Identifying resistance in wild and ornamental cherry towards bacterial canker caused by .

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.

Transposon Mutagenesis of Pathovars and to Identify Genes Involved in Bacterial Canker Disease of Cherry.

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.

An improved conjugation method for Pseudomonas syringae.

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.

Supercoiling of an excised genomic island represses effector gene expression to prevent activation of host resistance.

The plant pathogen Pseudomonas syringae pv. phaseolicola, which causes halo blight disease of beans, contains a 106 kb genomic island PPHGI-1. PPHGI-1 carries a gene, avrPphB, which encodes an effector protein that triggers a resistance response in certain bean cultivars.

A low frequency persistent reservoir of a genomic island in a pathogen population ensures island survival and improves pathogen fitness in a susceptible host.

The co-evolution of bacterial plant pathogens and their hosts is a complex and dynamic process. Host resistance imposes stress on invading pathogens that can lead to changes in the bacterial genome enabling the pathogen to escape host resistance. We have observed this phenomenon with the plant pathogen Pseudomonas syringae pv.

Early changes in apoplast composition associated with defence and disease in interactions between Phaseolus vulgaris and the halo blight pathogen Pseudomonas syringae Pv. phaseolicola.

The apoplast is the arena in which endophytic pathogens such as Pseudomonas syringae grow and interact with plant cells. Using metabolomic and ion analysis techniques, this study shows how the composition of Phaseolus vulgaris leaf apoplastic fluid changes during the first six hours of compatible and incompatible interactions with two strains of P. syringae pv.

Development of a therapeutic monoclonal antibody that targets secreted fatty acid-binding protein aP2 to treat type 2 diabetes.

The lipid chaperone aP2/FABP4 has been implicated in the pathology of many immunometabolic diseases, including diabetes in humans, but aP2 has not yet been targeted for therapeutic applications. aP2 is not only an intracellular protein but also an active adipokine that contributes to hyperglycemia by promoting hepatic gluconeogenesis and interfering with peripheral insulin action. Serum aP2 levels are markedly elevated in mouse and human obesity and strongly correlate with metabolic complications.

The Identification of Genes Important in Pseudomonas syringae pv. phaseolicola Plant Colonisation Using In Vitro Screening of Transposon Libraries.

The bacterial plant pathogen Pseudomonas syringae pv. phaseolicola (Pph) colonises the surface of common bean plants before moving into the interior of plant tissue, via wounds and stomata. In the intercellular spaces the pathogen proliferates in the apoplastic fluid and forms microcolonies (biofilms) around plant cells.

Discovery and characterization of olokizumab: a humanized antibody targeting interleukin-6 and neutralizing gp130-signaling.

Interleukin-6 (IL-6) is a critical regulator of the immune system and has been widely implicated in autoimmune disease. Here, we describe the discovery and characterization of olokizumab, a humanized antibody to IL-6. Data from structural biology, cell biology and primate pharmacology demonstrate the therapeutic potential of targeting IL-6 at "Site 3", blocking the interaction with the signaling co-receptor gp130.

In planta induced changes in the native plasmid profile of Pseudomonas syringae pathover phaseolicola strain 1302A.

Pseudomonas syringae pv. phaseolicola (Pph) strain 1302A, a causative agent of halo blight in the common bean Phaseolus vulgaris, contains four native plasmids designated pAV505 (150 kb), pAV506 (50 kb), pAV507 (47 kb) and pAV508 (42 kb). Pph 1302A also contains a 106 kb genomic island PPHGI-1 which shares features with integrative and conjugative elements (ICElands) and carries the effector gene avrPphB (hopAR1) which triggers a defensive response in bean cultivars carrying the matching R3 resistance gene.

Modulation of CSF-1-regulated post-natal development with anti-CSF-1 antibody.

Colony-stimulating factor-1 (CSF-1) regulates the survival, proliferation and differentiation of macrophages. CSF-1-deficient mice are osteopetrotic due to a lack of osteoclasts, while their tissue macrophage deficiencies and an absence of CSF-1 regulation of CSF-1 receptor-expressing cells in the female reproductive tract contribute to their pleiotropic phenotype. To further understand CSF-1 regulation of macrophages in vivo, we developed a neutralizing anti-mouse CSF-1 antibody which was expressed as a recombinant Fab' fragment and coupled to 40 kDa polyethylene glycol.