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Rio1 promotes rDNA stability and downregulates RNA polymerase I to ensure rDNA segregation

Maria G. Iacovella, Cristina Golfieri, Lucia F. Massari, Sara Busnelli, Cinzia Pagliuca, Marianna Dal Maschio, Valentina Infantino, Rosella Visintin, Karl Mechtler, Sébastien Ferreira-Cerca and Peter De Wulf ()
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Maria G. Iacovella: European Institute of Oncology
Cristina Golfieri: European Institute of Oncology
Lucia F. Massari: European Institute of Oncology
Sara Busnelli: European Institute of Oncology
Cinzia Pagliuca: European Institute of Oncology
Marianna Dal Maschio: European Institute of Oncology
Valentina Infantino: European Institute of Oncology
Rosella Visintin: European Institute of Oncology
Karl Mechtler: The Research Institute of Molecular Pathology
Sébastien Ferreira-Cerca: Lehrstuhl für Biochemie III, Universität Regensburg
Peter De Wulf: European Institute of Oncology

Nature Communications, 2015, vol. 6, issue 1, 1-16

Abstract: Abstract The conserved protein kinase Rio1 localizes to the cytoplasm and nucleus of eukaryotic cells. While the roles of Rio1 in the cytoplasm are well characterized, its nuclear function remains unknown. Here we show that nuclear Rio1 promotes rDNA array stability and segregation in Saccharomyces cerevisiae. During rDNA replication in S phase, Rio1 downregulates RNA polymerase I (PolI) and recruits the histone deacetylase Sir2. Both interventions ensure rDNA copy-number homeostasis and prevent the formation of extrachromosomal rDNA circles, which are linked to accelerated ageing in yeast. During anaphase, Rio1 downregulates PolI by targeting its subunit Rpa43, causing PolI to dissociate from the rDNA. By stimulating the processing of PolI-generated transcripts at the rDNA, Rio1 allows for rDNA condensation and segregation in late anaphase. These events finalize the genome transmission process. We identify Rio1 as an essential nucleolar housekeeper that integrates rDNA replication and segregation with ribosome biogenesis.

Date: 2015
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7643

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DOI: 10.1038/ncomms7643

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