Linked Life Data

18321796

Source:http://linkedlifedata.com/resource/pubmed/id/18321796

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2008-4-28
pubmed:abstractText
Yeast cells lacking MMS22 or MMS1 are hypersensitive to agents that perturb replisome progression but the cellular functions of these genes are unknown. In this study we investigate the involvement of budding yeast MMS22 and MMS1 in homologous recombination (HR). Recombination between sister chromatids or between homologous chromosomes induced by agents that block replisomes was severely defective in cells lacking MMS22 or MMS1. In contrast, HR induced by double-strand breaks was not affected by the absence of these genes. Major defects in MMS-induced HR were also observed in cells lacking the cullin RTT101, the histone acetyltransferase RTT109 and in cells lacking the histone chaperone ASF1, all of which interact genetically with MMS22 and MMS1. Finally, we show that cells lacking either MMS22 or MMS1 are defective in recovery from MMS-induced replisome stalling. These results identify Mms22 and Mms1 as S-phase specific recombination-promoting factors.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1568-7864
pubmed:author
pubmed:issnType
Print
pubmed:day
3
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
811-8
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Budding yeast Mms22 and Mms1 regulate homologous recombination induced by replisome blockage.
pubmed:affiliation
MRC Protein Phosphorylation Unit, Sir James Black Centre, University of Dundee, Hawkhill, Dundee DD1 5EH, Scotland, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't