PolySUMOylation of PCNA and Rad52 restricts centromeric recombination in fission yeast

Katarzyna Markowska, Ireneusz Litwin, Dorota Misiorna, Julia Kończak, Aleksandra Bogdańska, Paulina Tomaszewska, Michał Tracz, Mika Haenen and Karol Kramarz ()
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Katarzyna Markowska: University of Wrocław, Academic Excellence Hub - Research Centre for DNA Repair and Replication, Faculty of Biological Sciences
Ireneusz Litwin: University of Wrocław, Academic Excellence Hub - Research Centre for DNA Repair and Replication, Faculty of Biological Sciences
Dorota Misiorna: University of Wrocław, Academic Excellence Hub - Research Centre for DNA Repair and Replication, Faculty of Biological Sciences
Julia Kończak: University of Wrocław, Academic Excellence Hub - Research Centre for DNA Repair and Replication, Faculty of Biological Sciences
Aleksandra Bogdańska: University of Wrocław, Academic Excellence Hub - Research Centre for DNA Repair and Replication, Faculty of Biological Sciences
Paulina Tomaszewska: University of Wrocław, Department of Genetics and Cell Physiology, Faculty of Biological Sciences
Michał Tracz: University of Wrocław, Faculty of Biotechnology
Mika Haenen: University of Wrocław, Academic Excellence Hub - Research Centre for DNA Repair and Replication, Faculty of Biological Sciences
Karol Kramarz: University of Wrocław, Academic Excellence Hub - Research Centre for DNA Repair and Replication, Faculty of Biological Sciences

Nature Communications, 2025, vol. 16, issue 1, 1-19

Abstract: Abstract SUMOylation, a conserved post-translational modification in eukaryotes, regulates protein function, localization, and stability. However, the role of SUMO chains in genome maintenance is still emerging. Using Schizosaccharomyces pombe, we show that loss of SUMO chains results in spontaneous replication stress, DNA damage, and elevated centromeric recombination. To investigate SUMO-dependent interactome at the sites of Rad52 repair, we used a split-SUMO-ID proteomics approach. It allows the analysis of local SUMOylation content at the Rad52 repair sites, and enabled the identification of the essential replication factor PCNA. We found that SUMO chain-modified PCNA antagonizes Rad8-mediated PCNA polyubiquitination, modulating the choice of post-replication repair pathways at stalled forks within centromeres. In the absence of polySUMOylation, excessive PCNA polyubiquitination drives elevated recombination at centromeres. Artificial tethering of a SUMO chain to Rad52 suppresses this defect. Our findings uncover an essential role for SUMO chains in centromere maintenance by modulating DNA repair pathway choice under endogenous replication stress.

Date: 2025
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DOI: 10.1038/s41467-025-65862-1

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