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Título: | FUS (fused in sarcoma) is a component of the cellular response to topoisomerase I–induced DNA breakage and transcriptional stress |
Autor: | Martínez-Macías, María Isabel CSIC; Moore, Duncan AQ; Green, Ryan L.; Gómez-Herreros, Fernando CSIC ORCID; Naumann, Marcel; Hermann, Andreas; van Damme, Philip; Hafezparast, Majid; Caldecott, Keith W. | Fecha de publicación: | abr-2019 | Editor: | Life Science Alliance | Citación: | Life Science Alliance 2(2): e201800222 (2019) | Resumen: | FUS (fused in sarcoma) plays a key role in several steps of RNA metabolism, and dominant mutations in this protein are associated with neurodegenerative diseases. Here, we show that FUS is a component of the cellular response to topoisomerase I (TOP1)–induced DNA breakage; relocalising to the nucleolus in response to RNA polymerase II (Pol II) stalling at sites of TOP1-induced DNA breaks. This relocalisation is rapid and dynamic, reversing following the removal of TOP1-induced breaks and coinciding with the recovery of global transcription. Importantly, FUS relocalisation following TOP1-induced DNA breakage is associated with increased FUS binding at sites of RNA polymerase I transcription in ribosomal DNA and reduced FUS binding at sites of RNA Pol II transcription, suggesting that FUS relocates from sites of stalled RNA Pol II either to regulate pre-mRNA processing during transcriptional stress or to modulate ribosomal RNA biogenesis. Importantly, FUS-mutant patient fibroblasts are hypersensitive to TOP1-induced DNA breakage, highlighting the possible relevance of these findings to neurodegeneration. | Versión del editor: | http://dx.doi.org/10.26508/lsa.201800222 | URI: | http://hdl.handle.net/10261/204507 | DOI: | 10.26508/lsa.201800222 | E-ISSN: | 2575-1077 |
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