392 / 2019-02-22 15:47:13
PLANT NATRIURETIC PEPTIDE A and its novel receptor PNP-R2 antagonize salicylic acid-mediated signaling and cell death
PNP-A,LSD1,peptide-receptor pair,salicylic acid,cell death
摘要录用
Keun Pyo Lee / Shanghai Center for Plant Stress Biology and Center of Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
Kaiwei Liu / Shanghai Center for Plant Stress Biology and Center of Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
Eun Yu Kim / National Key Laboratory of Plant Molecular Genetics, CAS Center for Excellence in Molecular Plant Sciences, Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences
Laura Medina-Puche / Shanghai Center for Plant Stress Biology and Center of Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
Zihao Li / Shanghai Center for Plant Stress Biology and Center of Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
Rosa Lozano-Duran / Shanghai Center for Plant Stress Biology and Center of Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
Chanhong Kim / Shanghai Center for Plant Stress Biology and Center of Excellence in Molecular Plant Sciences, Chinese Academy of Sciences
The plant stress hormone salicylic acid (SA) participates in local and systemic acquired resistance, which eventually leads to a whole-plant resistance toward bacterial pathogens. However, if SA-mediated signaling is not appropriately controlled, plants must pay defense-associated fitness costs such as growth inhibition and cell death. Despite its importance, to date only a few components counteracting the SA-primed cell death pathway have been identified in Arabidopsis (Arabidopsis thaliana). These include other plant hormones such as jasmonic acid and abscisic acid, apoplastic reactive oxygen species (ROS) and proteins such as LESION SIMULATING DISEASE 1 (LSD1), a transcription coregulator. Here, we describe PLANT NATRIURETIC PEPTIDE A (PNP-A), a functional analog to vertebrate atrial natriuretic peptides, which appears to antagonize both the SA-mediated signaling and the SA-primed cell death. While loss of PNP-A potentiates SA-mediated signaling, exogenous application of synthetic PNP-A or overexpression of PNP-A significantly compromises the SA-mediated immune responses. Moreover, we identified a plasma membrane-localized receptor-like protein, PNP-R2, which interacts with PNP-A and initiates the PNP-A-mediated intracellular signaling. In summary, our work identifies a novel peptide-receptor pair which counteracts both SA-mediated signaling and SA-primed cell death in Arabidopsis.
重要日期
  • 会议日期

    06月16日

    2019

    06月21日

    2019

  • 05月01日 2019

    初稿截稿日期

  • 06月21日 2019

    注册截止日期

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