Готові списки джерел за темами / Transcription coupled repair factors (TCR)

Добірка наукової літератури з теми "Transcription coupled repair factors (TCR)"

Автор: Grafiati

Опубліковано: 6 вересня 2023

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Статті в журналах з теми "Transcription coupled repair factors (TCR)"

Guirouilh-Barbat, Josée, Christophe Redon, and Yves Pommier. "Transcription-coupled DNA Double-Strand Breaks Are Mediated via the Nucleotide Excision Repair and the Mre11-Rad50-Nbs1 Complex." Molecular Biology of the Cell 19, no. 9 (September 2008): 3969–81. http://dx.doi.org/10.1091/mbc.e08-02-0215.

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The cellular activity of Yondelis (trabectedin, Ecteinascidin 743, Et743) is known to depend on transcription-coupled nucleotide excision repair (TCR). However, the subsequent cellular effects of Et743 are not fully understood. Here we show that Et743 induces both transcription- and replication-coupled DNA double-strand breaks (DSBs) that are detectible by neutral COMET assay and as γ-H2AX foci that colocalize with 53BP1, Mre11, Ser1981-pATM, and Thr68-pChk2. The transcription coupled-DSBs (TC-DSBs) induced by Et743 depended both on TCR and Mre11-Rad50-Nbs1 (MRN) and were associated with DNA-PK–dependent γ-H2AX foci. In contrast to DNA-PK, ATM phosphorylated H2AX both in NER-proficient and -deficient cells, but its full activation was dependent on H2AX as well as DNA-PK, suggesting a positive feedback loop: DNA-PK-γ-H2AX-ATM. Knocking-out H2AX or inactivating DNA-PK reduced Et743's antiproliferative activity, whereas ATM and MRN tended to act as survival factors. Our results highlight the interplays between ATM and DNA-PK and their impacts on H2AX phosphorylation and cell survival. They also suggest that γ-H2AX may serve as a biomarker in patients treated with Et743 and that molecular profiling of tumors for TCR, MRN, ATM, and DNA-PK might be useful to anticipate tumor response to Et743 treatment.

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Li, Shisheng, Baojin Ding, Runqiang Chen, Christine Ruggiero, and Xuefeng Chen. "Evidence that the Transcription Elongation Function of Rpb9 Is Involved in Transcription-Coupled DNA Repair in Saccharomyces cerevisiae." Molecular and Cellular Biology 26, no. 24 (October 9, 2006): 9430–41. http://dx.doi.org/10.1128/mcb.01656-06.

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ABSTRACT Rpb9, a small nonessential subunit of RNA polymerase II, has been shown to have multiple transcription-related functions in Saccharomyces cerevisiae. These functions include promoting transcription elongation and mediating a subpathway of transcription-coupled repair (TCR) that is independent of Rad26, the homologue of human Cockayne syndrome complementation group B protein. Rpb9 is composed of three distinct domains: the N-terminal Zn1, the C-terminal Zn2, and the central linker. Here we show that the Zn1 and linker domains are essential, whereas the Zn2 domain is almost dispensable, for both transcription elongation and TCR functions. Impairment of transcription elongation, which does not dramatically compromise Rad26-mediated TCR, completely abolishes Rpb9-mediated TCR. Furthermore, Rpb9 appears to be dispensable for TCR if its transcription elongation function is compensated for by removing a transcription repression/elongation factor. Our data suggest that the transcription elongation function of Rpb9 is involved in TCR.

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Bucheli, Miriam, Lori Lommel, and Kevin Sweder. "The Defect in Transcription-Coupled Repair Displayed by a Saccharomyces cerevisiae rad26 Mutant Is Dependent on Carbon Source and Is Not Associated With a Lack of Transcription." Genetics 158, no. 3 (July 1, 2001): 989–97. http://dx.doi.org/10.1093/genetics/158.3.989.

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Abstract Nucleotide excision repair (NER) is an evolutionarily conserved pathway that removes DNA damage induced by ultraviolet irradiation and various chemical agents that cause bulky adducts. Two subpathways within NER remove damage from the genome overall or the transcribed strands of transcribing genes (TCR). TCR is a faster repair process than overall genomic repair and has been thought to require the RAD26 gene in Saccharomyces cerevisiae. Rad26 is a member of the SWI/SNF family of proteins that either disrupt chromatin or facilitate interactions between the RNA Pol II and transcription activators. SWI/SNF proteins are required for the expression or repression of a diverse set of genes, many of which are differentially transcribed in response to particular carbon sources. The remodeling of chromatin by Rad26 could affect transcription and/or TCR following formation of DNA damage and other stress-inducing conditions. We speculate that another factor(s) can substitute for Rad26 under particular growth conditions. We therefore measured the level of repair and transcription in two different carbon sources and found that the defect in the rad26 mutant for TCR was dependent on the type of carbon source. Furthermore, TCR did not correlate with transcription rate, suggesting that disruption of RAD26 leads to a specific defect in DNA repair and not transcription.

