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Nucleotide excision repair in cellular chromatin: studies with yeast from nucleotide to gene to genome.

Waters R, Evans K, Bennett M, Yu S, Reed S - Int J Mol Sci (2012)

Bottom Line: Here we review our development of, and results with, high resolution studies on global genome nucleotide excision repair (GGNER) in Saccharomyces cerevisiae.We consider results employing primarily MFA2 as a model gene, but also those with URA3 located at subtelomeric sequences.In the latter case we also see a role for acetylation at histone H4.

View Article: PubMed Central - PubMed

Affiliation: Institute of Cancer and Genetics, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK; E-Mails: evansKE3@cardiff.ac.uk (K.E.); bennettMR1@cardiff.ac.uk (M.B.); yuS@cardiff.ac.uk (S.Y.); reedSH1@cardiff.ac.uk (S.R.).

ABSTRACT
Here we review our development of, and results with, high resolution studies on global genome nucleotide excision repair (GGNER) in Saccharomyces cerevisiae. We have focused on how GGNER relates to histone acetylation for its functioning and we have identified the histone acetyl tranferase Gcn5 and acetylation at lysines 9/14 of histone H3 as a major factor in enabling efficient repair. We consider results employing primarily MFA2 as a model gene, but also those with URA3 located at subtelomeric sequences. In the latter case we also see a role for acetylation at histone H4. We then go on to outline the development of a high resolution genome-wide approach that enables one to examine correlations between histone modifications and the nucleotide excision repair (NER) of UV-induced cyclobutane pyrimidine dimers throughout entire genomes. This is an approach that will enable rapid advances in understanding the complexities of how compacted chromatin in chromosomes is processed to access DNA damage and then returned to its pre-damaged status to maintain epigenetic codes.

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Related in: MedlinePlus

The CPD distribution in a part of Chromosome 4. Black: CPD levels detected by the CPD antibody; Grey: theoretical CPD distribution. The bars represent standard deviations. For more detail see [45].
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f16-ijms-13-11141: The CPD distribution in a part of Chromosome 4. Black: CPD levels detected by the CPD antibody; Grey: theoretical CPD distribution. The bars represent standard deviations. For more detail see [45].

Mentions: DNA microarrays were developed decades ago for whole genome transcription profiling. The combination of these and chromatin immunoprecipitation, namely ChIP on chip, was an extension that enabled the identification of the binding sites of DNA-binding proteins and the covalent modifications to nucleosomes on a genome-wide basis [43,44]. We built on this technology by developing a genome wide ChIP on Chip approach that employs microarrays to monitor UV-induced DNA damage (CPDs) and its repair [45]. Consequently, this method means that we can identify the UV-induced changes in chromatin and the chromatin modifications that facilitate repair throughout an entire genome. The method is described in detail in our paper by Teng et al. [45]. A snapshot of the frequency of CPD induction in part of the yeast genome is shown in Figure 16 and the data for the entire yeast genome can be seen in the above paper [45].


Nucleotide excision repair in cellular chromatin: studies with yeast from nucleotide to gene to genome.

Waters R, Evans K, Bennett M, Yu S, Reed S - Int J Mol Sci (2012)

The CPD distribution in a part of Chromosome 4. Black: CPD levels detected by the CPD antibody; Grey: theoretical CPD distribution. The bars represent standard deviations. For more detail see [45].
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3472735&req=5

f16-ijms-13-11141: The CPD distribution in a part of Chromosome 4. Black: CPD levels detected by the CPD antibody; Grey: theoretical CPD distribution. The bars represent standard deviations. For more detail see [45].
Mentions: DNA microarrays were developed decades ago for whole genome transcription profiling. The combination of these and chromatin immunoprecipitation, namely ChIP on chip, was an extension that enabled the identification of the binding sites of DNA-binding proteins and the covalent modifications to nucleosomes on a genome-wide basis [43,44]. We built on this technology by developing a genome wide ChIP on Chip approach that employs microarrays to monitor UV-induced DNA damage (CPDs) and its repair [45]. Consequently, this method means that we can identify the UV-induced changes in chromatin and the chromatin modifications that facilitate repair throughout an entire genome. The method is described in detail in our paper by Teng et al. [45]. A snapshot of the frequency of CPD induction in part of the yeast genome is shown in Figure 16 and the data for the entire yeast genome can be seen in the above paper [45].

Bottom Line: Here we review our development of, and results with, high resolution studies on global genome nucleotide excision repair (GGNER) in Saccharomyces cerevisiae.We consider results employing primarily MFA2 as a model gene, but also those with URA3 located at subtelomeric sequences.In the latter case we also see a role for acetylation at histone H4.

View Article: PubMed Central - PubMed

Affiliation: Institute of Cancer and Genetics, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK; E-Mails: evansKE3@cardiff.ac.uk (K.E.); bennettMR1@cardiff.ac.uk (M.B.); yuS@cardiff.ac.uk (S.Y.); reedSH1@cardiff.ac.uk (S.R.).

ABSTRACT
Here we review our development of, and results with, high resolution studies on global genome nucleotide excision repair (GGNER) in Saccharomyces cerevisiae. We have focused on how GGNER relates to histone acetylation for its functioning and we have identified the histone acetyl tranferase Gcn5 and acetylation at lysines 9/14 of histone H3 as a major factor in enabling efficient repair. We consider results employing primarily MFA2 as a model gene, but also those with URA3 located at subtelomeric sequences. In the latter case we also see a role for acetylation at histone H4. We then go on to outline the development of a high resolution genome-wide approach that enables one to examine correlations between histone modifications and the nucleotide excision repair (NER) of UV-induced cyclobutane pyrimidine dimers throughout entire genomes. This is an approach that will enable rapid advances in understanding the complexities of how compacted chromatin in chromosomes is processed to access DNA damage and then returned to its pre-damaged status to maintain epigenetic codes.

Show MeSH
Related in: MedlinePlus