The pathogen effector BcSSP2 suppresses the NPC phase separation to facilitate Botrytis cinerea infection

Jiaojiao Wang (), Dewei Wu, Gaofeng Pei, Yupei Wang, Xiaokang Liu, Shiping Tian, Zhanquan Zhang, Xiaolin Zhang, Pilong Li (), Daoxin Xie () and Xiaoyi Shan ()
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Jiaojiao Wang: Beijing Forestry University
Dewei Wu: Tsinghua University
Gaofeng Pei: Tsinghua University; Tsinghua University-Peking University Joint Center for Life Sciences
Yupei Wang: Tsinghua University
Xiaokang Liu: Tsinghua University
Shiping Tian: Chinese Academy of Sciences
Zhanquan Zhang: Chinese Academy of Sciences
Xiaolin Zhang: Tsinghua University
Pilong Li: Tsinghua University; Tsinghua University-Peking University Joint Center for Life Sciences
Daoxin Xie: Tsinghua University
Xiaoyi Shan: Tsinghua University

Nature Communications, 2025, vol. 16, issue 1, 1-13

Abstract: Abstract Biomolecular phase separation-mediated immunity was recently uncovered as an important strategy of plants and animals for their survival in the challenging environment. Effectors are powerful weapons evolved by pathogens to overcome host defense response for effective infection. However, plant pathogen effectors were rarely identified to suppress the phase separation-mediated host defense response. Here, we report a pathogen effector that disrupts phase separation process in host cells to suppress host defense response and facilitate pathogen infection. We identify a host-internalized effector protein BcSSP2 from a disastrous pathogen Botrytis cinerea targets the central barrier of plant nuclear pore complex (NPC). BcSSP2 disrupts the phase separation of NUP62 and attenuates phase separation-dependent nuclear transport of immune regulator MPK3 to suppress plant defense response for effective pathogen infection. Intriguingly, BcSSP2 homologs are widely distributed among necrotrophic ascomycetes and also interfere with NUP62 phase separation, suggesting that disrupting plant NPC phase separation might be an evolutionarily conserved strategy evolved by these necrotrophic pathogens to facilitate their infection.

Date: 2025
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DOI: 10.1038/s41467-025-63632-7

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