Molecular mechanisms and genomic maps of DNA excision repair in Escherichia coli and humans

Hu, Jinchuan; Selby, Christopher P.; Adar, Sheera; Adebali, Ogün; Sancar, Aziz

doi:10.1074/jbc.r117.807453

Cited by 69 publications

(82 citation statements)

References 103 publications

(159 reference statements)

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“…Two key properties of TCR in mammalian cells are its dependence on CSB translocase and independence of XPC damage recognition protein. Hence, to determine whether rDNA is subject to TCR, we analyzed the XR-seq data (6,17,18) for CPD repair in a normal human fibroblast (NHF1) cell line, in a CSB mutant cell line, which is defective in TCR but carries out normal global repair, and in an XPC mutant cell line, which is known to perform normal TCR but is defective in global repair. Fig.…”

Section: Mapping Cpd Repair Of Rdna In Wt Csb and Xpc Mutant Human mentioning

confidence: 99%

“…Transcription-coupled repair is characterized by 3-10-fold higher efficiency of repair of the transcribed (template) strand (TS) compared with the nontranscribed (coding) strand (NTS) or nontranscribed regions of the genome (global repair) (3,4,6). In addition to the core excision repair proteins, TCR also depends on the transcription-repair coupling factor encoded by the mfd gene in E. coli (7) and the CSB gene in humans (8).…”

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confidence: 99%

“…Furthermore, TCR has also been implicated in rDNA repair in yeast (16). The availability of our recently generated, genome-wide, high-resolution repair-mapping procedure with single-nucleotide resolution led us to address rDNA repair using this more direct high-throughput assay (6,17,18). However, because rDNA is repetitive, it is not included or accurately annotated in many of the earlier and currently available releases of human and mouse genome assemblies.…”

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confidence: 99%

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Single-nucleotide resolution analysis of nucleotide excision repair of ribosomal DNA in humans and mice

Yang

Selby

et al. 2019

Journal of Biological Chemistry

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The unique nucleolar environment, the repetitive nature of ribosomal DNA (rDNA), and especially the possible involvement of RNA polymerase I (RNAPI) in transcription-coupled repair (TCR) have made the study of repair of rDNA both interesting and challenging. TCR, the transcription-dependent, preferential excision repair of the template strand compared with the nontranscribed (coding) strand has been clearly demonstrated in genes transcribed by RNAPII. Whether TCR occurs in rDNA is unresolved. In the present work, we have applied analytical methods to map repair events in rDNA using data generated by the newly developed XR-seq procedure, which measures excision repair genome-wide with single-nucleotide resolution. We find that in human and mouse cell lines, rDNA is not subject to TCR of damage caused by UV or by cisplatin.

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Section: Mapping Cpd Repair Of Rdna In Wt Csb and Xpc Mutant Human mentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Single-nucleotide resolution analysis of nucleotide excision repair of ribosomal DNA in humans and mice

Yang

Selby

et al. 2019

Journal of Biological Chemistry

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“…[44] Most individual reactions within metabolic pathways are reversible except for a few (near-)irreversible steps that oftentimes occur early in the pathway and are highly regulated (Figure 1). Similarly, complex biological processes as diverse as messenger RNA (mRNA) translation, [45][46][47][48] pre-mRNA splicing, [49,50] nucleotide excision repair of damaged DNA, [51] and discrimination of self-and non-self-peptides by T cells [52] all rely on a mix of sequential reversible and irreversible steps to effect what is called "kinetic proofreading" (Figure 4). As the name implies, this mechanism enhances biological specificity and fidelity beyond the level that can ordinarily be achieved by the difference in thermodynamic-free energy between correct and incorrect interactions.…”

Section: Kinetic Proofreading Partitioning and Trappingmentioning

confidence: 99%

Biological Pathway Specificity in the Cell—Does Molecular Diversity Matter?

Walter

2019

BioEssays

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Biology arises from the crowded molecular environment of the cell, rendering it a challenge to understand biological pathways based on the reductionist, low‐concentration in vitro conditions generally employed for mechanistic studies. Recent evidence suggests that low‐affinity interactions between cellular biopolymers abound, with still poorly defined effects on the complex interaction networks that lead to the emergent properties and plasticity of life. Mass‐action considerations are used here to underscore that the sheer number of weak interactions expected from the complex mixture of cellular components significantly shapes biological pathway specificity. In particular, on‐pathway—i.e., “functional”—become those interactions thermodynamically and kinetically stable enough to survive the incessant onslaught of the many off‐pathway (“nonfunctional”) interactions. Consequently, to better understand the molecular biology of the cell a further paradigm shift is needed toward mechanistic experimental and computational approaches that probe intracellular diversity and complexity more directly. Also see the video abstract here https://youtu.be/T19X_zYaBzg.

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“…Cells possess elaborate DNA repair mechanisms to cope with various types of DNA damage. Nucleotide excision repair, one of these repair mechanisms, removes a wide range of bulky and helix-distorting lesions, including UV radiation-induced cissyn cyclobutane pyrimidine dimers (CPDs) 3 and (6 -4) pyrimidine-pyrimidone photoproducts ((6 -4)PPs), and chemical carcinogens (e.g. benzo[a]pyrene) and cancer chemotherapeutics (e.g.…”

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confidence: 99%

Nucleotide excision repair capacity increases during differentiation of human embryonic carcinoma cells into neurons and muscle cells

Liu

Kakoki

et al. 2019

Journal of Biological Chemistry

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Embryonic stem cells can self-renew and differentiate, holding great promise for regenerative medicine. They also employ multiple mechanisms to preserve the integrity of their genomes. Nucleotide excision repair, a versatile repair mechanism, removes bulky DNA adducts from the genome. However, the dynamics of the capacity of nucleotide excision repair during stem cell differentiation remain unclear. Here, using immunoslot blot assay, we measured repair rates of UV-induced DNA damage during differentiation of human embryonic carcinoma (NTERA-2) cells into neurons and muscle cells. Our results revealed that the capacity of nucleotide excision repair increases as cell differentiation progresses. We also found that inhibition of the apoptotic signaling pathway has no effect on nucleotide excision repair capacity. Furthermore, RNA-Seq-based transcriptomic analysis indicated that expression levels of four core repair factors, xeroderma pigmentosum (XP) complementation group A (XPA), XPC, XPG, and XPF-ERCC1, are progressively up-regulated during differentiation, but not those of replication protein A (RPA) and transcription factor IIH (TFIIH). Together, our findings reveal that increase of nucleotide excision repair capacity accompanies cell differentiation, supported by the upregulated transcription of genes encoding DNA repair enzymes during differentiation of two distinct cell lineages.

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Molecular mechanisms and genomic maps of DNA excision repair in Escherichia coli and humans

Cited by 69 publications

References 103 publications

Single-nucleotide resolution analysis of nucleotide excision repair of ribosomal DNA in humans and mice

Single-nucleotide resolution analysis of nucleotide excision repair of ribosomal DNA in humans and mice

Biological Pathway Specificity in the Cell—Does Molecular Diversity Matter?

Nucleotide excision repair capacity increases during differentiation of human embryonic carcinoma cells into neurons and muscle cells

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