Ikoma, Japan—Farmers, gardeners, and botanists have long observed that plant diseases tend to flare up during periods of high humidity, particularly after rainfall. Humid conditions help bacteria enter plant leaves, and once inside, certain species create a waterlogged internal environment known as 'water-soaking.' This dilutes the plant's defenses and essentially turns the leaf into a bacterial incubator. Central to this process is the hormone abscisic acid (ABA), which controls the release of water via tiny leaf pores called stomata.
Over a decade ago, scientists discovered that bacteria can manipulate the host plant's ABA system by injecting effector proteins into cells, driving ABA up and thereby keeping stomata shut. However, the plant's side of this story remained unclear. Do plants actively defend themselves against water-soaking under high-humidity conditions? How do they sense rising humidity and turn that into a response?
In a recent study, a research team led by Assistant Professor Shigetaka Yasuda from the Nara Institute of Science and Technology (NAIST), Japan, set out to answer these questions. Their paper, which was made available online on December 19, 2025, and published in Volume 17 of the journal Nature Communications on January 21, 2026, was co-authored by Professor Yusuke Saijo from NAIST, Dr. Masanori Okamoto from RIKEN, Japan, Assistant Professors Akihisa Shinozawa and Izumi Yotsui from Tokyo University of Agriculture, Japan, and Professor Masatsugu Toyota from Saitama University, Japan.
Working with a small plant species called Arabidopsis thaliana and the bacterial pathogen Pseudomonas syringae, the team first found that high humidity rapidly induces the production of an enzyme called CYP707A3, which breaks down ABA. Lower ABA levels prompt stomata to open, releasing water from the spaces between leaf cells where bacteria grow. Plants lacking CYP707A3 were significantly more vulnerable to water-soaking, confirming its defensive role.
The researchers then traced this signaling chain upstream, revealing that rising humidity triggers an increase in calcium ions in leaf cells via channel proteins called CNGC2, CNGC4, and CNGC9. In turn, this activates the CAMTA3 transcription factor, which regulates the expression of specific genes that promote CYP707A3 production. Notably, breaking any link in this chain greatly impaired resistance to water-soaking.
To understand how the bacteria respond, the team used genetically modified P. syringae strains with different effector proteins removed. They found that the protein AvrPtoB is not only the main effector suppressing CYP707A3 under high humidity but also a modulator of ABA production. As Asst. Prof. Yasuda puts it: "Plants activate defenses to prevent water accumulation, while pathogens try to counteract this by hijacking the plant's water-retention system."
These findings reveal that plants sense high humidity as a warning and mount a molecular defense, and that bacteria have evolved specific mechanisms to dismantle it. "Our work provides insights that could support the development of new plant disease management strategies, particularly under high-humidity conditions that are expected to become more frequent with climate change," concludes Asst. Prof. Yasuda. "Examining whether similar defense mechanisms operate in major crops, such as rice, could help improve our understanding of disease resistance and support future crop protection approaches."
