dc.creator | Huertas Sánchez, Pablo | es |
dc.creator | García Rubio, María Luisa | es |
dc.creator | Wellinger, Ralf Erik | es |
dc.creator | Luna Varo, Rosa María | es |
dc.creator | Aguilera López, Andrés | es |
dc.date.accessioned | 2017-07-04T10:32:53Z | |
dc.date.available | 2017-07-04T10:32:53Z | |
dc.date.issued | 2006 | |
dc.identifier.citation | Huertas Sánchez, P., García Rubio, M.L., Wellinger, R.E., Luna Varo, R.M. y Aguilera López, A. (2006). An hpr1 point mutation that impairs transcription and mRNP biogenesis without increasing recombination. Molecular and Cellular Biology, 26 (20), 7451-7465. | |
dc.identifier.issn | 0270-7306 | es |
dc.identifier.uri | http://hdl.handle.net/11441/61926 | |
dc.description.abstract | THO/TREX, a conserved eukaryotic protein complex, is a key player at the interface between transcription
and mRNP metabolism. The lack of a functional THO complex impairs transcription, leads to transcriptiondependent
hyperrecombination, causes mRNA export defects and fast mRNA decay, and retards replication
fork progression in a transcription-dependent manner. To get more insight into the interconnection between
mRNP biogenesis and genomic instability, we searched for HPR1 mutations that differentially affect gene
expression and recombination. We isolated mutants that were barely affected in gene expression but exhibited
a hyperrecombination phenotype. In addition, we isolated a mutant, hpr1-101, with a strong defect in transcription,
as observed for lacZ, and a general defect in mRNA export that did not display a relevant hyperrecombination
phenotype. In THO single-null mutants, but not in the hpr1 point mutants studied, THO and its
subunits were unstable. Interestingly, in contrast to hyperrecombinant null mutants, hpr1-101 did not cause
retardation of replication fork progression. Transcription and mRNP biogenesis can therefore be impaired by
THO/TREX dysfunction without increasing recombination, suggesting that it is possible to separate the
mechanism(s) responsible for mRNA biogenesis defects from the further step of triggering transcriptiondependent
recombination. | es |
dc.description.sponsorship | Ministerio de Educación y Ciencia BMC2000-0409 SAF2003-00204 | es |
dc.description.sponsorship | Junta de Andalucía CVI102 | es |
dc.format | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | American Society for Microbiology | es |
dc.relation.ispartof | Molecular and Cellular Biology, 26 (20), 7451-7465. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.title | An hpr1 point mutation that impairs transcription and mRNP biogenesis without increasing recombination | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Genética | es |
dc.relation.projectID | BMC2000-0409 | es |
dc.relation.projectID | SAF2003-00204 | es |
dc.relation.projectID | CVI102 | es |
dc.relation.publisherversion | 10.1128/MCB.00684-06 | es |
dc.identifier.doi | 10.1128/MCB.00684-06 | es |
idus.format.extent | 15 p. | es |
dc.journaltitle | Molecular and Cellular Biology | es |
dc.publication.volumen | 26 | es |
dc.publication.issue | 20 | es |
dc.publication.initialPage | 7451 | es |
dc.publication.endPage | 7465 | es |
dc.identifier.sisius | 6655169 | es |
dc.contributor.funder | Ministerio de Educación y Ciencia (MEC). España | |
dc.contributor.funder | Junta de Andalucía | |