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Título

R-loops do not accumulate in transcription-defective hpr1-101 mutants: implications for the functional role of THO/TREX

AutorGómez-González, Belén CSIC ORCID; Aguilera, Andrés CSIC ORCID
Palabras claveAlleles
Cytidine deaminase
Nuclear proteins
Point mutation
RNA-binding proteins
Recombination
Ribonuclease H
Ribonucleaseproteins
Saccharomyces cerevisiae proteins
Transcription factors
Fecha de publicación18-may-2009
EditorOxford University Press
CitaciónNucleic Acids Research 37(13): 4315-4321 (2009)
ResumenTo get further insight into the effect that THO/TREX and R-loops have in transcription-associated recombination and transcription, we analyzed the ability to form R-loops of hpr1-101, a THO mutation that impairs transcription and mRNP biogenesis without triggering hyper-recombination. Human AID, a cytidine deaminase that acts on ssDNA displaced by RNA-DNA hybrids, strongly induced both hyper-recombination and hyper-mutation in hpr1-101, similar to hpr1Δ mutants. However, in contrast to hpr1Δ, AID-induced mutations in hpr1-101 occur at similar frequencies in both the transcribed and non-transcribed strands, implying that the enhanced AID action in these mutants is not caused by co-transcriptional R-loops. These results indicate for the first time that THO has a transcriptional function that is not mediated by R-loops, providing a new perspective for the understanding of the coupling of transcription with mRNP biogenesis and export.
Descripción7 páginas, 6 figuras, 1 tabla.
Versión del editorhttp://dx.doi.org/10.1093/nar/gkp385
URIhttp://hdl.handle.net/10261/42470
DOI10.1093/nar/gkp385
ISSN0305-1048
E-ISSN1362-4962
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