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Largo-Gosens, A.

Publications and source records attributed to Largo-Gosens, A..

3 recordsLinked to original sources

Zymoseptoria tritici stealth infection is facilitated by stage-specific down-regulation of a β-glucanase

Plant cell walls constitute a major defence barrier against pathogens, although it is unclear how specific cell wall components impact pathogen colonisation. Pathogens secrete cell wall degrading enzymes (CWDEs) to facilitate plant colonisation, but damaged, infected cells are often a source of cell wall-derived oligosaccharides that trigger host immunity. The mechanisms by which pathogens minimize the release of cell wall-derived oligosaccharides while colonizing the host remain to be elucidated. We combined biochemical, molecular genetics and transcriptomic analyses to functionally characterize a glycoside hydrolase (ZtGH45) from the wheat pathogen Zymoseptoria tritici. ZtGH45 gene is expressed during the necrotrophic phase of the fungus, coinciding with an accumulation of wheat {beta}-1,3/1,4-mixed-linked glucan (MLG)-derived oligosaccharides. We show that overexpression of ZtGH45 enhances {beta}-1,3/1,4-glucan hydrolysis and the derived oligosaccharides trigger an immune response in wheat, which hinders Z. tritici virulence. The results demonstrate that tight regulation of ZtGH45 is critical for the infection process to prevent early accumulation of MLG oligosaccharides that would prematurely induce host immunity counterbalancing fungal virulence. We suggest that the balance between plant cell wall degradation by fungal CWDE and the release of immunogenic wall-derived oligosaccharides governs the outcome of host invasion by pathogens.

plant biology↗

Linear β-1,2-glucans trigger immune hallmarks and disease resistance in plants

Immune responses in plants are triggered by molecular patterns or elicitors, recognized by plant pattern recognition receptors (PRRs). Such molecular patterns arise from host-pathogen interactions and the response cascade activated after their perception is known as pattern-triggered immunity (PTI). Glucans have emerged as key players in PTI, but certain glucans ability to stimulate defensive responses in plants remains understudied. This work focused on identifying novel glucan oligosaccharides acting as molecular patterns. The ability of various microorganism-derived glucans to prompt PTI responses was tested, revealing that specific microbial-derived glucans, such as short linear {beta}-1,2-glucans, trigger this response in plants by increasing reactive oxygen species (ROS) production, MAP kinase phosphorylation, and differential expression of defence-related genes in Arabidopsis thaliana. Pretreatments with {beta}-1,2-glucan trisaccharide (B2G3) improved Arabidopsis defence against bacterial and fungal infections in a hypersusceptible genotype. The knowledge generated was then transferred to the monocotyledonous model species maize and wheat, confirming that these plants also respond to {beta}-1,2-glucans, with increased ROS production and improved protection against fungal infections following B2G3 pretreatments. In summary, as with other {beta}-glucans, plants perceive {beta}-1,2-glucans as warning signals and stimulate defence responses against phytopathogens. HighlightsWe describe a new group of glycans present in the extracellular matrices of some plant-interacting microorganisms that are sensed by host surveillance systems and enhance the plants natural resistance to disease.

plant biology↗

Transcriptomic reprogramming in a susceptible Phaseolus vulgaris L. variety during Pseudomonas syringae attack: The key role of homogalacturonan methylation

The susceptibility of common bean varieties to Pseudomonas syringae pv. phaseolicola (Pph) has been well-documented. However, the molecular mechanism that drives this susceptibility has not been clarified yet. In an attempt to understand this process, 15-day-old common bean plants, variety rinon, were infected with Pph to analyze the transcriptomic changes during the first steps of the infection (at 2 and 9 h). RNA-seq analysis showed an upregulation of defense-and signaling-related genes at 2h, most of them being downregulated at 9h, suggesting that Pph would inhibit the transcriptomic reprogramming of the plant. This trend was also observed in the modulation of 101 cell wall (CW) related genes, suggesting that Pph could produce/induce changes in the CW. However, the changes in CW composition at early stages of Pph infection were related to homogalacturonan (HG) methylation and the formation of HG egg boxes. From all HG-related genes modulated by the infection, a common bean pectin methylesterase inhibitor 3 (PvPMEI3) gene - closely related to AtPMEI3 -- was detected. In addition, PMEI3 protein was located in the apoplast and its PME inhibitory activity was demonstrated. Therefore, PvPMEI3 seems to be a good candidate to play a key role in Pph infection. This premise was supported by the analysis of Arabidopsis pmei3 mutant, which showed susceptibility to Pph, in contrast to resistant Col-0 control plants. All these changes could be an attempt to reinforce the CW structure and thus, hinder the attack of the bacterium. However, these transcriptional and CW-remodeling processes are neither maintained during the necessary time, nor are deep enough to block the action of the pathogen, facilitating the well-known susceptibility of rinon variety to Pph.

plant biology↗