DEK oncoprotein participates in heterochromatin replication via SUMO-dependent nuclear bodies

Author:

Pierzynska-Mach Agnieszka1ORCID,Czada Christina2,Vogel Christopher2,Gwosch Eva2,Osswald Xenia2,Bartoschek Denis2,Diaspro Alberto13ORCID,Kappes Ferdinand4ORCID,Ferrando-May Elisa25ORCID

Affiliation:

1. Nanoscopy & NIC@IIT, Istituto Italiano di Tecnologia 1 , Genoa 16152 , Italy

2. Bioimaging Center, University of Konstanz 2 Department of Biology , , Konstanz 78464 , Germany

3. University of Genoa 3 DIFILAB, Department of Physics , , Genoa 16146 , Italy

4. Duke Kunshan University 4 , Division of Natural and Applied Sciences, Kunshan 215316 , People's Republic of China

5. German Cancer Research Center 5 , Heidelberg 69120 , Germany

Abstract

ABSTRACT The correct inheritance of chromatin structure is key for maintaining genome function and cell identity and preventing cellular transformation. DEK, a conserved non-histone chromatin protein, has recognized tumor-promoting properties, its overexpression being associated with poor prognosis in various cancer types. At the cellular level, DEK displays pleiotropic functions, influencing differentiation, apoptosis and stemness, but a characteristic oncogenic mechanism has remained elusive. Here, we report the identification of DEK bodies, focal assemblies of DEK that regularly occur at specific, yet unidentified, sites of heterochromatin replication exclusively in late S-phase. In these bodies, DEK localizes in direct proximity to active replisomes in agreement with a function in the early maturation of heterochromatin. A high-throughput siRNA screen, supported by mutational and biochemical analyses, identifies SUMO as one regulator of DEK body formation, linking DEK to the complex SUMO protein network that controls chromatin states and cell fate. This work combines and refines our previous data on DEK as a factor essential for heterochromatin integrity and facilitating replication under stress, and delineates an avenue of further study for unraveling the contribution of DEK to cancer development.

Funder

Horizon Europe Marie Sklodowska-Curie Actions

Deutsche Forschungsgemeinschaft

RWTH Aachen University

Istituto Italiano di Tecnologia

Duke Kunshan University

Publisher

The Company of Biologists

Subject

Cell Biology

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