ABF1-binding Sites Promote Efficient Global Genome Nucleotide Excision Repair

Yu, Shirong; Smirnova, Julia B.; Friedberg, Errol C.; Stillman, Bruce; Akiyama, Masahiro; Owen-Hughes, Tom; Waters, Raymond; Reed, Simon H.

doi:10.1074/jbc.m806830200

Cited by 22 publications

(30 citation statements)

References 46 publications

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“…We have reported that binding of the Abf1 component of the GG-NER complex to one of its DNA recognition sequences promotes efficient GG-NER both in vitro and in vivo (Yu et al 2009). Using standard chromatin immunoprecipitation (ChIP) and qPCR, we demonstrated Abf1 binding at a single Abf1 consensus binding site called the "I silencer," located at the yeast HMLALPHA locus (Yu et al 2009). Mutation of this DNA consensus site caused loss of Abf1 and GG-NER complex binding and reduced GG-NER efficiency extending from the mutated Abf1 DNA binding site.…”

Section: Gg-ner Is Organized and Initiated From Abf1 Binding Sites Fomentioning

confidence: 99%

“…Abf1 has a wide range of functions in processes including transcription (Buchman et al 1988;Miyake et al 2004;Yarragudi et al 2007;Schlecht et al 2008), gene silencing (Boscheron et al 1996;Zou et al 2006;Zhang et al 2012), replication (Rhode et al 1992), and NER (Yu et al 2004(Yu et al , 2009). We have reported that binding of the Abf1 component of the GG-NER complex to one of its DNA recognition sequences promotes efficient GG-NER both in vitro and in vivo (Yu et al 2009).…”

Section: Gg-ner Is Organized and Initiated From Abf1 Binding Sites Fomentioning

confidence: 99%

“…We identified the Saccharomyces cerevisiae protein complex of Rad7, Rad16, and Abf1, required for GG-NER in yeast, referred to as the GG-NER complex. We showed that efficient GG-NER requires Abf1 to be bound to specific DNA binding sites (Reed et al 1999), which can be found at hundreds of locations throughout the yeast genome (Yu et al 2009). The Rad16 protein is a member of the SWI/SNF super-family of chromatin remodeling factors.…”

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Global genome nucleotide excision repair is organized into domains that promote efficient DNA repair in chromatin

Evans

Eijk

et al. 2016

Genome Res.

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The rates at which lesions are removed by DNA repair can vary widely throughout the genome, with important implications for genomic stability. To study this, we measured the distribution of nucleotide excision repair (NER) rates for UV-induced lesions throughout the budding yeast genome. By plotting these repair rates in relation to genes and their associated flanking sequences, we reveal that, in normal cells, genomic repair rates display a distinctive pattern, suggesting that DNA repair is highly organized within the genome. Furthermore, by comparing genome-wide DNA repair rates in wild-type cells and cells defective in the global genome-NER (GG-NER) subpathway, we establish how this alters the distribution of NER rates throughout the genome. We also examined the genomic locations of GG-NER factor binding to chromatin before and after UV irradiation, revealing that GG-NER is organized and initiated from specific genomic locations. At these sites, chromatin occupancy of the histone acetyl-transferase Gcn5 is controlled by the GG-NER complex, which regulates histone H3 acetylation and chromatin structure, thereby promoting efficient DNA repair of UV-induced lesions. Chromatin remodeling during the GG-NER process is therefore organized into these genomic domains. Importantly, loss of Gcn5 significantly alters the genomic distribution of NER rates; this has implications for the effects of chromatin modifiers on the distribution of mutations that arise throughout the genome.

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Section: Gg-ner Is Organized and Initiated From Abf1 Binding Sites Fomentioning

confidence: 99%

Section: Gg-ner Is Organized and Initiated From Abf1 Binding Sites Fomentioning

confidence: 99%

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confidence: 99%

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Global genome nucleotide excision repair is organized into domains that promote efficient DNA repair in chromatin

Evans

Eijk

et al. 2016

Genome Res.

