Bacteria, Fabaceae, Hazel, Plant Toxins
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Bacterial diseases of hazelnut (Corylus avellana & Corylus spp.) and more

Bacterial blight

Xanthomonas arboricola
Scientific classification
Domain:Bacteria
Phylum:Pseudomonadota
Class:Gammaproteobacteria
Order:Xanthomonadales
Family:Xanthomonadaceae
Genus:Xanthomonas
Species:X. arboricola
Binomial name
Xanthomonas arboricola
Vauterin et al. 1995
Type strain
ATCC 49083

Xanthomonas arboricola pv. corylina

Xanthomonas arboricola is a species of bacteria. This phytopathogenic bacterium can cause disease in trees like Prunus, hazelnut and walnut.

  • Garrity, George M.; Brenner, Don J.; Krieg, Noel R.; Staley, James T. (eds.) (2005). Bergey’s Manual of Systematic Bacteriology, Volume Two: The Proteobacteria, Part C: The Alpha-, Beta-, Delta-, and Epsilonproteobacteria. New York, New York: Springer. ISBN 978-0-387-24145-6.

Hosts and symptoms

Xanthomonas arboricola has a vast host range, however, most symptoms are consistent throughout each of the cultivars such as hazelnut, walnut, and genus prunus (stone fruits). In X. pruni (syn. X. arboricola pv. pruni), the symptoms first usually begin with dark lesions forming on leaves. As the bacteria proliferate, bacterial ooze is noticeable as the necrotic lesions can become greasy. The discharge from the leaf can then spread inoculum to other leaves via rain splash. Infection can lead to an early defoliation of the plant, greatly affecting fruit production. Fruit will also show lesions similar to those found on the leaves. The lesions can cause significant rot of the fruit, thus decreasing or even eliminating any yield. While these are the primary symptoms, sometimes the bacteria can enter the twig over winter, and cause noticeable cankers in the spring; a dieback can happen if the stem cankers are severe enough.

 

Disease cycle

Xanthomonas arboricola can infect all green tissue of the plant. The disease cycle of Xanthomonas arboricola begins on the leaves of the infected plant where the bacteria will live in an epiphytic stage (gathering all nutrients and water from the air) until mid to late spring when sufficient rainsplash spreads the bacteria to new buds and fruits where it becomes pathogenic. With enough early spring rain, a repeating cycle can form in which infected leaves and young buds pass the disease to early season fruit and nutlets. With less rain, a late season infection of fruit and nuts will occur. After the infection of fruit and nuts in autumn, Xanthomonas arboricola will spread to dormant buds and wounds in leaves or branches and overwinter. Come early spring the Xanthomonas will once again enter an epiphytic stage on leaves emerging from previously infected dormant buds and repeat the cycle annually.

Environment impact on disease cycle

Incidence of infection can be correlated with rainfall events during the budding season of the walnut. The most important rains occurring during bud break events. This is due to the rainsplash moving inoculum from infected buds across other green tissues of the tree, most crucially to developing nuts.

Importance

Xanthomonas arboricola has an extraordinarily destructive potential when infecting crops. It is the most devastating blight on walnut, and can cause up to 100% yield loss if not properly managed. Its host range threatens stone fruits and other nuts. Epidemics have been reported in countries such as The United States, Iran, Turkey, and Italy. These outbreaks are not limited to just these countries, and without extensive epidemiological knowledge, it could spread with devastating effects. Through disease forecasting efforts, X. arboricola is known to have its highest virulence and growth rate at around 30 degrees Celsius. Temperature in addition to understanding regional humidity, could help prevent future epidemics in agriculture. Less moisture on the plants, and slightly cooler temperatures can hinder both the dispersal and growth of X. arboricola. In Australia an estimated 3.1 million AUD were lost on average due to yield losses from prunus spp. in years with pathogen prevalence. The pathogen’s capability to survive in woody tissue over winter, or after plant death proves a major challenge for plant pathologists to find an effective solution.[citation needed]

Management

Current management of bacterial walnut blight caused by Xanthomonas arboricola pv. juglandis is through copper-based bactericide sprays. Spraying is started just prior to early shoot emergence and continued at 7- to 10-day or longer intervals as necessary for disease control according to spring rainfall. This spraying regime is to continue until the end of August. Unfortunately, continuous use of copper-based bactericides lead to a buildup of copper in soil and can be related to yield loss in walnut orchards. A natural antibiotic produced by a strain of Streptomyces by the name of kasumin or kasugamycin has been found to have high efficacy against Xanthomonas arboricola pv. juglandis as a copper spray alternative under dry conditions. However, this same efficacy has not been found to hold up under moderate to heavy rainfall unless paired with a copper-based spray treatment.

With the overall lack of resistance and limited control measures, sanitation and irrigation are one of the most widely recommended modes of management. Proper irrigation and water management can help limit the amount of rain splash to prevent the rapid spread of disease. In preventing epidemics, it is recommended to plant certified propagation material; this inhibits the spread of epiphytic X. arboricola. Sanitation is crucial in stopping the distribution of this disease, given how widespread and destructive it can be.

