Many plant-associated microbes are pathogens that impair plant growth and reproduction. Plants respond to infection using a two-branched innate immune system. The first branch recognizes and responds to molecules common to many classes of microbes, including non-pathogens. The second responds to pathogen virulence factors, either directly or through their effects on host targets. These plant immune systems, and the pathogen molecules to which they respond, provide extraordinary insights into molecular recognition, cell biology and evolution across biological kingdoms. A detailed understanding of plant immune function will underpin crop improvement for food, fibre and biofuels production.

http://www.segenetica.es/cng2/cng2008/biblio/Ref-Marc-Valls---Jones-and-Dangl-Nat06.pdf

The plant immune system

https://www.ibric.org/myboard/down.php?Board=exp_qna&filename=pBBR1MCS.pdf&id=20940&fidx=1

Four new derivatives of the broad-host-range cloning vector pBBR1MCS, carrying different antibiotic-resistance cassettes.

Various gram-negative animal and plant pathogens use a novel, sec-independent protein secretion system as a basic virulence mechanism. It is becoming increasingly clear that these so-called type III secretion systems inject (translocate) proteins into the cytosol of eukaryotic cells, where the translocated proteins facilitate bacterial pathogenesis by specifically interfering with host cell signal transduction and other cellular processes. Accordingly, some type III secretion systems are activated by bacterial contact with host cell surfaces. Individual type III secretion systems direct the secretion and translocation of a variety of unrelated proteins, which account for species-specific pathogenesis phenotypes. In contrast to the secreted virulence factors, most of the 15 to 20 membrane-associated proteins which constitute the type III secretion apparatus are conserved among different pathogens. Most of the inner membrane components of the type III secretion apparatus show additional homologies to flagellar biosynthetic proteins, while a conserved outer membrane factor is similar to secretins from type II and other secretion pathways. Structurally conserved chaperones which specifically bind to individual secreted proteins play an important role in type III protein secretion, apparently by preventing premature interactions of the secreted factors with other proteins. The genes encoding type III secretion systems are clustered, and various pieces of evidence suggest that these systems have been acquired by horizontal genetic transfer during evolution. Expression of type III secretion systems is coordinately regulated in response to host environmental stimuli by networks of transcription factors. This review comprises a comparison of the structure, function, regulation, and impact on host cells of the type III secretion systems in the animal pathogens Yersinia spp., Pseudomonas aeruginosa, Shigella flexneri, Salmonella typhimurium, enteropathogenic Escherichia coli, and Chlamydia spp. and the plant pathogens Pseudomonas syringae, Erwinia spp., Ralstonia solanacearum, Xanthomonas campestris, and Rhizobium spp.

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Type III Protein Secretion Systems in Bacterial Pathogens of Animals and Plants

Nonpathogenic rhizobacteria can induce a systemic resistance in plants that is phenotypically similar to pathogen-induced systemic acquired resistance (SAR). Rhizobacteria-mediated induced systemic resistance (ISR) has been demonstrated against fungi, bacteria, and viruses in Arabidopsis, bean, carnation, cucumber, radish, tobacco, and tomato under conditions in which the inducing bacteria and the challenging pathogen remained spatially separated. Bacterial strains differ in their ability to induce resistance in different plant species, and plants show variation in the expression of ISR upon induction by specific bacterial strains. Bacterial determinants of ISR include lipopolysaccharides, siderophores, and salicylic acid (SA). Whereas some of the rhizobacteria induce resistance through the SA-dependent SAR pathway, others do not and require jasmonic acid and ethylene perception by the plant for ISR to develop. No consistent host plant alterations are associated with the induced state, but upon challenge inoculation, resistance responses are accelerated and enhanced. ISR is effective under field conditions and offers a natural mechanism for biological control of plant disease.

/pdf/systemic-resistance-induced-by-rhizosphere-bacteria-13ehvnz7fj.pdf

Systemic resistance induced by rhizosphere bacteria

The gram-positive bacterium Listeria monocytogenes is the causative agent of listeriosis, a highly fatal opportunistic foodborne infection. Pregnant women, neonates, the elderly, and debilitated or immunocompromised patients in general are predominantly affected, although the disease can also develop in normal individuals. Clinical manifestations of invasive listeriosis are usually severe and include abortion, sepsis, and meningoencephalitis. Listeriosis can also manifest as a febrile gastroenteritis syndrome. In addition to humans, L. monocytogenes affects many vertebrate species, including birds. Listeria ivanovii, a second pathogenic species of the genus, is specific for ruminants. Our current view of the pathophysiology of listeriosis derives largely from studies with the mouse infection model. Pathogenic listeriae enter the host primarily through the intestine. The liver is thought to be their first target organ after intestinal translocation. In the liver, listeriae actively multiply until the infection is controlled by a cell-mediated immune response. This initial, subclinical step of listeriosis is thought to be common due to the frequent presence of pathogenic L. monocytogenes in food. In normal indivuals, the continual exposure to listerial antigens probably contributes to the maintenance of anti-Listeria memory T cells. However, in debilitated and immunocompromised patients, the unrestricted proliferation of listeriae in the liver may result in prolonged low-level bacteremia, leading to invasion of the preferred secondary target organs (the brain and the gravid uterus) and to overt clinical disease. L. monocytogenes and L. ivanovii are facultative intracellular parasites able to survive in macrophages and to invade a variety of normally nonphagocytic cells, such as epithelial cells, hepatocytes, and endothelial cells. In all these cell types, pathogenic listeriae go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. In this way, listeriae disseminate in host tissues sheltered from the humoral arm of the immune system. Over the last 15 years, a number of virulence factors involved in key steps of this intracellular life cycle have been identified. This review describes in detail the molecular determinants of Listeria virulence and their mechanism of action and summarizes the current knowledge on the pathophysiology of listeriosis and the cell biology and host cell responses to Listeria infection. This article provides an updated perspective of the development of our understanding of Listeria pathogenesis from the first molecular genetic analyses of virulence mechanisms reported in 1985 until the start of the genomic era of Listeria research.

