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Acute Smc5/6 depletion reveals its primary role in rDNA replication by restraining recombination at fork pausing sites
Umeå University, Faculty of Medicine, Department of Medical Biochemistry and Biophysics.
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2018 (English)In: PLoS Genetics, ISSN 1553-7390, E-ISSN 1553-7404, Vol. 14, no 1, article id e1007129Article in journal (Refereed) Published
Abstract [en]

Smc5/6, a member of the conserved SMC family of complexes, is essential for growth in most organisms. Its exact functions in a mitotic cell cycle are controversial, as chronic Smc5/6 loss-of-function alleles produce varying phenotypes. To circumvent this issue, we acutely depleted Smc5/6 in budding yeast and determined the first cell cycle consequences of Smc5/6 removal. We found a striking primary defect in replication of the ribosomal DNA (rDNA) array. Each rDNA repeat contains a programmed replication fork barrier (RFB) established by the Fob1 protein. Fob1 removal improves rDNA replication in Smc5/6 depleted cells, implicating Smc5/6 in the management of programmed fork pausing. A similar improvement is achieved by removing the DNA helicase Mph1 whose recombinogenic activity can be inhibited by Smc5/6 under DNA damage conditions. DNA 2D gel analyses further show that Smc5/6 loss increases recombination structures at RFB regions; moreover, mph1 Delta and fob1 Delta similarly reduce this accumulation. These findings point to an important mitotic role for Smc5/6 in restraining recombination events when protein barriers in rDNA stall replication forks. As rDNA maintenance influences multiple essential cellular processes, Smc5/6 likely links rDNA stability to overall mitotic growth.

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PUBLIC LIBRARY SCIENCE , 2018. Vol. 14, no 1, article id e1007129
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Biochemistry and Molecular Biology
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URN: urn:nbn:se:umu:diva-144968DOI: 10.1371/journal.pgen.1007129ISI: 000423718600006PubMedID: 29360860OAI: oai:DiVA.org:umu-144968DiVA, id: diva2:1184560
Available from: 2018-02-21 Created: 2018-02-21 Last updated: 2018-06-09Bibliographically approved

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Marjavaara, LisetteChabes, Andrei

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