Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2009-11-30
pubmed:abstractText
The role of many splicing factors in pre-mRNA splicing and the involvement of these factors in the processing of specific transcripts have often been defined through the analysis of loss-of-function mutants in vivo. Here we show that inactivating the nonsense-mediated mRNA decay (NMD) results in an enhancement of splicing phenotypes associated with several S. cerevisiae splicing factor mutations. Tiling microarrays showed that inactivation of the NMD factor Upf1p in the prp17Delta and prp18Delta mutant strains results in a larger spectrum of splicing defects than what is observed in the single mutants, including new transcripts previously shown unaffected by Prp17p or Prp18p inactivation. Inactivation of Upf1p in the second step/recycling factor prp22-1 mutant and in the nam8Delta and mud1Delta U1 snRNP component mutants also increase unspliced precursor accumulation of several specific transcripts. In addition, deletion of UPF1 partially suppresses the growth defects associated with the prp17Delta or prp22-1 mutations, demonstrating a positive genetic interaction between NMD and splicing factor mutants. These results show that RNA surveillance by NMD can mask some of the effects of splicing factor mutations, and that the roles of splicing factors cannot be fully understood in vivo unless RNA degradation systems that degrade unspliced precursors are also inactivated.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-10775271, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-10970881, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-11030620, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-11988574, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-14690599, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-15452114, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-16483935, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-16738408, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-17352659, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-17361132, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-17369403, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-17388687, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-17486100, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-17531985, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-18202663, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-18322460, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-18583613, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-18691155, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-18691968, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-2138057, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-2676722, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-3017708, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-3888403, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-7489518, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-7568198, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-8029003, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-8346213, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-8449403, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-9630245, http://linkedlifedata.com/resource/pubmed/commentcorrection/19850912-9717241
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1469-9001
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2236-47
pubmed:dateRevised
2010-9-27
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Nonsense-mediated mRNA decay mutes the splicing defects of spliceosome component mutations.
pubmed:affiliation
Department of Chemistry and Biochemistry and the Molecular Biology Institute, University of California at Los Angeles, Los Angeles, California 90095-1569, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural