Mitochondrial ROS trigger interorganellular signaling and prime ER processes to establish enhanced plant immunity.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 41032619.
- Also identified by DOI 10.1126/sciadv.ady9234 and PMC identifier 12487925.
- Licence recorded as CC BY-NC.
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Abstract
Reactive oxygen species (ROS) are key signaling molecules in plant development and immunity, but current understanding is primarily focused on apoplastic and chloroplastic ROS. Mitochondria are also a key source of intracellular ROS, yet their contribution to plant immunity is poorly characterized. Here, we studied mitochondrial ROS (mROS) function in plant-pathogen interactions, deploying genetically encoded sensors, assorted fluorescent markers, and genetic approaches to track mROS, specifically H<sub>2</sub>O<sub>2</sub>, dynamics and identify interorganelle contact sites. We unexpectedly found a mitochondria-endoplasmic reticulum (ER) ROS signal cascade functioning independently of apoplastic and chloroplastic ROS in plant immunity. mROS initiate immune responses induced by the oomycete pathogen <i>Phytophthora parasitica</i> and promote mitochondria-ER association. These enhanced mitochondria-ER membrane associations are required for transfer of mROS signals and initiation of extensive unfolded protein responses. We conclude that mROS transfer via mitochondria-ER membranes to the ER lumen is an underappreciated yet essential component in plant defense.
Medical subject headings
- Mitochondria
- Endoplasmic Reticulum
- Reactive Oxygen Species
- Plant Immunity
- Signal Transduction
- Arabidopsis