Active projects are underway to breed for resistance for Xanthomonas arboricola, however, it is difficult to implement resistant varieties of the susceptible hosts. Current efforts to breed resistance have yet to be fully successful. A study in the United States developed partial resistance; all resistance genotypes continued to show at least one symptom. One of the best modes of controlling the spread of the disease is by testing nursery plants for the bacteria before planting. This helps to guarantee that quarantined fields are not introduced to the bacteria by a foreign contaminate. Providing healthy planting material can help stop the relative spread of Xanthomonas arboricola, however, this is good practice and not a definitive solution.[citation needed]

External links

Taxon identifiersWikidata: Q8043052 BacDive: 17602 CoL: 7FV85 EoL: 973442 GBIF: 5427649 IRMNG: 10033423ITIS: 967753 LPSN: xanthomonas.html#arboricola NCBI: 56448 NZOR: 6cd76fa1-9cb4-4537-b107-798c41dcac21 uBio: 2115800

Categories: 

Bacterial canker

Cultures of Pseudomonas syringae van Hall taken from bean halo blight colonies

Pseudomonas syringae pv avellanae

Pseudomonas syringae is a rod-shaped, Gram-negative bacterium with polar flagella. As a plant pathogen, it can infect a wide range of species, and exists as over 50 different pathovars, all of which are available to researchers from international culture collections such as the NCPPB, ICMP, and others.

Pseudomonas syringae
Cultures of Pseudomonas syringae
Scientific classification
Domain:Bacteria
Phylum:Pseudomonadota
Class:Gammaproteobacteria
Order:Pseudomonadales
Family:Pseudomonadaceae
Genus:Pseudomonas
Species:P. syringae
Binomial name
Pseudomonas syringae
Van Hall, 1904
Type strain
ATCC 19310
CCUG 14279
CFBP 1392
CIP 106698
ICMP 3023
LMG 1247
NCAIM B.01398
NCPPB 281
NRRL B-1631
Pathovars
P. s. pv. aceris
P. s. pv. aptata
P. s. pv. atrofaciens
P. s. pv. dysoxylis
P. s. pv. japonica
P. s. pv. lapsa
P. s. pv. panici
P. s. pv. papulans
P. s. pv. persicae 
(Prunier, Luisetti &. Gardan)
Young, Dye & Wilkie
P. s. pv. pisi
P. s. pv. syringae
P. s. pv. morsprunorum

Pseudomonas syringae is a member of the genus Pseudomonas, and based on 16S rRNA analysis, it has been placed in the P. syringae group. It is named after the lilac tree (Syringa vulgaris), from which it was first isolated.

  • Anzai, Y; Kim, H; Park, JY; Wakabayashi, H; Oyaizu, H (2000). “Phylogenetic affiliation of the pseudomonads based on 16S rRNA sequence”. International Journal of Systematic and Evolutionary Microbiology. 50 (4): 1563–89. doi:10.1099/00207713-50-4-1563. PMID 10939664.
  • Kreig, N. R.; Holt, J. G., eds. (1984). Bergey’s Manual of Systematic Biology. Baltimore: Williams and Wilkins. pp. 141–99.

A phylogenomic analysis of 494 complete genomes from the entire Pseudomonas genus showed that P. syringae does not form a monophyletic species in the strict sense, but a wider evolutionary group that also included other species as well, such as P. avellanae, P. savastanoi, P. amygdali, and P. cerasi.

Pseudomonas syringae tests negative for arginine dihydrolase and oxidase activity, and forms the polymer levan on sucrose nutrient agar. Many, but not all, strains secrete the lipodepsinonapeptide plant toxin syringomycin, and it owes its yellow fluorescent appearance when cultured in vitro on King’s B medium to production of the siderophore pyoverdin.

Pseudomonas syringae also produces ice nucleation active (INA) proteins which cause water (in plants) to freeze at fairly high temperatures (−1.8 to −3.8 °C (28.8 to 25.2 °F)), resulting in injury. Since the 1970s, P. syringae has been implicated as an atmospheric “biological ice nucleator”, with airborne bacteria serving as cloud condensation nuclei. Recent evidence has suggested the species plays a larger role than previously thought in producing rain and snow. They have also been found in the cores of hailstones, aiding in bioprecipitation. These INA proteins are also used in making artificial snow.

Bacterial speck on tomato in Upstate New York

Pseudomonas syringae pathogenesis is dependent on effector proteins secreted into the plant cell by the bacterial type III secretion system. Nearly 60 different type III effector families encoded by hop genes have been identified in P. syringae. Type III effectors contribute to pathogenesis chiefly through their role in suppressing plant defense. Owing to early availability of the genome sequence for three P. syringae strains and the ability of selected strains to cause disease on well-characterized host plants, including Arabidopsis thaliana, Nicotiana benthamiana, and the tomato, P. syringae has come to represent an important model system for experimental characterization of the molecular dynamics of plant-pathogen interactions.

