Biology subjects

Gaudreault-Lafleur, F.

Publications and source records attributed to Gaudreault-Lafleur, F..

3 recordsLinked to original sources

bioRxiv2026

Extracellular water withdrawal drives disease resistance in the phyllosphere

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.

plant biology↗

bioRxiv2026

Atypical immunity induced by extracellular water in plants

Microbial pathogens require nutrients and water to support their growth and proliferation. Pathogen-mediated resource acquisition is orchestrated by the secretion of virulence factors that have evolved a diversity of forms (from effector proteins to small toxins), but which have converged in function (resource acquisition). A key observable virulence mechanism employed by a large number of microbial pathogens to cause disease is to induce a water-rich niche in the extracellular space (i.e. the apoplast) of their host, known as water-soaked lesions. Given the ubiquity of this virulence mechanism, we asked whether plants respond to pathogen-induced extracellular water to activate immune programs. We find that inducing a water-soaked apoplast induces an atypical transcriptional response, yet results in a functional immune response that restricts pathogen growth as effectively as canonical pattern-triggered immunity. Genetic and functional analyses reveal a role for the immune phytohormone salicylic acid (SA) in mediating apoplastic water-induced immunity (AWII). These results suggest that plants engage in an immune-priming program in response to apoplastic water accumulation, suggesting that the pathogenic niches induced during infection may be perceived as danger signals.

plant biology↗

bioRxiv2024

Chloroplastic ROS bursts initiate salicylic acid biosynthesis in plant immunity

Chloroplasts are essential centers of signal integration and transduction in plants. They are involved in the biosynthesis of primary and specialized metabolites, including salicylic acid (SA), a key defense phytohormone synthesized via the conserved chorismate biosynthetic pathway. However, the identity of the signal(s) that ultimately triggers SA induction in chloroplasts upon perception of a biotic threat has remained elusive. Here, we provide evidence of a functional link between chloroplast-derived reactive oxygen species (cROS) and SA production. We observe that inhibiting ROS bursts generated from photosystem II during plant immune activation completely abrogates the induction of SA synthesis in response to immunity-inducing signals, without affecting SA-independent immune responses. Indeed, time course analyses show that the induction of SA marker genes parallels that of cROS production during an immune response. Consistent with this, preventing cROS induction is sufficient to nullify the immune protection normally conferred by activating immunity prior to an infection. Analyses of transcriptomes and photosynthetic efficiency show that two conserved effectors from the phytopathogen Pseudomonas syringae, HopM1 and AvrE1, redundantly disrupt photosynthesis and cROS bursts. These effects reduce SA accumulation and are mediated via the impact of HopM1 and AvrE1 in inducting host abscisic acid signaling. Our results suggest that a change in chloroplastic redox homeostasis induced by biotic stressors acts as an initiator of plant immunity through the production of SA, and that this response is targeted by conserved pathogen effector proteins.

plant biology↗