling factor) facilitates removal of RNA polymerase stalled at transcriptional blockages and recruitment of repair proteins to DNA lesions on the transcribed strand. Here we demonstrate that the loss of Mfd has a depressive effect on stationary-phase mutagenesis. An association between Mfd mutagenesis and aspects of transcription is discussed.

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Maddukuri, Leena, Dominika Dudzińska, and Barbara Tudek. "Bacterial DNA repair genes and their eukaryotic homologues: 4. The role of nucleotide excision DNA repair (NER) system in mammalian cells." Acta Biochimica Polonica 54, no. 3 (September 23, 2007): 469–82. http://dx.doi.org/10.18388/abp.2007_3222.

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The eukaryotic cell encounters more than one million various kinds of DNA lesions per day. The nucleotide excision repair (NER) pathway is one of the most important repair mechanisms that removes a wide spectrum of different DNA lesions. NER operates through two sub pathways: global genome repair (GGR) and transcription-coupled repair (TCR). GGR repairs the DNA damage throughout the entire genome and is initiated by the HR23B/XPC complex, while the CSB protein-governed TCR process removes DNA lesions from the actively transcribed strand. The sequence of events and the role of particular NER proteins are currently being extensively discussed. NER proteins also participate in other cellular processes like replication, transcription, chromatin maintenance and protein turnover. Defects in NER underlay severe genetic disorders: xeroderma pigmentosum (XP), Cockayne syndrome (CS) and trichothiodystrophy (TTD).

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Crowley, David J., and Philip C. Hanawalt. "Induction of the SOS Response Increases the Efficiency of Global Nucleotide Excision Repair of Cyclobutane Pyrimidine Dimers, but Not 6-4 Photoproducts, in UV-IrradiatedEscherichia coli." Journal of Bacteriology 180, no. 13 (July 1, 1998): 3345–52. http://dx.doi.org/10.1128/jb.180.13.3345-3352.1998.

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ABSTRACT Nucleotide excision repair (NER) is responsible for the removal of a variety of lesions from damaged DNA and proceeds through two subpathways, global repair and transcription-coupled repair. InEscherichia coli, both subpathways require UvrA and UvrB, which are induced following DNA damage as part of the SOS response. We found that elimination of the SOS response either genetically or by treatment with the transcription inhibitor rifampin reduced the efficiency of global repair of the major UV-induced lesion, the cyclobutane pyrimidine dimer (CPD), but had no effect on the global repair of 6-4 photoproducts. Mutants in which the SOS response was constitutively derepressed repaired CPDs more rapidly than did wild-type cells, and this rate was not affected by rifampin. Transcription-coupled repair of CPDs occurred in the absence of SOS induction but was undetectable when the response was expressed constitutively. These results suggest that damage-inducible synthesis of UvrA and UvrB is necessary for efficient repair of CPDs and that the levels of these proteins determine the rate of NER of UV photoproducts. We compare our findings with recent data from eukaryotic systems and suggest that damage-inducible stress responses are generally critical for efficient global repair of certain types of genomic damage.

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Poli, Jérôme, Susan M. Gasser, and Manolis Papamichos-Chronakis. "The INO80 remodeller in transcription, replication and repair." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1731 (August 28, 2017): 20160290. http://dx.doi.org/10.1098/rstb.2016.0290.

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The accessibility of eukaryotic genomes to the action of enzymes involved in transcription, replication and repair is maintained despite the organization of DNA into nucleosomes. This access is often regulated by the action of ATP-dependent nucleosome remodellers. The INO80 class of nucleosome remodellers has unique structural features and it is implicated in a diverse array of functions, including transcriptional regulation, DNA replication and DNA repair. Underlying these diverse functions is the catalytic activity of the main ATPase subunit, which in the context of a multisubunit complex can shift nucleosomes and carry out histone dimer exchange. In vitro studies showed that INO80 promotes replication fork progression on a chromatin template, while in vivo it was shown to facilitate replication fork restart after stalling and to help evict RNA polymerase II at transcribed genes following the collision of a replication fork with transcription. More recent work in yeast implicates INO80 in the general eviction and degradation of nucleosomes following high doses of oxidative DNA damage. Beyond these replication and repair functions, INO80 was shown to repress inappropriate transcription at promoters in the opposite direction to the coding sequence. Here we discuss the ways in which INO80's diverse functions help maintain genome integrity. This article is part of the themed issue ‘Chromatin modifiers and remodellers in DNA repair and signalling’.

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