Biology subjects

Mansfield, J. W.

Publications and source records attributed to Mansfield, J. W..

4 recordsLinked to original sources

bioRxiv2026

Managing the phyllosphere: Agronomic practices influence the ecology and evolution of Pseudomonas syringae in cherry orchards

Bacterial canker, caused the Pseudomonas syringae species complex, is a major constraint on sweet cherry production worldwide. However, the influence of agronomic practices on pathogen ecology, dispersal and evolution under field conditions remains poorly understood. Here, we combined a factorial-design field experiment with whole-genome sequencing to investigate the effects of polytunnel covering and nitrogen fertigation on phyllosphere populations and the dynamics of a key pathogen, P. syringae pathovar syringae 9644 (Pss9644) in young cherry trees. Epiphytic P. syringae populations initially resembled those in surrounding woodland environments. Over time, pathogenic phylogroup 2d lineages became dominant, particularly on uncovered trees. Diversity of P. syringae populations was higher in uncovered treatments. Polytunnel covering markedly altered community composition and limited rain-splash dispersal of Pss9644 from stem cankers to leaves, thereby interrupting a key stage of the disease cycle. By contrast, nitrogen fertigation had no detectable effect on phyllosphere community structure, but enhanced plant growth and reduced lesion expansion following inoculation. Whole-genome sequencing of re-isolated Pss9644 strains revealed limited short-term genomic diversification, with single-nucleotide polymorphisms detected in 22 re-isolates. In total, 36 mutations were identified across the chromosome although no mutation affected virulence or motility. Taken together, our results show that agronomic practices influence both pathogen ecology and disease outcomes through distinct mechanisms: polytunnel covering primarily limits pathogen dispersal and reshapes phyllosphere communities, while nitrogen fertigation enhances plant growth and reduces disease severity. These findings highlight the potential to integrate canopy management and nutrient strategies to mitigate bacterial canker risk in commercial cherry production.

microbiology↗

bioRxiv2024

Genetic dissection of the tissue-specific roles of type III effectors and phytotoxins in the pathogenicity of Pseudomonas syringae pv. syringae to cherry

When compared with other phylogroups (PGs) of the Pseudomonas syringae (Ps) species complex, Ps pv. syringae strains within PG2 have a reduced repertoire of type III effectors (T3Es) but produce several phytotoxins. Effectors within the cherry pathogen Pss9644 were grouped based on their frequency in strains from Prunus as: the conserved effector locus (CEL) common to most Ps pathogens; a CORE of effectors common to PG2; a set of PRUNUS effectors common to cherry pathogens; and a FLEXIBLE set of T3Es. Pss9644 also contains gene clusters for biosynthesis of toxins syringomycin/syringopeptin and syringolin A. After confirmation of virulence gene expression, mutants with a sequential series of T3E and toxin deletions were pathogenicity tested on wood, leaves and fruits of sweet cherry (Prunus avium) and leaves of ornamental cherry (Prunus incisa). The toxins had a key role in disease development in fruits but were less important in leaves and wood. An effectorless mutant retained some pathogenicity to fruit but not wood or leaves. Striking redundancy was observed amongst effector groups. The CEL effectors have important roles during the early-stages of leaf infection and acted synergistically with toxins in all tissues. Deletion of separate groups of T3Es had much more effect in Prunus incisa than in sweet cherry. Mixed inocula were used to complement the toxin mutations in trans and indicated that strain mixtures may be important in the field. Our results highlight the niche-specific role of toxins in cherry tissues and the complexity of effector redundancy in the pathogen Pss9644.

microbiology↗

bioRxiv2018

Comparative genomics of Pseudomonas syringae reveals convergent gene gain and loss associated with specialisation onto cherry (Prunus avium)

O_LIGenome-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.s pv. morsprunorum (Psm) races 1 and 2, P.s pv. syringae (Pss) and P.s pv. avii.\nC_LIO_LIGenome-based phylogenetic analyses revealed Psm races and P.s pv. avii clades were distinct and were each monophyletic, whereas cherry-pathogenic strains of Pss were interspersed amongst strains from other host species.\nC_LIO_LIA maximum likelihood approach was used to predict effectors associated with host specialisation on cherry. Pss possesses a smaller repertoire of type III effectors but has more toxin biosynthesis clusters compared with Psm and P.s pv. avii. Evolution of cherry pathogenicity was correlated with gain of genes such as hopAR1 and hopBB1 through putative phage transfer and horizontal transfer, respectively. By contrast, loss of the avrPto/hopAB redundant effector group was observed in cherry-pathogenic clades. Ectopic expression of hopAB and hopC1 triggered the hypersensitive reaction in cherry leaves, confirming computational predictions.\nC_LIO_LICherry canker provides a fascinating example of convergent evolution of pathogenicity that is explained by the mix of effector and toxin repertoires acting on a common host.\nC_LI

microbiology↗

bioRxiv2017

Characterisation of the pathogenicity of strains of Pseudomonas syringae towards cherry and plum

Bacterial canker is a major disease of cherry and other stone fruits caused by several pathovars of Pseudomonas syringae. These are P.s pv. morsprunorum race 1 (Psm R1), P.s pv. morsprunorum race 2 (Psm R2) and P.s pv. syringae (Pss). Psm R1 and R2 were originally designated as races of the same pathovar, however phylogenetic analysis has revealed them to be distantly related. This study characterised the pathogenicity of P. syringae on cherry and plum, in the field and the laboratory. The field experiment identified variation in host cultivar susceptibility to the different pathogen clades. The cherry cultivar Merton Glory exhibited a broad resistance to all clades, whilst cultivar Van showed race-specific resistance. Psm R1 may be divided into a race structure with some strains pathogenic to both cherry and plum and others only pathogenic to plum. The results of laboratory-based pathogenicity tests were compared to results obtained on whole-trees. Only cut shoot inoculations were found to be sensitive enough to detect cultivar variation in susceptibility. Measuring population growth of bacteria in detached leaves reliably discriminated pathogens from non-pathogens. In addition, symptom appearance discriminated Psm races from non-pathogens which triggered a rapid hypersensitive response (HR). The pathogen Pss rapidly induced disease lesions and therefore may exhibit a more necrotrophic lifestyle than hemi-biotrophic Psm races. This in-depth study of pathogenic interactions, identification of host resistance and optimisation of laboratory assays, will provide a framework for future genetic dissection of virulence and host resistance mechanisms.

plant biology↗