P-109 - An apoplastic fungal effector disrupts N-glycosylation of ZmLecRK1 for degradation to suppress disease resistance in maize

Wednesday, July 16, 2025

13:30 - 15:15

Location: Confex Hall 3

Effector Interference Mechanisms

Presenting Author(s)

WZ

Wangsheng Zhu

China agricultural university
Beijing, Beijing, China (People's Republic)

Author(s)

cL

chuang Liu

China Agricultural University
Beijing, Beijing, China (People's Republic)
ZL

Zhenju Li

China Agricultural University
Beijing, Beijing, China (People's Republic)
JC

Junbin Chen

China Agricultural University
Beijing, Beijing, China (People's Republic)

Pathogens deploy effector proteins to suppress host immune responses and enable successful colonization in plants. The apoplastic proteins are the major virulence effectors in pathogenicity; whether and how they directly attack extracellular immune receptors remains unclear. Here, we identify an apoplastic effector FgLPMO9A from Fusarium graminearum as a specific inhibitor of maize immune receptor ZmLecRK1-mediated resistance. FgLPMO9A is a member of the polysaccharide monooxygenase family that depolymerizes polysaccharides. Knocking out FgLPMO9A compromises F. graminearum pathogenicity in maize, while the growth of which is fully restored in the zmlecrk1 mutants. FgLPMO9A interacts with the extracellular S-domain of ZmLecRK1 and disrupts N-glycosylation at the N341 site, leading to ZmLecRK1 degradation via the vesicle-activated degradation pathway. Finally, ZmLecRK1 with N341Q substitution significantly enhances resistance to F. graminearum infection in maize. Taken together, we demonstrate that F. graminearum dampens maize immunity by deploying the apoplastic effector to induce extracellular immune receptor degradation.