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Desai, Shyamal D., Hui Zhang, Alexandra Rodriguez-Bauman, Jin-Ming Yang, Xiaohua Wu, Murugesan K. Gounder, Eric H. Rubin, and Leroy F. Liu. "Transcription-Dependent Degradation of Topoisomerase I-DNA Covalent Complexes." Molecular and Cellular Biology 23, no. 7 (April 1, 2003): 2341–50. http://dx.doi.org/10.1128/mcb.23.7.2341-2350.2003.

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ABSTRACT Topoisomerase I (Top I)-DNA covalent complexes represent a unique type of DNA lesion whose repair and processing remain unclear. In this study, we show that Top I-DNA covalent complexes transiently arrest RNA transcription in normal nontransformed cells. Arrest of RNA transcription is coupled to activation of proteasomal degradation of Top I and the large subunit of RNA polymerase II. Recovery of transcription occurs gradually and depends on both proteasomal degradation of Top I and functional transcription-coupled repair (TCR). These results suggest that arrest of the RNA polymerase elongation complex by the Top I-DNA covalent complex triggers a 26S proteasome-mediated signaling pathway(s) leading to degradation of both Top I and the large subunit of RNA polymerase II. We propose that proteasomal degradation of Top I and RNA polymerase II precedes repair of the exposed single-strand breaks by TCR.

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Atanassov, Boyko, Aneliya Velkova, Emil Mladenov, Boyka Anachkova, and George Russev. "Comparison of the Global Genomic and Transcription-Coupled Repair Rates of Different Lesions in Human Cells." Zeitschrift für Naturforschung C 59, no. 5-6 (June 1, 2004): 445–53. http://dx.doi.org/10.1515/znc-2004-5-628.

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There are two subclasses of nucleotide excision repair (NER). One is the global genomic repair (GGR) which removes lesions throughout the genome regardless of whether any specific sequence is transcribed or not. The other is the transcription-coupled repair (TCR), which removes lesions only from the transcribed DNA sequences. There are data that GGR rates depend on the chemical nature of the lesions in a manner that the lesions inflicting larger distortion on the DNA double helix are repaired at higher rate. It is not known whether the TCR repair rates depend on the type of lesions and in what way. To address this question human cells were transfected with pEGFP and pEYFP plasmids treated with UV light, cis-diamminedichloroplatinum(II) (cisplatin) and angelicin and 24 h later the restored fluorescence was measured and used to calculate the respective NER rates. In a parallel series of experiments the same plasmids were incubated in repair-competent protein extracts to determine GGR rates in the absence of transcription. From the two sets of data, the TCR rates were calculated. We found out that cisplatin, UV light and angelicin lesions were repaired by GGR with different efficiency, which corresponded to the degree of DNA helix distortion induced by these agents. On the other hand the three lesions were repaired by TCR at very similar rates which showed that TCR efficiency was not directly connected with the chemical nature of the lesions.

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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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van den Boom, Vincent, Elisabetta Citterio, Deborah Hoogstraten, Angelika Zotter, Jean-Marc Egly, Wiggert A. van Cappellen, Jan H. J. Hoeijmakers, Adriaan B. Houtsmuller, and Wim Vermeulen. "DNA damage stabilizes interaction of CSB with the transcription elongation machinery." Journal of Cell Biology 166, no. 1 (June 28, 2004): 27–36. http://dx.doi.org/10.1083/jcb.200401056.

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The Cockayne syndrome B (CSB) protein is essential for transcription-coupled DNA repair (TCR), which is dependent on RNA polymerase II elongation. TCR is required to quickly remove the cytotoxic transcription-blocking DNA lesions. Functional GFP-tagged CSB, expressed at physiological levels, was homogeneously dispersed throughout the nucleoplasm in addition to bright nuclear foci and nucleolar accumulation. Photobleaching studies showed that GFP-CSB, as part of a high molecular weight complex, transiently interacts with the transcription machinery. Upon (DNA damage-induced) transcription arrest CSB binding these interactions are prolonged, most likely reflecting actual engagement of CSB in TCR. These findings are consistent with a model in which CSB monitors progression of transcription by regularly probing elongation complexes and becomes more tightly associated to these complexes when TCR is active.

