Linked Life Data

8659101

Source:http://linkedlifedata.com/resource/pubmed/id/8659101

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-8-1
pubmed:abstractText
This report provides genetic evidence that two vaccinia virus genes, A18R and G2R, both of which affect the fidelity of viral transcription in vivo, interact with each other or act on a common biochemical pathway. Previous experiments with the antipoxviral drug isatin-beta-thiosemicarbazone suggest that lethal mutation of gene G2R would compensate for mutations in gene A18R. We therefore tested the hypothesis that gene G2R is an extragenic suppressor of A18R mutations. First, we constructed a recombinant which contains both a G2R deletion mutation and an A18R temperature-sensitive mutation and found that this recombinant was viable. Second, we isolated both cold-sensitive and temperature-insensitive phenotypic revertants of A18R temperature-sensitive mutants and found in both cases that the revertants contained G2R mutations. In the case of the cold-sensitive revertants, we were able to prove that the cold-sensitive phenotype mapped to the G2R gene. Combined with the biochemical data on A18R and G2R, these results imply that the A18R and G2R genes interact with each other either directly or indirectly in a fashion which affects the fidelity of intermediate and late viral transcription.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
220
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
10-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Mutation of vaccinia virus gene G2R causes suppression of gene A18R ts mutants: implications for control of transcription.
pubmed:affiliation
Department of Molecular Genetics and Microbiology, University of Florida, Gainesville 32610, USA. condit@icbr.ifas.ufl.edu.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.