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Commensal lifestyle regulated by a negative feedback loop between Arabidopsis ROS and the bacterial T2SS

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  • Frederickson Entila

    (Huazhong Agricultural University
    Max Planck Institute for Plant Breeding Research)

  • Xiaowei Han

    (Huazhong Agricultural University
    Huazhong Agricultural University
    Chinese Academy of Agricultural Sciences)

  • Akira Mine

    (JST PRESTO
    Kyoto University)

  • Paul Schulze-Lefert

    (Max Planck Institute for Plant Breeding Research)

  • Kenichi Tsuda

    (Huazhong Agricultural University
    Max Planck Institute for Plant Breeding Research
    Huazhong Agricultural University
    Chinese Academy of Agricultural Sciences)

Abstract

Despite the plant health-promoting effects of plant microbiota, these assemblages also comprise potentially detrimental microbes. How plant immunity controls its microbiota to promote plant health under these conditions remains largely unknown. We find that commensal bacteria isolated from healthy Arabidopsis plants trigger diverse patterns of reactive oxygen species (ROS) production dependent on the immune receptors and completely on the NADPH oxidase RBOHD that selectively inhibited specific commensals, notably Xanthomonas L148. Through random mutagenesis, we find that L148 gspE, encoding a type II secretion system (T2SS) component, is required for the damaging effects of Xanthomonas L148 on rbohD mutant plants. In planta bacterial transcriptomics reveals that RBOHD suppresses most T2SS gene expression including gspE. L148 colonization protected plants against a bacterial pathogen, when gspE was inhibited by ROS or mutation. Thus, a negative feedback loop between Arabidopsis ROS and the bacterial T2SS tames a potentially detrimental leaf commensal and turns it into a microbe beneficial to the host.

Suggested Citation

  • Frederickson Entila & Xiaowei Han & Akira Mine & Paul Schulze-Lefert & Kenichi Tsuda, 2024. "Commensal lifestyle regulated by a negative feedback loop between Arabidopsis ROS and the bacterial T2SS," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
  • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-44724-2
    DOI: 10.1038/s41467-024-44724-2
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