Extracellular water withdrawal drives disease resistance in the phyllosphere
Abstract
A central question in immunity is how hosts arrest pathogen growth. Diverse plant pathogens create a water-soaked niche in host tissue essential for pathogenesis, yet how water shapes infection outcome is unknown. Using genetics and hyperspectral imaging, we show that extracellular water status is rate-limiting for both compatible and incompatible interactions. We find that the hypersensitive response of effector-triggered immunity (ETI) is, mechanistically, a desiccation event. Water loss imposes osmotic stress that arrests bacterial division while the pathogen remains alive and metabolically active, rather than killing it. Restoring apoplastic water reverses this stasis and licenses growth despite intact immune signaling and cell death. Water status, not immune signaling per se , gates pathogen growth. This reframes ETI as a controlled desiccation mechanism and identifies hydration as a decisive lever on disease outcome.
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BibTeX
@misc{roussinleveillee2026extracellular,
title = {{Extracellular water withdrawal drives disease resistance in the phyllosphere}},
author = {Charles Roussin-Léveillée and Sabrina Gauthier and Yezhou Hu and Jie Zhu and Faye Gaudreault- Lafleur and Soline Marty and Antoine Pelletier and Alexis Roy and Laurent D. Noël and Gitta Coaker and Xiufang Xin and Peter Moffett},
howpublished = {HAL},
year = {2026},
month = aug,
doi = {10.64898/2026.08.27.747301},
url = {https://hal.science/hal-05761639v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Extracellular water withdrawal drives disease resistance in the phyllosphere
AU - Charles Roussin-Léveillée
AU - Sabrina Gauthier
AU - Yezhou Hu
AU - Jie Zhu
AU - Faye Gaudreault- Lafleur
AU - Soline Marty
AU - Antoine Pelletier
AU - Alexis Roy
AU - Laurent D. Noël
AU - Gitta Coaker
AU - Xiufang Xin
AU - Peter Moffett
PY - 2026
DA - 2026/08/28
PB - HAL
DO - 10.64898/2026.08.27.747301
UR - https://hal.science/hal-05761639v1
AB - A central question in immunity is how hosts arrest pathogen growth. Diverse plant pathogens create a water-soaked niche in host tissue essential for pathogenesis, yet how water shapes infection outcome is unknown. Using genetics and hyperspectral imaging, we show that extracellular water status is rate-limiting for both compatible and incompatible interactions. We find that the hypersensitive response of effector-triggered immunity (ETI) is, mechanistically, a desiccation event. Water loss imposes osmotic stress that arrests bacterial division while the pathogen remains alive and metabolically active, rather than killing it. Restoring apoplastic water reverses this stasis and licenses growth despite intact immune signaling and cell death. Water status, not immune signaling per se , gates pathogen growth. This reframes ETI as a controlled desiccation mechanism and identifies hydration as a decisive lever on disease outcome.
ER -