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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

Exponential phase repair competent cells or those with rad16 deleted were un-irradiated (U) subjected to 70 J/m2 of UV and either sampled immediately (0) or at various repair times after UV (1, 2, 4 h). The Relative levels of histone H3 acetylation at lysine 9/14 was measured at the −2 nucleosome of the MFA2 gene (A) or in total chromatin via the Western blots shown and quantified in (B) [19].
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f10-ijms-13-11141: Exponential phase repair competent cells or those with rad16 deleted were un-irradiated (U) subjected to 70 J/m2 of UV and either sampled immediately (0) or at various repair times after UV (1, 2, 4 h). The Relative levels of histone H3 acetylation at lysine 9/14 was measured at the −2 nucleosome of the MFA2 gene (A) or in total chromatin via the Western blots shown and quantified in (B) [19].

Mentions: The result above poses the question as to what factors govern this UV-induced change in chromatin that facilitates efficient GG-NER? Thus we went on to investigate if any proteins with roles in GG-NER could govern these UV-induced parameters. We were intrigued to discover that the UV-induced histone H3 acetylation required the GG-NER specific protein Rad16 (Figure 10) [19].


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)

Exponential phase repair competent cells or those with rad16 deleted were un-irradiated (U) subjected to 70 J/m2 of UV and either sampled immediately (0) or at various repair times after UV (1, 2, 4 h). The Relative levels of histone H3 acetylation at lysine 9/14 was measured at the −2 nucleosome of the MFA2 gene (A) or in total chromatin via the Western blots shown and quantified in (B) [19].
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f10-ijms-13-11141: Exponential phase repair competent cells or those with rad16 deleted were un-irradiated (U) subjected to 70 J/m2 of UV and either sampled immediately (0) or at various repair times after UV (1, 2, 4 h). The Relative levels of histone H3 acetylation at lysine 9/14 was measured at the −2 nucleosome of the MFA2 gene (A) or in total chromatin via the Western blots shown and quantified in (B) [19].
Mentions: The result above poses the question as to what factors govern this UV-induced change in chromatin that facilitates efficient GG-NER? Thus we went on to investigate if any proteins with roles in GG-NER could govern these UV-induced parameters. We were intrigued to discover that the UV-induced histone H3 acetylation required the GG-NER specific protein Rad16 (Figure 10) [19].

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