Pseudomonas syringae

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A Microbial Biorealm page on the genus Pseudomonas syringae

Contents

Classification

Higher order taxa

Domain: Bacteria

Phylum: Proteobacteria

Class: Gamma proteobacteria

Order: Pseudomonadales

family: Pseudomonadaceae

genus: Pseudomonas

species: P. syringae

Species

Pseudomonas syringae

Description and significance

Pseudomonas syringae is a rod shaped Gram-negative bacteria, with an aerobic metabolism, and polar flagella. It is a plant pathogen that can be characterized by its inability to properly utilize arginine, because it lacks the assistance of the arginine dihydrolase system. This species of bacteria is actually represented by over 50 different pathovar strains, which is a set of bacterial strains with similar characteristics differentiated by their distinctive pathogenicity toward one or more plant hosts. Each strain of Pseudomonas syringae is specific for a particular plant. All Pseudomonas syringae strains lack a specific cytochrome C oxidase in their respiratory electron transport chain, which causes a negative oxidase reaction to result. It is a nutritionally versatile organism that thrives on damaged plant tissues, and most notably, colonizes the surface of plant leaves. Each strain is specific to a particular species of plant for which it infects. However, it should be noted that not all strains of Pseudomonas syringae are necessarily pathogenic and can develop in non-host plants as well. Non-pathogenic strains have been researched as potential sources of inoculations for plants, serving as a form of antifungal treatment. This in turn generated great interest in sequencing the various genomes of the different strains of P. syringae, in order to better understand the potential utilization of these plant pathogens in agriculture, the identification of genes that are specifically expressed in plants, and enhance the capability of utilizing the ice nucleation properties found within this bacterial species. Besides the use of this bacterium as an antifungal agent against post-harvest rots, it has been found that it has the capability to prevent/ reduce the effects of frost damage on cash crops such as those of the citrus industry. Genomic sequences led to the discovery on a genomic island that produces the nucleation protein necessary for the formation of ice within P. syringae. This discovery has led to the capability of producing artificial snow, a necessity for some ski resorts.

The original strain of Pseudomonas syringae was first isolated in 1902 by van Hall from a diseased lilac (Syringa vulgaris), thus leading to the taxonomic designation of syringae. In the subsequent years to follow, more and more strains were isolated on lesions of other plant species. Initially, each strain was classified as its own distinct species, but as scientists investigated further, more similarities were brought to light, eventually leading to their classification under a single species. [1, 2]


Genome structure

The genomes of several strains of Pseudomonas syringae have been sequenced. Most strains contain around 6 million base pairs in their chromosomes, but of course, there are variations in their genomic sequences depending on the strain. The two completed genomic sequences are from Pseudomonas syringae pv. syringae B728a and Pseudomonas syringae pv. tomato str. DC3000. Both strains contain one circular chromosome, but Pseudomonas syringae pv. tomato str. DC3000 was found to contain 2 plasmids, while Pseudomonas syringae pv. syringae B728a was found to contain no plasmids. Apparently, the plasmids were unique to a particular strain, in order to suit a specific environmental adaptation for gene and phenotypic expression under the right conditions. The genomic islands of particular interest included those responsible the production of ice nucleation surface proteins and pathogenic properties of the bacteria. [6, 11]

Cell structure and metabolism

Pseudomonas syringae are rod-shaped Gram-negative aerobic bacteria. They have multiple polar flagella, used for motility [1]. It has also been found that they produce a pilus-like structure due to the actions of hypersensitive response and pathogenicity genes. Comparing this surface appendage to that of other bacteria, which share similar cell surface structures, it has been determined that this pilus is a common structure in pathogenic bacteria, necessary for the contamination of eukaryotic cells [3]. Some P. syringae contain unique cell surface proteins that are necessary for the formation of ice. By deleting the gene that codes for this particular surface protein, one can significantly reduce favorable conditions necessary for the formation of ice, or induce the formation of ice by synthetically producing this protein which, acts as an ice nucleation site [5, 2]. Because each strain of P. syringae is phenotypically different from one another, it is hard to make generalizations about the species cell structures and appearance. For example, Pseudomonas syringae pv. syringae B301D is distinctly colored yellowish green, due to the production of a fluorescent siderophore in iron limited growth conditions. This characteristic is not necessarily true for all strains. [4]

