Skip to main content
ISMPMI Congress 2025 Main banner
Icon Legend
This session is not in your schedule.
This session is in your schedule. Click again to remove it.

Poster

Session: Session 2 Presenting Authors at Posters (Odds)

P-177 - Ustilago maydis tumor-associated effector HAP1 targets maize SnRK1 to regulate starch-driven hypertrophy in maize

Wednesday, July 16, 2025
13:30 - 15:15  
Location: Confex Hall 3
Effector Interference Mechanisms

    Author(s)

  • YL

    Yoon Joo Lee

    University of Cologne
    Cologne, Nordrhein-Westfalen, Germany

    • Presenting Author(s)

  • DZ

    Dong Zhang

    University of Cologne
    cologne, Nordrhein-Westfalen, Germany

    • Author(s)

  • SS

    Sara Stolze

    Max Planck Institute for Plant Breeding Research, Proteomics Group
    Koeln, Nordrhein-Westfalen, Germany

  • GS

    Georgios Saridis

    AG Döhlemann, Terrestrische Mikrobiologie
    Köln, Nordrhein-Westfalen, Germany

  • ME

    Malaika K. Ebert, PI

    PI
    North Dakota State University
    Fargo, North Dakota, United States

  • HN

    Hirofumi Nakagami

    Group leader
    Max Planck Institute for Plant Breeding Research
    Koeln, Nordrhein-Westfalen, Germany

  • GD

    Gunther Doehlemann

    Professor
    University of Cologne
    Cologne, Nordrhein-Westfalen, Germany

Ustilago maydis infection in maize is known to cause hypertrophic leaf tumors, yet the underlying mechanisms driving excessive cell growth remain unknown. Here, we identify an effector, HAP1 (Hypertrophy-Associated Protein 1), as a virulence factor that regulates mesophyll cell hypertrophy. Through CRISPR-Cas9 mutagenesis, we demonstrate that HAP1 contributes to endoreduplication and starch accumulation in infected tissues. RNA-sequencing revealed HAP1-dependent upregulation of starch biosynthesis genes and cell cycle genes, while defense-related WRKY transcription factors are suppressed, linking HAP1 to metabolic reprogramming and immune modulation. To understand how HAP1 drives metabolic reprogramming, we explored its host targets and found that it interacts with maize SnRK1α2 and trehalose-6-phosphate synthase (TPS). Hap1 promotes the phosphorylation of SnRK1 downstream targets in a corporative manner with two additional HAP1-interacting U. maydis effectors, HIP1 and HIP2, enhancing its binding to SnRK1α2. Overall, our findings suggest that HAP1 drives maize metabolic reprogramming by targeting the SnRK1-TPS signaling pathway, diverting carbon flux toward starch synthesis while suppressing host defense responses to regulate hypertrophy.