Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-1-5
pubmed:abstractText
Global genome nucleotide excision repair (GG-NER) removes DNA damage from nontranscribing DNA. In Saccharomyces cerevisiae, the RAD7 and RAD16 genes are specifically required for GG-NER. We have reported that autonomously replicating sequence-binding factor 1 (ABF1) protein forms a stable complex with Rad7 and Rad16 proteins. ABF1 functions in transcription, replication, gene silencing, and NER in yeast. Here we show that binding of ABF1 to its DNA recognition sequence found at multiple genomic locations promotes efficient GG-NER in yeast. Mutation of the I silencer ABF1-binding site at the HMLalpha locus caused loss of ABF1 binding, which resulted in a domain of reduced GG-NER efficiency on one side of the ABF1-binding site. During GG-NER, nucleosome positioning at this site was not altered, and this correlated with an inability of the GG-NER complex to reposition nucleosomes in vitro.We discuss how the GG-NER complex might facilitate GG-NER while preventing unregulated gene transcription during this process.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
9
pubmed:volume
284
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
966-73
pubmed:dateRevised
2011-8-1
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
ABF1-binding sites promote efficient global genome nucleotide excision repair.
pubmed:affiliation
Department of Pathology, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't