Due to the great variety in this particular species, generalizing the metabolism of Pseudomonas syringae is an obvious impossibility. The metabolism of each strain is for the most part unique, depending on the strain’s preferred host plant. For the most part they are chemo heterotrophic organisms that depend on the host organism for nutrients. Most P. syringae live on the surfaces of leaves, thus they obtain their required nutrients from the nutrients that diffuse onto the leaf surface. Studies suggest that the disease causing nature of this microbe is often a result of over population on the leaf surface. It should be noted that the relation between nutrient availability and the population size of P. syringae is still largely obscure, as no direct connection has been made between increased availability of nutrients and an increase in population size in scientific studies. However, these organisms are not limited to their disease causing lifestyle. These hardy microorganisms can survive as saprophytes (living off dead organic material) as well, when environmental conditions are not favorable for a pathogenic lifestyle. Another way for P. syringae to adapt to unfavorable weather conditions is the formation of lesions on the host, which was the primary indication of pathogenic activity in past case studies, when these organisms were first heavily studied. In fact, the characterization of P. syringae as a pathogen was so prevalent, that its other methods of survival became largely overlooked as result. Only recently, has the versatility of P. syringae begun to gain greater attention and interest. [1, 2]

Ecology

P. syringae is largely associated with plants and it is widely known as a plant pathogen. The environment in which it lives is known as the phyllosphere. Researchers speculate that most strains live primarily on the surface of leaf epidermis, thus distinguishing P. syringae as an epiphytic bacterium. It shares its environment with other microorganisms as well, depending on the particular species of the host as well as weather conditions. The phyllosphere can be regarded as a fairly extreme environment for bacteria due to the frequency, variation and rapid change in the surrounding environment that it is exposed to on a daily basis. Although it may not be deliberate in its disease causing effects to its host, as populations of P. syringae flourish, they often end up destroying their own habitat in the form of disease, lesions, and frost damage, potentially leading to their own demise. Some strains will form lesions on the plant surfaces to aid in their survival during unfavorable weather conditions. These microbes tend to thrive in cool wet conditions, with rain as an essential component of their ability to survive and move to new hosts. In hot dry weather, P. syringae populations often dramatically decrease in relative size and abundance. Once again, there are exceptions to these generalizations, depending on the particular strain. [2]

Pathology

Not all strains of P. syringae are pathogenic. The strains that are pathogenic cause disease on their hosts through the release of toxins and cell wall degrading enzymes. The result of disease occurring in the plant is actually a function of the pathogen population size and not just the presence of a pathogen. A sign of pathogenic activity by P. syringae on plant leaves is usually indicated by the presence of lesions or, depending on the strain of P. syringae, spots that develop on leaf surfaces. They exude an array of effector proteins into the host plant cells using a type III secretion device. There are a couple types of genes that may be associate with the pathogenic qualities of P. syringae. These include the Hrp genes which elicit the hypersensitive reaction in susceptible plants; however, there is still no real proof that these genes are responsible for the formation of lesions found on infected plants. Researchers have only determined that the Hrp genes maybe a necessary component for the microbe to interact with and invade the host organism. The other gene suspected of causing the symptoms of disease in the host plant are the genes of the gacS and gacA regulon. These genes were found to be pathovar specific [1, 2]. These genes, along with the open reading frames of sypA, sypB, and sypC in the DNA, are required for the formation of the lesions in plants and/or for secretion of toxins Syringopeptin and Syringomycin. Both of these toxins function as virulence determinants between the plant and P. syringae. Currently, there still a lot of research being done to further identify the factors that benefit the pathogenic nature of P. syringae. [7]

