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dc.contributor.authorHe, Feng
dc.contributor.authorPeltz, Stuart W.
dc.contributor.authorDonahue, Janet L.
dc.contributor.authorRosbash, Michael
dc.contributor.authorJacobson, Allan
dc.date2022-08-11T08:09:36.000
dc.date.accessioned2022-08-23T16:37:19Z
dc.date.available2022-08-23T16:37:19Z
dc.date.issued1993-08-01
dc.date.submitted2009-04-02
dc.identifier.citationProc Natl Acad Sci U S A. 1993 Aug 1;90(15):7034-8. <a href="http://www.pnas.org/content/90/15/7034.full.pdf+html">Link to article on publisher's website</a>
dc.identifier.issn0027-8424 (Print)
dc.identifier.pmid8346213
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38987
dc.description.abstractNonsense-mediated mRNA decay, the accelerated turnover of mRNAs transcribed from genes containing early nonsense mutations, is dependent on the product of the UPF1 gene in yeast. Mutations that inactivate UPF1 lead to the selective stabilization of mRNAs containing early nonsense mutations but have no effect on the half-lives of almost all other mRNAs. Since the transcripts of nonsense alleles are not typical cellular constituents, we sought to identify those RNAs that comprise normal substrates of the nonsense-mediated mRNA decay pathway. Many yeast pre-mRNAs contain early in-frame nonsense codons and we consider it possible that a role of this pathway is to accelerate the degradation of pre-mRNAs present in the cytoplasm. Consistent with this hypothesis, we find that, in a strain lacking UPF1 function, the CYH2, RP51B, and MER2 pre-mRNAs are stabilized 2- to 5-fold and are associated with ribosomes. We conclude that a major source of early nonsense codon-containing cytoplasmic transcripts in yeast is pre-mRNAs and that the UPF1 protein may be part of a cellular system that ensures that potentially deleterious nonsense fragments of polypeptides do not accumulate.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=8346213&dopt=Abstract">Link to Article in PubMed</a>
dc.subjectGene Expression Regulation, Fungal
dc.subject*Genes, Fungal
dc.subjectIntrons
dc.subjectNucleic Acid Precursors
dc.subjectProtein Biosynthesis
dc.subject*RNA Splicing
dc.subjectRNA, Fungal
dc.subjectRNA, Messenger
dc.subjectRibosomes
dc.subjectSaccharomyces cerevisiae
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleStabilization and ribosome association of unspliced pre-mRNAs in a yeast upf1- mutant
dc.typeArticle
dc.source.journaltitleProceedings of the National Academy of Sciences of the United States of America
dc.source.volume90
dc.source.issue15
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2813&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1814
dc.identifier.contextkey808580
refterms.dateFOA2022-08-23T16:37:19Z
html.description.abstract<p>Nonsense-mediated mRNA decay, the accelerated turnover of mRNAs transcribed from genes containing early nonsense mutations, is dependent on the product of the UPF1 gene in yeast. Mutations that inactivate UPF1 lead to the selective stabilization of mRNAs containing early nonsense mutations but have no effect on the half-lives of almost all other mRNAs. Since the transcripts of nonsense alleles are not typical cellular constituents, we sought to identify those RNAs that comprise normal substrates of the nonsense-mediated mRNA decay pathway. Many yeast pre-mRNAs contain early in-frame nonsense codons and we consider it possible that a role of this pathway is to accelerate the degradation of pre-mRNAs present in the cytoplasm. Consistent with this hypothesis, we find that, in a strain lacking UPF1 function, the CYH2, RP51B, and MER2 pre-mRNAs are stabilized 2- to 5-fold and are associated with ribosomes. We conclude that a major source of early nonsense codon-containing cytoplasmic transcripts in yeast is pre-mRNAs and that the UPF1 protein may be part of a cellular system that ensures that potentially deleterious nonsense fragments of polypeptides do not accumulate.</p>
dc.identifier.submissionpathoapubs/1814
dc.contributor.departmentDepartment of Molecular Genetics and Microbiology
dc.source.pages7034-8


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