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Poster

Session: Session 1 Presenting Authors at Posters (Evens)

P-224 - Viral DNA replication triggers changes in nuclear architecture across domains of life: new insights from geminiviruses

Tuesday, July 15, 2025
09:55 - 11:30  
Location: Confex Hall 3
Microbial infection strategies (pathogens & non-pathogens)

    Presenting Author(s)

  • KK

    Kyoka Kuroiwa

    Department of Plant Biochemistry, Centre for Plant Molecular Biology (ZMBP), Eberhard Karls University
    Tübingen, Baden-Wurttemberg, Germany

    • Author(s)

  • CS

    Chaonan Shi

    PhD
    Department of Plant Biochemistry, Centre for Plant Molecular Biology (ZMBP), Eberhard Karls University
    Tübingen, Baden-Wurttemberg, Germany

  • MG

    Man Gao

    Post-doc
    Center for Plant Molecular Biology
    Tuebingen, Baden-Wurttemberg, Germany

  • CS

    Christoph Sicking

    Leibniz Institute DSMZ-German Collection of Microorganisms and Cell Cultures
    Braunschweig, Niedersachsen, Germany

  • BK

    Björn Krenz

    Leibniz Institute DSMZ
    Braunschweig, Niedersachsen, Germany

  • RL

    Rosa Lozano-Durán

    University of Tü​bingen
    Tübingen, GERMANY

Geminiviruses replicate in the nucleus using the host DNA replication machinery. Their viral DNA replication seems to induce a major reorganization in the cellular chromatin structure, characterized by its condensation and marginalization to the nuclear periphery. This phenomenon is called virus-induced reorganization of cellular chromatin (ROCC) and suggested to favor the formation of a nuclear viral replication factory. Strikingly, ROCC is observed not only in plants during infection by geminiviruses, but also in animals during infection by independently evolved DNA viruses, implying its convergent evolution. While this hints at the ROCC’s importance for these viruses, little is known about its induction, let alone the underlying molecular mechanisms and outcomes for both virus and host. Here, we demonstrate our advancements on the molecular characterization of ROCC triggered by tomato yellow leaf curl virus (TYLCV). We show that replication of a single-stranded DNA template by the TYLCV replication-associated protein is sufficient to induce ROCC, even in the absence of the virus. We also show the specific recruitment of host DNA replication machinery to the potential viral replication factory during ROCC. This work pinpoints the minimal requirement of virus-derived components for ROCC and supports the idea that this change in the nuclear architecture leads to formation of a viral replication factory.