These findings suggest that it would be beneficial for plants to recognize rain as an early risk factor for infectious diseases. High humidity, which is usually associated with rain, enhances the effects of bacterial pathogen effectors, such as HopM1, and establishes an aqueous apoplast for aggressive host colonization 17. In addition, raindrops negatively regulate stomatal closure, which facilitates pathogen entry into leaf tissues 13, 15, 16. Likewise, raindrops contain fungi such as Alternaria sp., Fusarium sp., Cladosporium sp., Phoma sp., Rhizopus sp., and Botrytis cinerea 14. Natural raindrops contain bacteria at a concentration of 1.06 × 10 4 (/cm 3) 11, including plant pathogens such as Pseudomonas syringae 12, Xanthomonas campestris, and Pantoea ananatis 13. The anticipation of potentially pathogenic microorganisms through sensing climatological changes and their specific detection thus constitute two distinct layers of the plant immune system.Īmong the climatological factors that affect the outcome of plant–microbe interactions, rain is a major cause of devastating plant diseases, as fungal spores and bacteria are spread through rain-dispersed aerosols or ballistic particles splashed from neighboring infected plants. Such responses enable plants to prepare for the potential increased risk of infection at the time when microbes are anticipated to be most infectious. In addition to PTI and ETI, plant immunity can be induced periodically in the absence of pathogen threat, a process controlled by the circadian clock and driven by daily oscillations in humidity as well as light–dark cycles 8, 9, 10. These ligand–receptor systems are largely dependent on a transient increase in intracellular calcium concentration ( i), followed by the initiation of phosphorylation-dependent signaling cascades, including mitogen-activated protein kinases (MAPKs) and calcium-dependent protein kinases, that orchestrate a complex transcriptional network and the activity of immune mediators 6, 7. ETI often culminates in a hypersensitive response as well as acute and localized cell death at the site of infection accompanied by profound transcriptional changes of defense-related genes to retard pathogen growth 4, 5. While adapted pathogens have evolved virulence effectors that can circumvent PTI, plants also deploy disease resistance ( R) genes, primarily encoding nucleotide-binding LRR proteins, which mount effector-triggered immunity (ETI) 3, 4, 5. In plants, pattern-recognition receptors (PRRs), such as leucine-rich repeat receptor-like kinases (LRR-RLKs) and LRR receptor proteins (LRR-RPs), specifically recognize microbe-associated molecular patterns (MAMPs) as non-self molecules, leading to the activation of pattern-triggered immunity (PTI) to limit pathogen proliferation 1, 2. Innate immunity is an evolutionarily conserved front line of defense across the plant and animal kingdoms. Nature Communications volume 13, Article number: 1216 ( 2022) Mechanosensory trichome cells evoke a mechanical stimuli–induced immune response in Arabidopsis thaliana
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