We found that the fungal pathogen Fusarium graminearum secretes an apoplastic effector that disrupts N-glycosylation of the maize immune receptor ZmLecRK1, leading to its degradation by selective autophagy. This mechanism enables the pathogen to evade host defences and successfully colonize maize.
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References
Couto, D. & Zipfel, C. Regulation of pattern recognition receptor signalling in plants. Nat. Rev. Immunol. 16, 537–552 (2016). A review article that discusses how PRRs detect pathogens and activate immune responses.
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Li, Z. J. et al. Natural variations of maize ZmLecRK1 determine its interaction with ZmBAK1 and resistance patterns to multiple pathogens. Mol. Plant 17, 1606–1623 (2024). This paper reports the cloning and functional characterization of the multipathogen resistance gene ZmLecRK1 in maize.
Zhang, S. C. et al. A conserved Phytophthora apoplastic trypsin-like serine protease targets the receptor-like kinase BAK1 to dampen plant immunity. Nat. Plants 11, 1401–1415 (2025). This paper reports that a soybean receptor-like kinase BAK1 is directly targeted by a Phytophthora apoplastic protease.
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This is a summary of: Liu, C. et al. An apoplastic fungal effector disrupts N-glycosylation of ZmLecRK1, inducing its degradation to suppress disease resistance in maize. Nat. Plants https://doi.org/10.1038/s41477-025-02112-8 (2025).
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Glycosylation disruption is a new virulence strategy for a plant fungal pathogen. Nat. Plants 11, 1989–1990 (2025). https://doi.org/10.1038/s41477-025-02113-7
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DOI: https://doi.org/10.1038/s41477-025-02113-7
