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Roussin-Leveillee, C.

Publications and source records attributed to Roussin-Leveillee, C..

7 recordsLinked to original sources

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↗

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↗

Glycan recognition by a plant sentinel immune receptor

Pathogens target and degrade the extracellular matrix surrounding plant cells. A central question is how cell wall-derived damage-associated molecular patterns (DAMPs) are recognized and integrated to trigger immune responses. We address this question by determining the structure of the multidomain receptor IGP1 in both apo form and bound to the cellulose-derived DAMP cellotriose. Structural analyses reveal that constitutive Leucine Rich Repeat-malectin interactions preconfigure IGP1 for ligand recognition and that the receptor features a highly specific sugar-binding pocket in the LRR domain capable of distinguishing fine variations in glycan structures. By directly sensing cello-oligomers, IGP1 acts as a cell wall sentinel that links pathogen-induced wall degradation to immune alerting, equipping plants to mount rapid and robust defense responses.

plant biology↗

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↗

Light prevents pathogen-induced aqueous microenvironments via potentiation of salicylic acid signaling

Upon establishment of an infection, many plant pathogens induce an aqueous microenvironment in the extracellular space of their host, resulting in water-soaked lesions. In the case of Pseudomonas syringae (Pst), this is accomplished through the activity of water-soaking effectors that stimulate abscisic acid (ABA) production and signaling, which results in stomatal closure. This reduces transpiration and induces a microenvironment favorable for bacterial growth. Stomata are also highly sensitive to environmental conditions, including light and circadian rhythm. Here, we show that a period of darkness is required for water-soaking, and that a constant light regime abrogates the water-soaking activity of Pst effectors. Additionally, we show that constant light induces resistance against Pst and that this effect requires salicylic acid (SA). An increase in SA production upon infection under constant light did not affect effector-induced ABA signaling, but rather abrogated ABAs ability to induce stomatal closure. Indeed, under normal diurnal light regimes, application of a SA analog is sufficient to prevent the ability of the pathogen to induce stomatal closure and a water-rich niche in the apoplast. Our results provide a novel approach to interfering with a common virulence strategy, as well as providing a physiological mechanism by which SA functions in defense against certain pathogens.

plant biology↗

Natural variation in the Arabidopsis AGO2 gene is associated with susceptibility to potato virus X

RNA silencing functions as an anti-viral defence in plants through the action of DICER-like (DCL) and ARGONAUTE (AGO) proteins. However, there are few known examples of functional variation in RNA silencing components. The AGO2 protein is important for antiviral defense against multiple viruses and has been shown to be a major limiting factor to infection by potato virus X (PVX) of Arabidopsis thaliana but not Nicotiana benthamiana. We show that the AGO2 proteins from these two plants have differential activity against PVX, suggesting that variation in AGO2 is important in plant-virus interactions. Consistent with this, we find that the Arabidopsis thaliana AGO2 gene shows a high incidence of polymorphisms between accessions, with evidence of selective pressure. AGO2 protein variants can be assigned to two groups, in near equal frequency, based on an amino acid change and small deletions in the protein N-terminus. Inoculation of a large number of Arabidopsis accessions shows strong correlation between these alleles and resistance or susceptibility to PVX. These observations were validated using genetic and transgenic complementation analysis, which showed that one type of AGO2 variant is specifically affected in its antiviral activity, without interfering with other AGO2-associated functions such as anti-bacterial resistance or DNA methylation. Our results demonstrate a novel type of genetically-encoded virus resistance and suggest that plant-virus interactions have influenced natural variation in RNA silencing components.

plant biology↗

ARGONAUTE5 Mediates Fine-Tuning of Vegetative-to-Reproductive Phase Transition Through Its Interaction with miR156 in Arabidopsis

Vegetative-to-reproductive phase change is a finely tuned process in plants, largely controlled by the age-regulated microRNA156 (miR156), which functions by suppressing the transcripts of SQUAMOSA-PROMOTER BINDING LIKE (SPL) transcription factors. ARGONAUTE proteins (AGO) are essential effectors of miRNA-mediated gene regulation. However, which AGO(s) mediate(s) the control of flowering time remains unclear. Here, we demonstrate a role for AGO5 in vegetative-to-reproductive phase transition through the modulation of SPL transcription factors. We show that AGO5 interacts physically and functionally with miR156 and that ago5 mutants present an early flowering phenotype in Arabidopsis. Furthermore, in ago5 mutants, the repression of flowering caused by miR156 overexpression is largely reversed, whereas leaf morphology remains unaffected. Our results thus indicate a specific role for AGO5 in mediating miR156 activity in meristematic, but not vegetative, tissue. As such, our data suggest a spatiotemporal regulation of the miR156 aging pathway, mediated through different AGO proteins in different tissues.

plant biology↗