Humidity-driven ABA depletion determines plant-pathogen competition for leaf water
Shigetaka Yasuda1, Akihisa Shinozawa2, Yuanjie Weng3
1Graduate School of Science and Technology, Nara Institute of Science and Technology, Ikoma, Japan. shige-yasuda@bs.naist.jp.
Nature Communications
|December 19, 2025
Summary
High humidity triggers plant defense against bacterial pathogens by reducing abscisic acid (ABA) levels. This involves ABA 8'-hydroxylase (CYP707A3) and calcium signaling, limiting bacterial water-soaking and infection.
Area of Science:
- Plant Pathology
- Plant Physiology
- Molecular Biology
Background:
- Bacterial phytopathogens like Pseudomonas syringae pv. tomato (Pst) DC3000 cause water-soaked lesions under high humidity, aiding infection.
- Plant resistance mechanisms against humidity-driven bacterial infections are not well understood.
Purpose of the Study:
- To investigate the role of abscisic acid (ABA) metabolism and signaling in Arabidopsis thaliana resistance to bacterial infection under high humidity.
Main Methods:
- Analysis of CYP707A3 gene expression in response to humidity.
- Investigating the role of calcium channels (CNGC2, CNGC4, CNGC9) and CAMTA3 in ABA regulation.
- Assessing the impact of Pst DC3000 type III secretion effectors on water-soaking.
Main Results:
- Elevated humidity induces CYP707A3 expression, decreasing ABA levels and promoting stomatal opening to limit bacterial spread.
- High humidity increases cytosolic Ca2+ via CNGC2/CNGC4 (partially CNGC9), activating CAMTA3 to induce CYP707A3.
- Pst DC3000 effectors, like AvrPtoB, counteract plant defenses to facilitate water-soaking.
Conclusions:
- CYP707A3-mediated ABA catabolism is crucial for plant resistance to bacterial pathogens under high humidity.
- A signaling pathway involving Ca2+ influx and CAMTA3 regulates CYP707A3 induction in response to humidity.
- Plants and bacteria compete for leaf water, with bacterial effectors manipulating host responses.
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