ArticleNature plants2025
An apoplastic fungal effector disrupts N-glycosylation of ZmLecRK1, inducing its degradation to suppress disease resistance in maize.
Article in Nature plants, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- N-glycosylation code diversifies paralogous chitinases to balance plant immunity and growth.Nature plants · 2026Article
- O-Glycosylated expansinScience advances · 2026Article
- The oligosaccharyltransferase TaOST1B promotes viral infection by enhancement of RNA silencing suppression in wheat.Nature communications · 2026Article
- A new plant SUMO ligase, MPEL1, synergizes with MAPK16 to regulate resistance against Fusarium pathogens.The EMBO journal · 2026Article
- CgCFEM1 and CgCFEM2 modulate virulence in Colletotrichum gloeosporioides by integrated regulation of TOR and cAMP-PKA signaling pathways.BMC microbiology · 2026Article
- Stagonosporopsis cucurbitacearum Effector Protein ScAA9 Contributes to Virulence and Triggers Plant Immune Responses.Molecular plant pathology · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Pathogens deploy effectors to suppress host immune responses and enable successful colonization in plants. While apoplastic effectors have major roles in pathogenicity, whether and how they directly attack extracellular immune receptors remains unclear. Here we identify an apoplastic effector FgLPMO9A from the fungal pathogen Fusarium graminearum that directly inhibits maize immune receptor ZmLecRK1-mediated resistance. FgLPMO9A belongs to the polysaccharide monooxygenase family, which depolymerizes polysaccharides. Deletion of FgLPMO9A attenuates F. graminearum virulence on maize, but this defect is fully rescued in the zmlecrk1 mutants. FgLPMO9A interacts with the extracellular S-domain of ZmLecRK1 and disrupts N-glycosylation at the N341 site, thereby promoting ZmLecRK1 degradation via the NBR1-mediated autophagy pathway. Notably, the ZmLecRK1 variant with the N341Q substitution confers enhanced resistance to F. graminearum in maize. We demonstrate that F. graminearum dampens maize immunity by deploying an apoplastic effector to induce extracellular immune receptor degradation.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.