Application to Biotechnology

Pseudomonas syringae is perhaps the best studied bacterial plant pathogen to date. This is because it serves as a model organism for studying the interaction between plants and bacterial pathogens. Researchers in educational institutions as well as government branches, such as the United States Department of Agricultural, have invested a great deal in understanding the metabolic lifestyle of this organism in order to better prevent post harvest rots and combat the possible outbreak of a plant pathogen with the capability to destroy thousands of crops. These microbes hold a number of special characteristics and produce a wide variety of potentially useful compounds. For example, they show a high resistance to copper and antibiotics. In fact, they encode genes that bestow resistance to cationic antimicrobial peptides and antibiotics [1, 2, and 6]. Pseudomonas syringae is also a microbe of great interest for its ice nucleation properties. It was discovered that these bacteria produce surface proteins that were essential in the formation of ice crystals at sub-zero temperatures on plant surfaces. By eliminating the genes that were responsible for the production of this protein, a significant amount of frost damage could be prevented on cash crops. This surface protein could also be exploited to induce the production of artificial snow, allowing places like ski resorts to produce snow even when it would normally be too warm. [1, 2, 5, and 6]

Current Research

There is continuing research on the mechanism of the pathogenic nature of Pseudomonas syringae. The type III effector repertoire of P. syringae pv. syringae B728a has recently been studied to determine its role in the survival and the disease causing effects of this microbe. This was done by placing the microbe on a host plant (bean plant), as well as a non-host plant (a tobacco plant). They found that the effectors have different cell death-modulating activities and distinct roles when they infected the susceptible bean and tobacco hosts. They found no direct connection between the cell death-eliciting and defense-eliciting activity, nor did they find a stringent relationship between cell death-suppressing activity and defense-interfering activity in the infected host organisms. They also discovered several effectors with quantitative avirulence activities on their susceptible hosts, but with growth-promoting effects on a species on which it does not cause disease. They determined that P. syringae pv. syringae B728a may have evolved a large repertoire of effectors to become more efficient at colonizing non-host plants of unrelated species to promote their own fitness. [8]

It has recently been determined that one of the major targets of the effectors secreted by P. syringae is the abscisic acid signaling pathway. A significant portion of effector-induced genes were determined to be closely associated with the abscisic acid biosynthesis and also responses to this plant hormone. Genes that are up regulated by effector delivery shared a 42% overlap with abscisic acid-responsive genes. These genes were also found to be components of networks that were induced by osmotic stress and drought. Researchers concluded that a major virulence strategy for P. syringae was the manipulation of the host plant hormone homeostasis, leading to the inhibition of the plants defense mechanisms toward the microbe. [9]

Researchers have also found another mechanism by which P. syringae overcomes a host’s innate immunity to pathogenic activity. They found that one of the effectors secreted by P. syringae, HopAI1, inhibits the Arabidopsis mitogen-activated protein kinases that are activated when exposed to pathogen-associated molecular patterns. Their research indicates that HopAI1 inactivates mitogen-activated protein kinases by removing the phosphate group from phosphothreonine through phosphothreonine lyase activity, essential for HopAI1 function. As a result, HopAI1 suppresses the fortification of the plant’s cell wall defense, as well as the transcriptional activity of pathogen-associated molecular pattern response genes. [10]

References

1) Hirano, S.S. and C.D. Upper (1990) Population biology and epidemiology of Pseudomonas syringae Annual Reviews in Phytopathology 28:155-177 - http://arjournals.annualreviews.org/doi/pdf/10.1146/annurev.py.28.090190.001103

2) Hirano, S.S. and C.D. Upper (2000) Bacteria in the Leaf Ecosystem with Emphasis on Pseudomonas syringae — a Pathogen, Ice Nucleus, and Epiphyte. Microbiology and Molecular Biology Reviews 64 624-653 - http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=10974129

