Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 116, Issue 38, Pages 19187-19192Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1910886116
Keywords
Arabidopsis; autophagy; peroxisome; ROS; stomata
Categories
Funding
- Japan Society for the Promotion of Science KAKENHI [18H02468, 26711019, 15K14552, 19K16171, 17K07457]
- Japan Foundation for Applied Enzymology
- Cooperative Research Grant of the Plant Transgenic Design Initiative (PTraD) at Gene Research Center, University of Tsukuba
- Cooperative Research Project Program of the Medical Institute of Bioregulation, Kyushu University
- NIBB Collaborative Research Program [17-518]
- Grants-in-Aid for Scientific Research [19K16171, 18H02468, 15K14552, 26711019, 17K07457] Funding Source: KAKEN
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Reactive oxygen species (ROS) function as key signaling molecules to inhibit stomatal opening and promote stomatal closure in response to diverse environmental stresses. However, how guard cells maintain basal intracellular ROS levels is not yet known. This study aimed to determine the role of autophagy in the maintenance of basal ROS levels in guard cells. We isolated the Arabidopsis autophagy-related 2 (atg2) mutant, which is impaired in stomatal opening in response to light and low CO2 concentrations. Disruption of other autophagy genes, including ATG5, ATG7, ATG10, and ATG12, also caused similar stomatal defects. The atg mutants constitutively accumulated high levels of ROS in guard cells, and antioxidants such as ascorbate and glutathione rescued ROS accumulation and stomatal opening. Furthermore, the atg mutations increased the number and aggregation of peroxisomes in guard cells, and these peroxisomes exhibited reduced activity of the ROS scavenger catalase and elevated hydrogen peroxide (H2O2) as visualized using the peroxisome-targeted H2O2 sensor HyPer. Moreover, such ROS accumulation decreased by the application of 2-hydroxy-3-butynoate, an inhibitor of peroxisomal H2O2-producing glycolate oxidase. Our results showed that autophagy controls guard cell ROS homeostasis by eliminating oxidized peroxisomes, thereby allowing stomatal opening.
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