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Apoplastic calcium executes a shut-down function on plant peroxidases: a hypothesis.
1Zentrum für Biochemie und Molekularbiologie, Universität Kiel, Kiel, Germany. cplieth@zbm.uni-kiel.de
Plant Signaling & Behavior
|May 15, 2012
Summary
Calcium depletion switches off peroxidases (POs) during heat stress, leading to reactive oxygen species (ROS) accumulation. This calcium-mediated mechanism (CaDIRA) may explain plant stress responses.
Area of Science:
- Plant Physiology
- Biochemistry
- Stress Biology
Background:
- Peroxidase (PO) activity is regulated by apoplastic calcium concentrations.
- PO heat stability is also influenced by calcium levels.
Purpose of the Study:
- To propose a scenario where calcium acts as a heat-triggered switch-off mechanism for peroxidases.
- To explain the role of calcium depletion in initiating reactive oxygen species (ROS) accumulation under heat stress.
Main Methods:
- The study presents a theoretical scenario based on existing literature.
- It hypothesizes a mechanism involving apoplastic calcium depletion and ROS accumulation.
Main Results:
- Heat stress triggers apoplastic calcium depletion, switching off peroxidases.
- This calcium depletion initiates apoplastic ROS accumulation, termed CaDIRA (Calcium depletion-initiated ROS accumulation).
- CaDIRA may trigger self-amplifying cellular events and systemic plant stress responses.
Conclusions:
- Calcium plays a crucial role in modulating PO activity under heat stress.
- The CaDIRA hypothesis offers a potential explanation for unexplained plant stress signaling observations.
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