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Two nuclear effectors of the rice blast fungus modulate host immunity via transcriptional reprogramming

Author

Listed:
  • Seongbeom Kim

    (Seoul National University)

  • Chi-Yeol Kim

    (Seoul National University)

  • Sook-Young Park

    (Sunchon National University)

  • Ki-Tae Kim

    (Seoul National University)

  • Jongbum Jeon

    (Seoul National University)

  • Hyunjung Chung

    (Seoul National University
    Crop Cultivation and Environment Research Division, National Institute of Crop Science, Rural Development Administration)

  • Gobong Choi

    (Seoul National University)

  • Seomun Kwon

    (Seoul National University
    Heinrich-Heine University Düsseldorf, Institute for Microbiology, Cluster of Excellence on Plant Sciences)

  • Jaeyoung Choi

    (Seoul National University
    Smart Farm Research Center, Korea Institute of Science and Technology)

  • Junhyun Jeon

    (Yeungnam University)

  • Jong-Seong Jeon

    (Kyung Hee University)

  • Chang Hyun Khang

    (University of Georgia)

  • Seogchan Kang

    (The Pennsylvania State University)

  • Yong-Hwan Lee

    (Seoul National University
    Seoul National University
    Seoul National University)

Abstract

Pathogens utilize multiple types of effectors to modulate plant immunity. Although many apoplastic and cytoplasmic effectors have been reported, nuclear effectors have not been well characterized in fungal pathogens. Here, we characterize two nuclear effectors of the rice blast pathogen Magnaporthe oryzae. Both nuclear effectors are secreted via the biotrophic interfacial complex, translocated into the nuclei of initially penetrated and surrounding cells, and reprogram the expression of immunity-associated genes by binding on effector binding elements in rice. Their expression in transgenic rice causes ambivalent immunity: increased susceptibility to M. oryzae and Xanthomonas oryzae pv. oryzae, hemibiotrophic pathogens, but enhanced resistance to Cochliobolus miyabeanus, a necrotrophic pathogen. Our findings help remedy a significant knowledge deficiency in the mechanism of M. oryzae–rice interactions and underscore how effector-mediated manipulation of plant immunity by one pathogen may also affect the disease severity by other pathogens.

Suggested Citation

  • Seongbeom Kim & Chi-Yeol Kim & Sook-Young Park & Ki-Tae Kim & Jongbum Jeon & Hyunjung Chung & Gobong Choi & Seomun Kwon & Jaeyoung Choi & Junhyun Jeon & Jong-Seong Jeon & Chang Hyun Khang & Seogchan K, 2020. "Two nuclear effectors of the rice blast fungus modulate host immunity via transcriptional reprogramming," Nature Communications, Nature, vol. 11(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-19624-w
    DOI: 10.1038/s41467-020-19624-w
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    Cited by:

    1. Ziwei Zhu & Jun Xiong & Hao Shi & Yuchen Liu & Junjie Yin & Kaiwei He & Tianyu Zhou & Liting Xu & Xiaobo Zhu & Xiang Lu & Yongyan Tang & Li Song & Qingqing Hou & Qing Xiong & Long Wang & Daihua Ye & T, 2023. "Magnaporthe oryzae effector MoSPAB1 directly activates rice Bsr-d1 expression to facilitate pathogenesis," Nature Communications, Nature, vol. 14(1), pages 1-12, December.
    2. Xuetao Shi & Xin Xie & Yuanwen Guo & Junqi Zhang & Ziwen Gong & Kai Zhang & Jie Mei & Xinyao Xia & Haoxue Xia & Na Ning & Yutao Xiao & Qing Yang & Guo-Liang Wang & Wende Liu, 2024. "A fungal core effector exploits the OsPUX8B.2–OsCDC48-6 module to suppress plant immunity," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    3. You-Jin Lim & Yoon-Ju Yoon & Hyunjun Lee & Gobong Choi & Seongbeom Kim & Jaeho Ko & Jea Hyeoung Kim & Ki-Tae Kim & Yong-Hwan Lee, 2024. "Nuclear localization sequence of MoHTR1, a Magnaporthe oryzae effector, for transcriptional reprogramming of immunity genes in rice," Nature Communications, Nature, vol. 15(1), pages 1-14, December.
    4. Weiliang Zuo & Jasper R. L. Depotter & Sara Christina Stolze & Hirofumi Nakagami & Gunther Doehlemann, 2023. "A transcriptional activator effector of Ustilago maydis regulates hyperplasia in maize during pathogen-induced tumor formation," Nature Communications, Nature, vol. 14(1), pages 1-12, December.

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