Linked Life Data

8299167

Source:http://linkedlifedata.com/resource/pubmed/id/8299167

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1994-3-8
pubmed:abstractText
We have tested the ability of mutants of three additional genes in the excision repair pathway of Saccharomyces cerevisiae to suppress the hyper-recombination and rad52 double-mutant lethality phenotypes of the rad3-102 (formerly rem1-2) mutation. Such suppression has previously been observed with mutant alleles of RAD1 and RAD4. We had hypothesized that the rad3-102 mutation created elevated levels of DNA lesions which could be processed by the products of the RAD1 and RAD4 genes into recombinogenic double-strand breaks requiring the RAD52 product for repair. In this report, we show that the RAD2, RAD7, and RAD10 genes are also necessary for this processing. We discuss our observations of varying levels of mitotic crossing-over in Rem- rad double-mutant strains.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0172-8083
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:geneSymbol
RAD1, RAD10, RAD2, RAD4, RAD7, rad3-102, rem1-2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
481-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Interaction of excision repair gene products and mitotic recombination functions in yeast.
pubmed:affiliation
Division of Biology, Kansas State University, Manhattan 66506.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't