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ACA pumps maintain leaf excitability during herbivore onslaught.

Nikou Fotouhi1, Michaela Fischer-Stettler2, Gioia Lenzoni1

  • 1Department of Plant Molecular Biology, University of Lausanne, 1015 Lausanne, Switzerland.

Current Biology : CB
|April 12, 2022
PubMed
Summary

Plant electrical signaling, crucial for defense against insect attacks, fails in specific calcium pump mutants (aca10 aca12). This failure, linked to vascular issues, highlights the role of these genes in maintaining plant excitability under stress.

Keywords:
aphidelectrical signalinsectjasmonatephloemsenescence

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Area of Science:

  • Plant signaling and molecular genetics
  • Plant-insect interactions
  • Plant physiology

Background:

  • Plants generate electrical signals, such as slow wave potentials, in response to damage, facilitating communication.
  • The robustness of these electrical signals under severe damage conditions suggests underlying genetic mechanisms for maintaining tissue excitability.
  • Group insect attacks pose a significant threat, necessitating efficient plant defense responses.

Purpose of the Study:

  • To identify genes responsible for maintaining plant tissue excitability during coordinated insect attacks.
  • To investigate the role of P-Type II Ca2+-ATPase genes in electrical signaling and plant defense.
  • To understand the mechanisms underlying electrical signaling failure under stress conditions.

Main Methods:

  • Mechanical wounding and insect (Spodoptera littoralis) attack assays on wild-type and Arabidopsis thaliana aca10 aca12 mutant plants.
  • Electrophysiological recordings to measure leaf-to-leaf electrical signals (slow wave potentials).
  • Genetic rescue experiments involving the expression of ACA10 in specific vascular tissues.

Main Results:

  • Arabidopsis aca10 aca12 mutants exhibited catastrophic failure of electrical signaling and increased susceptibility to Spodoptera littoralis attack.
  • Electrical signaling failure was associated with petiole base deformation, chlorosis, and premature senescence, suggesting vascular dysfunction.
  • Expression of ACA10 in phloem companion cells rescued electrical signaling and defense, while expression in xylem contact cells provided partial rescue.
  • Prolonged darkness also induced electrical signaling failure in aca10 aca12 mutants, indicating a broader role in stress response.

Conclusions:

  • The plant vasculature functions as a capacitor, and ACA10/ACA12 are critical for restoring membrane potentials in vascular cells during energy-depleting stresses.
  • Failure to restore vascular cell excitability in aca10 aca12 mutants leads to signaling collapse and increased herbivore damage.
  • Non-invasive electrophysiology is a valuable tool for studying early senescence events and plant stress responses.