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“…Rad7-Rad16-Abf1 can generate superhelical torsion in DNA in vitro (Yu et al 2004), suggesting a model in which the complex binds to ABF1 sites in DNA in the absence of UV irradiation. Following UV irradiation, the complex uses ATP hydrolysis to translocate on DNA, generating conformational changes and eventually stalling at damaged sites to facilitate the recruitment of Rad4 (Guzder et al 1998;Yu et al 2009). …”

Section: ; Tremblay Et Al 2008)mentioning

confidence: 99%

DNA Repair Mechanisms and the Bypass of DNA Damage in Saccharomyces cerevisiae

2013

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DNA repair mechanisms are critical for maintaining the integrity of genomic DNA, and their loss is associated with cancer predisposition syndromes. Studies in Saccharomyces cerevisiae have played a central role in elucidating the highly conserved mechanisms that promote eukaryotic genome stability. This review will focus on repair mechanisms that involve excision of a single strand from duplex DNA with the intact, complementary strand serving as a template to fill the resulting gap. These mechanisms are of two general types: those that remove damage from DNA and those that repair errors made during DNA synthesis. The major DNA-damage repair pathways are base excision repair and nucleotide excision repair, which, in the most simple terms, are distinguished by the extent of single-strand DNA removed together with the lesion. Mistakes made by DNA polymerases are corrected by the mismatch repair pathway, which also corrects mismatches generated when single strands of non-identical duplexes are exchanged during homologous recombination. In addition to the true repair pathways, the postreplication repair pathway allows lesions or structural aberrations that block replicative DNA polymerases to be tolerated. There are two bypass mechanisms: an error-free mechanism that involves a switch to an undamaged template for synthesis past the lesion and an error-prone mechanism that utilizes specialized translesion synthesis DNA polymerases to directly synthesize DNA across the lesion. A high level of functional redundancy exists among the pathways that deal with lesions, which minimizes the detrimental effects of endogenous and exogenous DNA damage.

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“…1,9 This relatively simple picture has been recently expanded by a study showing that most Ribi gene promoters are demarcated, at positions ranging from 250 to 50 bp upstream of PAC and RRPE, by one or more binding sites for the GRFs Abf1, Reb1, Tbf1 and Rap1. 15 All of these proteins possess a Myb-like DNA-binding domain, bind to several hundreds of promoter regions in the S. cerevisiae genome and are multifunctional, being involved in processes other than transcription initiation, such as DNA repair, 16,17 telomere regulation, 18,19 and transcription termination. 20 The observation that all the yeast regulons involved in rRNA maturation and ribosome production (including snoRNA genes in addition to RP and Ribi genes 21 ) share GRF-associated promoters raises questions about the physiologic significance of these transcription factors in regulon modulation according to cell growth conditions.…”

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Transcriptional control of yeast ribosome biogenesis: A multifaceted role for general regulatory factors

2017

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In Saccharomyces cerevisiae, a group of more than 200 co-regulated genes (Ribi genes) is involved in ribosome biogenesis. This regulon has recently been shown to rely on a small set of transcriptional regulators (mainly Abf1, but also Reb1, Tbf1 and Rap1) previously referred to as general regulatory factors (GRFs) because of their widespread binding and action at many promoters and other specialized genomic regions. Intriguingly, Abf1 binding to Ribi genes is differentially modulated in response to distinct nutrition signaling pathways. Such a dynamic promoter association has the potential to orchestrate both activation and repression of Ribi genes in synergy with neighboring regulatory sites and through the functional interplay of histone acetyltransferases and deacetylases.

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ABF1-binding Sites Promote Efficient Global Genome Nucleotide Excision Repair

Cited by 22 publications

References 46 publications

Global genome nucleotide excision repair is organized into domains that promote efficient DNA repair in chromatin

Global genome nucleotide excision repair is organized into domains that promote efficient DNA repair in chromatin

DNA Repair Mechanisms and the Bypass of DNA Damage in Saccharomyces cerevisiae

Transcriptional control of yeast ribosome biogenesis: A multifaceted role for general regulatory factors

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