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D'Errico, Mariarosaria, Massimo Teson, Angelo Calcagnile, Tiziana Nardo, Naomi De Luca, Chiara Lazzari, Silvia Soddu, Giovanna Zambruno, Miria Stefanini, and Eugenia Dogliotti. "Differential Role of Transcription-Coupled Repair in UVB–Induced Response of Human Fibroblasts and Keratinocytes." Cancer Research 65, no. 2 (January 15, 2005): 432–38. http://dx.doi.org/10.1158/0008-5472.432.65.2.

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Abstract Most solar radiation–induced skin cancers arise in keratinocytes. In the human epidermis, protection against cancer is thought to be mediated mainly by nucleotide excision repair (NER) of UVB-induced cyclobutane pyrimidine dimers, and by elimination of the damaged cells by apoptosis. NER consists of two subpathways: global genome repair (GGR) and transcription-coupled repair (TCR). Here, we investigate the impact of defects in NER subpathways on the cellular response to UVB-induced damage by comparing primary human keratinocytes and fibroblasts from normal, XP-C (GGR-defective), and CS-A (TCR-defective) individuals. We show that human keratinocytes are more resistant to UVB killing than fibroblasts and present higher levels of UVB-induced DNA repair synthesis due to a more efficient GGR. The CS-A defect is associated with a strong apoptotic response in fibroblasts but not in keratinocytes. Following an UVB dose of 1,000 J/m2, no p53-mediated transactivation of mdm2 is observed in CS-A fibroblasts, whereas the p53-mdm2 circuit is fully activated in CS-A keratinocytes. Thus, in fibroblasts, the signal for apoptosis originates from DNA photoproducts in the transcribed strand of active genes, whereas in keratinocytes, it is largely TCR-independent. This study shows that the response to UVB radiation is cell type–specific in humans and provides the first evidence that a deficiency in TCR has a different impact depending on the cell type. These findings have important implications for the mechanism of skin cancer protection after UVB damage and may explain the lack of skin cancer in patients with Cockayne syndrome.

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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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Chen, Xuefeng, Christine Ruggiero, and Shisheng Li. "Yeast Rpb9 Plays an Important Role in Ubiquitylation and Degradation of Rpb1 in Response to UV-Induced DNA Damage." Molecular and Cellular Biology 27, no. 13 (April 23, 2007): 4617–25. http://dx.doi.org/10.1128/mcb.00404-07.

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ABSTRACT Rpb9, a nonessential subunit of RNA polymerase II (Pol II), has multiple transcription-related functions in Saccharomyces cerevisiae, including transcription elongation and transcription-coupled repair (TCR). Here we show that, in response to UV radiation, Rpb9 also functions in promoting ubiquitylation and degradation of Rpb1, the largest subunit of Pol II. This function of Rpb9 is not affected by any pathways of nucleotide excision repair, including TCR mediated by Rpb9 itself and by Rad26. Rpb9 is composed of three distinct domains: the N-terminal Zn1, the C-terminal Zn2, and the central linker. The Zn2 domain, which is dispensable for transcription elongation and TCR functions, is essential for Rpb9 to promote Rpb1 degradation, whereas the Zn1 and linker domains, which are essential for transcription elongation and TCR functions, play a subsidiary role in Rpb1 degradation. Coimmunoprecipitation analysis suggests that almost the full length of Rpb9 is required for a strong interaction with the core Pol II: deletion of the Zn2 domain causes dramatically weakened interaction, whereas deletion of Zn1 and the linker resulted in undetectable interaction. Furthermore, we show that Rpb1, rather than the whole Pol II complex, is degraded in response to UV radiation and that the degradation is primarily mediated by the 26S proteasome.

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Більше джерел

Дисертації з теми "Transcription coupled repair factors (TCR)"

Yang, Margaret Hwae-Ling. "Mutations flanking the DNA channel through RNA polymerase II affect transcription-coupled repair in Saccharomyces cerevisiae /." view abstract or download file of text, 2007. http://proquest.umi.com/pqdweb?did=1417800941&sid=1&Fmt=2&clientId=11238&RQT=309&VName=PQD.

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Thesis (Ph. D.)--University of Oregon, 2007.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 80-87). Also available for download via the World Wide Web; free to University of Oregon users.

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