/pdf/listeria-pathogenesis-and-molecular-virulence-determinants-31rj0tq40k.pdf

Listeria pathogenesis and molecular virulence determinants.

Compartmentation of antifungal compounds in oil cells of avocado fruit mesocarp and its effect on susceptibility to Colletotrichum gloeosporioides

A protein-lipopolysaccharide (PLP) complex was isolated from dialyzed log-phase culture fluids of Verticillium albo-atrum by DEAE-cellulose chromatography, agarose gel filtration and column electrophoresis. Excised cotton leaves supplied 5 μg/ml of the purified PLP for 24 to 36 h were indistinguishable from leaves on the fungus-infected plants. The purified PLP was somewhat unstable, tending to aggregate and precipitate in very low ionic strength solutions and degrading to lower molecular weight products in very high ionic strength solutions. The PLP had a molecular weight of c. 3 × 10 6 and was a major component of log-phase Verticillium cultures. Older cultures contained progressively larger quantities of related lower molecular weight materials, presumed to be PLP degradation products. The PLP was highly acidic and was composed of about 70% polysaccharide and 15% each of protein and lipid. Combined gas chromatography-mass spectrometry showed that the polysaccharide contained glucose, galactose, mannose and galacturonic acid.

Isolation of a protein-lipopolysaccharide complex from Verticillium albo-atrum

Mycolaminarans (water-soluble β-1,3-glucans) from Phytophthora cinnamomi, P. palmivora and P. megasperma var. sojae produced wilting symptoms on Persea indica, soybean, cacao and tomato at 0·01 to 0·5 mg/ml. The same symptoms were also observed with mycolaminaran phosphate, algal laminaran, pustulan (β-1,6-glucan) and carboxymethyl cellulose but different plant responses were produced by pectin and Carbowax and by the α-glucans, dextran and soluble starch. Plant responses to the mycolaminarans appeared to be caused by cellular toxicity rather than by vessel plugging because 14C-mycolaminaran became systematically distributed through P. indica plants and was entirely metabolized to various higher and lower size polymrs within 24 h. Low amounts of the neutral mycolaminaran (0·1 mg/ml maximum) were detected in filtrates of young log-phase cultures of P. megasperma var. sojae grown on synthetic medium.

Phytotoxicity of mycolaminarans—β-1,3-glucans from Phytophthora spp☆

Purified lipopolysaccharides (LPS) from four races of Pseudomonas syringae pv. glycinea were assayed for phytoalexin elicitor activity in soybean cotyledons, and isolated O-chain fractions were chemically characterized. The LPS were weak elicitors of glyceollin accumulation, but no race specificity was noted. SDS-Polyacrylamide gel electrophoresis showed considerable size heterogeneity in the LPS but only slight differences were noted between preparations from the various races. The major components of the O-chain fractions from all races were rhamnose and N-acetylglucosamine. The ratio of these components in preparations from race 4 differed significantly from those of races 1, 5 and 6.

Purification and composition of lipopolysaccharides from Pseudomonas syringae pv. glycinea

Cosmid clone pPsp01 from race 1 Pseudomonas syringae pv. phaseolicola isolate 3121 conferred a unique pattern of soybean cultivar reactions when expressed in P. s. pv. glycinea R4. The avirulence phenotype was shown to result from the presence in clone pPsp01 of an avrD allele as well as an additional avirulence gene located approximately 5-kb upstream. The new gene, called avrPphC, shows high identity to and is phenotypically identical to avrC, previously cloned from P. s. pv. glycinea race 0. avrD and avrPphC occur on an approximately 120-kb indigenous plasmid in P. s. pv. phaseolicola 3121. Although commonly observed in Xanthomonas campestris, this is the first noted occurrence of multiple avirulence genes on a single plasmid in Pseudomonas syringae. Unlike avrD, however, avrPphC does not appear to occur widely in pathovars of Pseudomonas syringae.

Noel T. Keen

Papers

Compartmentation of antifungal compounds in oil cells of avocado fruit mesocarp and its effect on susceptibility to Colletotrichum gloeosporioides

Isolation of a protein-lipopolysaccharide complex from Verticillium albo-atrum

Phytotoxicity of mycolaminarans—β-1,3-glucans from Phytophthora spp☆

Purification and composition of lipopolysaccharides from Pseudomonas syringae pv. glycinea

Avirulence gene avrPphC from Pseudomonas syringae pv. phaseolicola 3121: a plasmid-borne homologue of avrC closely linked to an avrD allele.