4.8 Article

Plant helper immune receptors are Ca2+-permeable nonselective cation channels

期刊

SCIENCE
卷 373, 期 6553, 页码 420-+

出版社

AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.abg7917

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资金

  1. National Science Foundation [IOS-1758400, IOS-1457257]
  2. National Institutes of Health [GM137286, GM135218]
  3. Howard Hughes Medical Institute (HHMI)
  4. Basic Science Research Program through the National Research Foundation of Korea Fellowship - Ministry of Education [2014R1A6A3A03058629]
  5. Deutsche Forschungsgemeinschaft [SFB/CRC1101]
  6. Reinhard Frank Stiftung (Project helperless plant)
  7. National Key Laboratory of Plant Molecular Genetics
  8. Institute of Plant Physiology and Ecology/Center for Excellence in Molecular Plant Sciences
  9. Chinese Academy of Sciences Strategic Priority Research Program [XDB27040214]
  10. University of Tubingen
  11. National Research Foundation of Korea [2014R1A6A3A03058629] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Plant nucleotide-binding leucine-rich repeat receptors (NLRs) play a crucial role in regulating immunity and cell death, with helper NLRs being essential for the function of many sensor NLRs. NRG1.1 and ADR1 are two helper NLRs that mediate cell death through Ca2+ influx, by forming Ca2+-permeable cation channels to directly regulate cytoplasmic Ca2+ levels.
Plant nucleotide-binding leucine-rich repeat receptors (NLRs) regulate immunity and cell death. In Arabidopsis, a subfamily of helper NLRs is required by many sensor NLRs. Active NRG1.1 oligomerized, was enriched in plasma membrane puncta, and conferred cytoplasmic calcium ion (Ca2+) influx in plant and human cells. NRG1.1-dependent Ca2+ influx and cell death were sensitive to Ca2+ channel blockers and were suppressed by mutations affecting oligomerization or plasma membrane enrichment. Ca2+ influx and cell death mediated by NRG1.1 and ACTIVATED DISEASE RESISTANCE 1 (ADR1), another helper NLR, required conserved negatively charged N-terminal residues. Whole-cell voltage-clamp recordings demonstrated that Arabidopsis helper NLRs form Ca2+-permeable cation channels to directly regulate cytoplasmic Ca2+ levels and consequent cell death. Thus, helper NLRs transduce cell death signals directly.

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