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Phosphoproteomic Strategy for Profiling Osmotic Stress Signaling in Arabidopsis
Published on: June 25, 2020
iTRAQ Mitoproteome Analysis Reveals Mechanisms of Programmed Cell Death in Arabidopsis thaliana Induced by Ochratoxin
Yan Wang1,2, Xiaoli Peng3,4, Zhuojun Yang3
1Institute of Food Science and Technology, Chinese Academy of Agricultural Sciences, Beijing 100193, China. pxlpxh@163.com.
Abstract:
Ochratoxin A (OTA) is one of the most common and dangerous mycotoxins in the world. Previous work indicated that OTA could elicit spontaneous HR-like lesions formation Arabidopsis thaliana, reactive oxygen species (ROS) play an important role in OTA toxicity, and their major endogenous source is mitochondria. However, there has been no evidence as to whether OTA induces directly PCD in plants until now. In this study, the presence of OTA in Arabidopsisthaliana leaves triggered accelerated respiration, increased production of mitochondrial ROS, the opening of ROS-dependent mitochondrial permeability transition pores and a decrease in mitochondrial membrane potential as well as the release of cytochrome c into the cytosol. There were 42 and 43 significantly differentially expressed proteins identified in response to exposure to OTA for 8 and 24 h, respectively, according to iTRAQ analysis. These proteins were mainly involved in perturbation of the mitochondrial electron transport chain, interfering with ATP synthesis and inducing PCD. Digital gene expression data at transcriptional level was consistent with the cell death induced by OTA being PCD. These results indicated that mitochondrial dysfunction was a prerequisite for OTA-induced PCD and the initiation and execution of PCD via a mitochondrial-mediated pathway.
Insights
Ochratoxin A (OTA) induces programmed cell death (PCD) in Arabidopsis thaliana by disrupting mitochondrial function. This mycotoxin triggers ROS production and mitochondrial damage, leading to plant cell death.
Area of Science:
- Plant Pathology
- Toxicology
- Molecular Biology
Background:
- Ochratoxin A (OTA) is a prevalent and hazardous mycotoxin.
- Previous studies linked OTA to plant lesions and reactive oxygen species (ROS) production, primarily from mitochondria.
- The direct induction of programmed cell death (PCD) by OTA in plants remained unconfirmed.
Purpose of the Study:
- To investigate whether Ochratoxin A directly induces programmed cell death (PCD) in Arabidopsis thaliana.
- To elucidate the role of mitochondria and ROS in OTA-induced plant cell death.
Main Methods:
- Exposure of Arabidopsis thaliana leaves to OTA.
- Measurement of respiration, mitochondrial ROS production, mitochondrial membrane potential, and cytochrome c release.
- iTRAQ quantitative proteomics analysis to identify differentially expressed proteins.
- Digital gene expression analysis.
Main Results:
- OTA exposure led to accelerated respiration, increased mitochondrial ROS, and mitochondrial permeability transition pore opening.
- A decrease in mitochondrial membrane potential and cytochrome c release into the cytosol were observed.
- Proteomic analysis revealed significant changes in proteins involved in the mitochondrial electron transport chain and ATP synthesis.
- Gene expression data supported OTA-induced PCD via a mitochondrial pathway.
Conclusions:
- Mitochondrial dysfunction is a critical prerequisite for OTA-induced PCD in plants.
- OTA initiates and executes PCD through a mitochondrial-mediated pathway.
- This study provides direct evidence for OTA-induced PCD in plants, mediated by mitochondrial damage.
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