<p>Plants are challenged by multiple biotic (for example, pathogens) and abiotic (for example, heavy metals) stressors. Some transition metals can enhance a plant’s defence against pathogens, but the mechanism remains unclear. Here we demonstrate that an <i>Arabidopsis</i> head-to-head gene pair of intracellular nucleotide-binding leucine-rich repeat (NLR) receptors, both expressed in the endodermis of roots, antagonistically control transition metal-enhanced immunity. One NLR, STM2, binds transition metal ions, such as Cd<sup>2+</sup>, Cu<sup>2+</sup> and Zn<sup>2+</sup>, with its LRR domain to enhance its NAD<sup>+</sup> hydrolytic activity and immune responses via the EDS1/PAD4/ADR1 module, triggering enhanced resistance to bacterial wilt <i>Ralstonia solanacearum</i>. The other NLR, STM1, suppresses STM2 to protect plants from transition metal-enhanced immunity and growth inhibition in the presence of excess metals. STM1 also dampens resistance to the pathogen. Our study defines an NLR activated by transition metals and reveals a trade-off between susceptibility to pathogens and sensitivity to transition metals that are pervasive in soil.</p>

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Transition metal-enhanced immunity in Arabidopsis roots via an NLR pair

  • Cheng Gao,
  • Sisi Chen,
  • Jie Chen,
  • Zhong Tang,
  • Shu-Yao Chen,
  • Xin-Yuan Huang,
  • Peng Wang,
  • Suomeng Dong,
  • Jeffery L. Dangl,
  • Li Wan,
  • Fang-Jie Zhao

摘要

Plants are challenged by multiple biotic (for example, pathogens) and abiotic (for example, heavy metals) stressors. Some transition metals can enhance a plant’s defence against pathogens, but the mechanism remains unclear. Here we demonstrate that an Arabidopsis head-to-head gene pair of intracellular nucleotide-binding leucine-rich repeat (NLR) receptors, both expressed in the endodermis of roots, antagonistically control transition metal-enhanced immunity. One NLR, STM2, binds transition metal ions, such as Cd2+, Cu2+ and Zn2+, with its LRR domain to enhance its NAD+ hydrolytic activity and immune responses via the EDS1/PAD4/ADR1 module, triggering enhanced resistance to bacterial wilt Ralstonia solanacearum. The other NLR, STM1, suppresses STM2 to protect plants from transition metal-enhanced immunity and growth inhibition in the presence of excess metals. STM1 also dampens resistance to the pathogen. Our study defines an NLR activated by transition metals and reveals a trade-off between susceptibility to pathogens and sensitivity to transition metals that are pervasive in soil.