Prp4 kinase grants the license to splice: control of weak splice sites during spliceosome activation
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- dc.contributor.author Eckert, Danielaca
- dc.contributor.author Andrée, Nicoleca
- dc.contributor.author Razanau, Alehca
- dc.contributor.author Zock-Emmenthal, Susanneca
- dc.contributor.author Lützelberger, Martinca
- dc.contributor.author Plath, Susannca
- dc.contributor.author Schmidt, Henningca
- dc.contributor.author Guerra Moreno, Ángelca
- dc.contributor.author Cozzuto, Lucaca
- dc.contributor.author Ayté del Olmo, Joséca
- dc.contributor.author Käufer, Norbert F.ca
- dc.date.accessioned 2016-01-13T16:46:22Z
- dc.date.available 2016-01-13T16:46:22Z
- dc.date.issued 2016
- dc.description.abstract The genome of the fission yeast Schizosaccharomyces pombe encodes 17 kinases that are essential for cell growth. These include the cell-cycle regulator Cdc2, as well as several kinases that coordinate cell growth, polarity, and morphogenesis during the cell cycle. In this study, we further characterized another of these essential kinases, Prp4, and showed that the splicing of many introns is dependent on Prp4 kinase activity. For detailed characterization, we chose the genes res1 and ppk8, each of which contains one intron of typical size and position. Splicing of the res1 intron was dependent on Prp4 kinase activity, whereas splicing of the ppk8 intron was not. Extensive mutational analyses of the 5' splice site of both genes revealed that proper transient interaction with the 5' end of snRNA U1 governs the dependence of splicing on Prp4 kinase activity. Proper transient interaction between the branch sequence and snRNA U2 was also important. Therefore, the Prp4 kinase is required for recognition and efficient splicing of introns displaying weak exon1/5' splice sites and weak branch sequences.ca
- dc.description.sponsorship We thank the DAAD (Deutscher Akademischer Austausch Dienst, German Academic Exchange Service) for their support of this project as part of the Spanish–German exchange program,which enabled DE to work in José Ayté’s laboratoryat the Universitat Pompeu Fabra (Barcelona, Spain). The Spanish Ministry of Science and Innovation (BFU2012-31939), PLAN E and FEDER to JA and a Georg-Christoph-Lichtenberg scholarship to AR, provided by the federal state of Niedersachsen (Germany).
- dc.format.mimetype application/pdfca
- dc.identifier.citation Eckert D, Andrée N, Razanau A, Zock-Emmenthal S, Lützelberger M, Plath S et al. Prp4 kinase grants the license to splice: control of weak splice sites during spliceosome activation. PLoS genetics. 2016;12(1):e1005768. DOI: 10.1371/journal.pgen.1005768ca
- dc.identifier.doi http://dx.doi.org/10.1371/journal.pgen.1005768
- dc.identifier.issn 1553-7390
- dc.identifier.uri http://hdl.handle.net/10230/25573
- dc.language.iso engca
- dc.publisher Public Library of Science (PLoS)ca
- dc.relation.ispartof PLoS genetics. 2016;12(1):e1005768
- dc.relation.projectID info:eu-repo/grantAgreement/ES/3PN/BFU2012-31939
- dc.rights © 2016 Eckert et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditedca
- dc.rights.accessRights info:eu-repo/semantics/openAccessca
- dc.rights.uri http://creativecommons.org/licenses/by/4.0/ca
- dc.subject.other Schizosaccharomyces pombe -- Metabolismeca
- dc.title Prp4 kinase grants the license to splice: control of weak splice sites during spliceosome activationca
- dc.type info:eu-repo/semantics/articleca
- dc.type.version info:eu-repo/semantics/publishedVersionca