Publications by authors named "Michelle Hulin"

Treating plant bacterial diseases is notoriously difficult because of the lack of available antimicrobials. Pseudomonas syringae pathovar syringae (Pss) is a major pathogen of cherry (Prunus avium) causing bacterial canker of the stem, leaf and fruit, impacting productivity and leading to a loss of trees. In an attempt to find a treatment for this disease, naturally occurring bacteriophage (phage) that specifically target Pss is being investigated as a biocontrol strategy.

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When compared with other phylogroups (PGs) of the Pseudomonas syringae species complex, P. syringae pv. syringae (Pss) strains within PG2 have a reduced repertoire of type III effectors (T3Es) but produce several phytotoxins.

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Pathogen infection is a dynamic process. Here, we employ single-cell transcriptomics to investigate plant response heterogeneity. By generating an Arabidopsis thaliana leaf atlas encompassing 95,040 cells during infection by a fungal pathogen, Colletotrichum higginsianum, we unveil cell-type-specific gene expression, notably an enrichment of intracellular immune receptors in vasculature cells.

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Pathogens produce diverse effector proteins to manipulate host cellular processes. However, how functional diversity is generated in an effector repertoire is poorly understood. Many effectors in the devastating plant pathogen Phytophthora contain tandem repeats of the "(L)WY" motif, which are structurally conserved but variable in sequences.

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Effectors play a central role in determining the outcome of plant-pathogen interactions. As key virulence proteins, effectors are collectively indispensable for disease development. By understanding the virulence mechanisms of effectors, fundamental knowledge of microbial pathogenesis and disease resistance have been revealed.

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Nicotinamide adenine dinucleotide (NAD) has emerged as a key component in prokaryotic and eukaryotic immune systems. The recent discovery that Toll/interleukin-1 receptor (TIR) proteins function as NAD hydrolases (NADase) links NAD-derived small molecules with immune signaling. We investigated pathogen manipulation of host NAD metabolism as a virulence strategy.

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Many strains of Pseudomonas colonise plant surfaces, including the cherry canker pathogens, Pseudomonas syringae pathovars syringae and morsprunorum. We have examined the genomic diversity of P. syringae in the cherry phyllosphere and focused on the role of prophages in transfer of genes encoding Type 3 secreted effector (T3SE) proteins contributing to the evolution of virulence.

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Bacterial canker is a major disease of stone fruits and is a critical limiting factor to sweet cherry () production worldwide. One important strategy for disease control is the development of resistant varieties. Partial varietal resistance in sweet cherry is discernible using shoot or whole tree inoculations; however, these quantitative differences in resistance are not evident in detached leaf assays.

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Bacterial canker of , affecting economically important stone fruit crops including cherry, peach, apricot and plum, is caused by the plant pathogen (.). Strains from two pathovars- pv.

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In order to achieve saturating transposon mutagenesis of the genome of plant pathogenic strains of Pseudomonas syringae we needed to improve plasmid conjugation frequency. Manipulation of the growth stage of donor and recipient cells allowed the required increase in frequency and facilitated conjugation of otherwise recalcitrant strains.

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Bacterial canker disease is a major limiting factor in the growing of cherry and other species worldwide. At least five distinct clades within the bacterial species complex are known to be causal agents of the disease. The different pathogens commonly coexist in the field.

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is a globally distributed soilborne fungal pathogen causing root rots, bulb rots, crown rots and vascular wilts on a range of horticultural plants. Pathogenic isolates are highly host specific and are classified as . is an important ornamental crop and both the quality and yield of flowers and bulbs can be severely affected by a basal rot caused by f.

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Fusarium proliferatum is a component of the onion basal rot disease complex. We present an annotated F. proliferatum draft genome sequence, totaling 45.

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Genome-wide analyses of the effector- and toxin-encoding genes were used to examine the phylogenetics and evolution of pathogenicity amongst diverse strains of Pseudomonas syringae causing bacterial canker of cherry (Prunus avium), including pathovars P. syringae pv morsprunorum (Psm) races 1 and 2, P. syringae pv syringae (Pss) and P.

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Background: Pseudomonas syringae can cause stem necrosis and canker in a wide range of woody species including cherry, plum, peach, horse chestnut and ash. The detection and quantification of lesion progression over time in woody tissues is a key trait for breeders to select upon for resistance.

Results: In this study a general, rapid and reliable approach to lesion quantification using image recognition and an artificial neural network model was developed.

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There has been a recent and rapid increase in the number of species of the genus Zygosaccharomyces which now comprises Z. bailii, Z. bisporus, Z.

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