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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

UV induced histone H3 acetylation (A) and the accessibility of the RsaI restriction site (B) within the MFA2 regulatory region post UV for NER defective rad4 and rad 14 mutants [16].
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Related In: Results  -  Collection

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f9-ijms-13-11141: UV induced histone H3 acetylation (A) and the accessibility of the RsaI restriction site (B) within the MFA2 regulatory region post UV for NER defective rad4 and rad 14 mutants [16].

Mentions: Surprisingly both this event and the UV induced histone acetylation occurred in rad4 and rad14 NER defective cells. However, in these instances neither event decreased as in NER-competent cells and where repair occurred (Figure 9) [16]. This indicates that functional NER is not required to trigger these events but that it is required to restore these events to their pre-DNA damage levels. The roles of SWI/SNF and INO80 in NER have been researched in greater depth by the research groups of Smerdon and McHugh, so further details can be obtained from their reviews in this issue.


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)

UV induced histone H3 acetylation (A) and the accessibility of the RsaI restriction site (B) within the MFA2 regulatory region post UV for NER defective rad4 and rad 14 mutants [16].
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f9-ijms-13-11141: UV induced histone H3 acetylation (A) and the accessibility of the RsaI restriction site (B) within the MFA2 regulatory region post UV for NER defective rad4 and rad 14 mutants [16].
Mentions: Surprisingly both this event and the UV induced histone acetylation occurred in rad4 and rad14 NER defective cells. However, in these instances neither event decreased as in NER-competent cells and where repair occurred (Figure 9) [16]. This indicates that functional NER is not required to trigger these events but that it is required to restore these events to their pre-DNA damage levels. The roles of SWI/SNF and INO80 in NER have been researched in greater depth by the research groups of Smerdon and McHugh, so further details can be obtained from their reviews in this issue.

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