The Npl3 hnRNP prevents R-loop-mediated transcription–replication conflicts and genome instability

Transcription is a major obstacle for replication fork (RF) progression and a cause of genome instability. Part of this instability is mediated by cotranscriptional R loops, which are believed to increase by suboptimal assembly of the nascent messenger ribonucleoprotein particle (mRNP). However, no...

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Detalles Bibliográficos
Autores: Santos Pereira, José María, Herrero, Ana B., García Rubio, María Luisa, Marín Rodríguez, Antonio, Moreno, Sergio, Aguilera López, Andrés
Tipo de recurso: artículo
Fecha de publicación:2013
País:España
Institución:Universidad de Sevilla (US)
Repositorio:idUS. Depósito de Investigación de la Universidad de Sevilla
OAI Identifier:oai:idus.us.es:11441/29092
Acceso en línea:http://hdl.handle.net/11441/29092
https://doi.org/10.1101/gad.229880.113
Access Level:acceso abierto
Palabra clave:R loops
transcription-associated genome instability
transcription–replication conflicts
Npl3
hnRNPs
DNA damage response
Descripción
Sumario:Transcription is a major obstacle for replication fork (RF) progression and a cause of genome instability. Part of this instability is mediated by cotranscriptional R loops, which are believed to increase by suboptimal assembly of the nascent messenger ribonucleoprotein particle (mRNP). However, no clear evidence exists that heterogeneous nuclear RNPs (hnRNPs), the basic mRNP components, prevent R-loop stabilization. Here we show that yeast Npl3, the most abundant RNA-binding hnRNP, prevents R-loop-mediated genome instability. npl3Δ cells show transcription-dependent and R-loop-dependent hyperrecombination and genome-wide replication obstacles as determined by accumulation of the Rrm3 helicase. Such obstacles preferentially occur at long and highly expressed genes, to which Npl3 is preferentially bound in wild-type cells, and are reduced by RNase H1 overexpression. The resulting replication stress confers hypersensitivity to double-strand break-inducing agents. Therefore, our work demonstrates that mRNP factors are critical for genome integrity and opens the option of using them as therapeutic targets in anti-cancer treatment.