3) Cody and Gross (1987) Characterization of Pyoverdinpss, the Fluorescent Siderophore Produced by Pseudomonas syringae pv. syringae. Applied Environmental Microbiology 53(5): 928–934 http://www.pubmedcentral.nih.gov/pagerender.fcgi?artid=203788&pageindex=1

4) He, S. Y., Kalkkinen, N., Nurmiaho-Lassila, E., Roine, E., Romantschuk, M., Wei, W., and Yuan, J. (1997) Hrp pilus: An hrp-dependent bacterial surface appendage produced by Pseudomonas syringae pv. tomato DC3000 Proc. Natl. Acad. Sci. USA Vol. 94, pp. 3459-3464 - http://www.pnas.org/cgi/reprint/94/7/3459.pdf

5) Maki, Galyan, Chang-Chien and Caldwell (1974) Ice Nucleation Induced by Pseudomonas syringae. Applied Environmental Microbiology 28(3): 456-459 - http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=186742&blobtype=pdf

6) Feil, H., Feil, W.S., Chain, P., Larimer, F., DiBartolo, G., Copeland, A., Lykidis, A., Trong, S., Nolan, M., Goltsman, E., Thiel, J., Malfatti, S., Loper, J.E., Lapidus, A., Detter, J.C., Land, M., Richardson, P.M., Kyrpides, N.C., Ivanova, N., and Lindow, S.E. (2005) Comparison of the complete genome sequences of Pseudomonas syringae pv. syringae B728a and pv. tomato DC3000. Proc. Natl. Acad. Sci. USA 2005 August 2; 102(31): 11064–11069. - http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16043691

7) Scholz-Schroeder, B.K., Soule, J.D., and Gross, D.C. (2003) The sypA, sypS, and sypC synthetase genes encode twenty-two modules involved in the nonribosomal peptide synthesis of syringopeptin by Pseudomonas syringae pv. syringae B301D. Molecular Plant-Microbe Interactions 16:271-80 - http://www.apsnet.org/mpmi/pdfs/2003/0123-01R.pdf

8) Vinatzer, B.A., Teitzel, G.M., Lee, M.W., Jelenska, J., Hotton, S., Fairfax, K., Jenrette, J., and Greenberg, J.T. (2006) The type III effector repertoire of Pseudomonas syringae pv. syringae B728a and its role in survival and disease on host and non-host plants. Molecular Microbiology 62 (1), 26–44. - http://www.blackwell-synergy.com/action/showPdf?submitPDF=Full+Text+PDF+%28582+KB%29&doi=10.1111%2Fj.1365-2958.2006.05350.x&cookieSet=1

9) de Torres-Zabala, M., Truman, W., Bennett, M.H., Lafforgue, G., Mansfield, J.W., Egea, P.R., Bögre, L., and Grant, M. (2007) Pseudomonas syringae pv. tomato hijacks the Arabidopsis abscisic acid signalling pathway to cause disease. The EMBO Journal (2007) 26, 1434–1443 http://www.nature.com/emboj/journal/v26/n5/full/7601575a.html

10) Zhang, J., Shao, F., Li, Y., Cui, H., Chen, L., Li, H., Zou, Y., Long, C., Lan, L., Chai, J., Chen, S., Tang, X., and Zhou, J.-M. (2007) A Pseudomonas syringae Effector Inactivates MAPKs to Suppress PAMP-Induced Immunity in Plants. Cell Host & Microbe (2007) – Elsevier, Volume 1, Issue 3, 17 May 2007, 175-185 - http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B8G3Y-4NRM084-5&_user=4429&_coverDate=05%2F17%2F2007&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000059602&_version=1&_urlVersion=0&_userid=4429&md5=8b73b66fd5325f85ba5518e787fa24c7

11) http://www.pseudomonas-syringae.org/

Edited by David Sze, student of Rachel Larsen and Kit Pogliano

KMG

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