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Assessing Stomatal Response to Live Bacterial Cells using Whole Leaf Imaging
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Bacterial infection systemically suppresses stomatal density.

Christian Dutton1,2, Hanna Hõrak1, Christopher Hepworth1,3

  • 1Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield, S10 2TN, UK.

Plant, Cell & Environment
|May 3, 2019
PubMed
Summary
This summary is machine-generated.

Plants develop fewer stomata on new leaves after pathogen attack, reducing entry points. This long-term defense involves altered leaf development and requires specific signaling pathways for disease resistance.

Keywords:
Arabidopsis thalianaPseudomonas syringaeflagellin receptorlipid transfer proteinplant pathogensalicylic acidstomatal developmentsystemic signal

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Area of Science:

  • Plant pathology
  • Plant physiology
  • Molecular plant-microbe interactions

Background:

  • Plant pathogens frequently enter hosts through stomata, which plants can close upon sensing an attack.
  • Plants possess a rapid stomatal closure response, but a longer-term developmental response to pathogens was previously unknown.

Purpose of the Study:

  • To investigate if plants exhibit a long-term, systemic stomatal response to pathogen infection.
  • To elucidate the mechanisms and signaling pathways involved in this developmental defense.

Main Methods:

  • Infection of Arabidopsis thaliana with Pseudomonas syringae.
  • Analysis of leaf development, stomatal density, and cell size post-infection.
  • Application of bacterial peptide flg22 and phytohormone salicylic acid.
  • Genetic analysis involving flagellin receptors, salicylic acid pathways, and AZI1.

Main Results:

  • Infected Arabidopsis leaves showed reduced stomatal density (up to 20%) due to larger epidermal cells and stomata.
  • Systemic reduction in stomatal density was induced by flg22 and salicylic acid.
  • Flagellin receptors, salicylic acid, and AZI1 were essential for this developmental response.
  • Reduced stomatal density correlated with lower bacterial colonization and slower disease progression.

Conclusions:

  • Plants mount a long-term, systemic defense by altering new leaf development to reduce stomatal density.
  • This response, mediated by pathways involving flg22, salicylic acid, and AZI1, enhances resistance to subsequent pathogen infection.
  • The findings suggest a link between developmental plasticity and innate immunity, akin to systemic acquired resistance.