History

Tomato plant leaf infected with bacterial speck

In 1961, Paul Hoppe of the U.S. Department of Agriculture studied a corn fungus by grinding up infected leaves each season, then applying the powder to test corn for the following season to track the disease. A surprise frost occurred that year, leaving peculiar results. Only plants infected with the diseased powder incurred frost damage, leaving healthy plants unfrozen. This phenomenon baffled scientists until graduate student Steven E. Lindow of the University of Wisconsin–Madison with D.C. Arny and C. Upper found a bacterium in the dried leaf powder in the early 1970s. Steven E. Lindow, now a plant pathologist at the University of California, Berkeley, found that when this particular bacterium was introduced to plants where it is originally absent, the plants became very vulnerable to frost damage. He went on to identify the bacterium as P. syringae, investigate the role of P. syringae in ice nucleation and in 1977, discover the mutant ice-minus strain. He was later successful at producing the ice-minus strain of P. syringae through recombinant DNA technology, as well.

Ice-minus bacteria is a common name given to a variant of the common bacterium Pseudomonas syringae (P. syringae). This strain of P. syringae lacks the ability to produce a certain surface protein, usually found on wild-type P. syringae. The “ice-plus” protein (INA protein, “Ice nucleation-active” protein) found on the outer bacterial cell wall acts as the nucleating centers for ice crystals.[Love, J.; Lesser, W. (April 1989). “The Potential Impact of Ice-Minus Bacteria as a Frost Protestant in New York Tree Fruit Production” (PDF). Northeastern Journal of Agricultural and Resource Economics. 18 (1): 26–34. doi:10.1017/S0899367X00000234.] This facilitates ice formation, hence the designation “ice-plus”. The ice-minus variant of P. syringae is a mutant, lacking the gene responsible for ice-nucleating surface protein production. This lack of surface protein provides a less favorable environment for ice formation. Both strains of P. syringae occur naturally, but recombinant DNA technology has allowed for the synthetic removal or alteration of specific genes, enabling the ice-minus strain to be created from the ice-plus strain in the lab.

Production

To systematically create the ice-minus strain of P. syringae, its ice-forming gene must be isolated, amplified, deactivated and reintroduced into P. syringae bacterium. The following steps are often used to isolate and generate ice-minus strains of P. syringae:

  1. Digest P. syringae’s DNA with restriction enzymes.
  2. Insert the individual DNA pieces into a plasmid. Pieces will insert randomly, allowing for different variations of recombinant DNA to be produced.
  3. Transform the bacterium Escherichia coli (E.coli) with the recombinant plasmid. The plasmid will be taken in by the bacteria, rendering it part of the organism’s DNA.
  4. Identify the ice-gene from the numerous newly developed E. coli recombinants. Recombinant E. coli with the ice-gene will possess the ice-nucleating phenotype, these will be “ice-plus”.
  5. With the ice nucleating recombinant identified, amplify the ice gene with techniques such as polymerase chain reactions (PCR).
  6. Create mutant clones of the ice gene through the introduction of mutagenic agents such as UV radiation to inactivate the ice gene, creating the “ice-minus” gene.
  7. Repeat previous steps (insert gene into plasmid, transform E. coli, identify recombinants) with the newly created mutant clones to identify the bacteria with the ice-minus gene. They will possess the desired ice-minus phenotype.
  8. Insert the ice-minus gene into normal, ice-plus P. syringae bacterium.
  9. Allow recombination to take place, rendering both ice-minus and ice-plus strains of P. syringae.

Economic importance

Icy lingonberry

In the United States alone, it has been estimated that frost accounts for approximately $1 billion in crop damage each year.[citation needed] As P. syringae commonly inhabits plant surfaces, its ice nucleating nature incites frost development, freezing the buds of the plant and destroying the occurring crop. The introduction of an ice-minus strain of P. syringae to the surface of plants would incur competition between the strains. Should the ice-minus strain win out, the ice nucleate provided by P. syringae would no longer be present, lowering the level of frost development on plant surfaces at normal water freezing temperature – 0 °C (32 °F). Even if the ice-minus strain does not win out, the amount of ice nucleate present from ice-plus P. syringae would be reduced due to competition. Decreased levels of frost generation at normal water freezing temperature would translate into a lowered quantity of crops lost due to frost damage, rendering higher crop yields overall.

The ice nucleating nature of P. syringae incites frost development, freezing the buds of the plant and destroying the occurring crop. The introduction of an ice-minus strain of P. syringae to the surface of plants would reduce the amount of ice nucleate present, rendering higher crop yields. The recombinant form was developed as a commercial product known as Frostban. Field-testing of Frostban in 1987 was the first release of a genetically modified organism into the environment. The testing was very controversial and drove the formation of US biotechnology policy. Frostban was never marketed.

Controversy

At the time of Lindow’s work on ice-minus P. syringae, genetic engineering was considered to be very controversial. Jeremy Rifkin and his Foundation on Economic Trends (FET) sued the NIH in federal court to delay the field trials, arguing that NIH had failed to conduct an Environmental Impact Assessment and had failed to explore the possible effects “Ice-minus” bacteria might have on ecosystems and even global weather patterns.[Bratspies, Rebecca (2007). “Some Thoughts on the American Approach to Regulating Genetically Modified Organisms” (PDF). Kansas Journal of Law and Public Policy. 16 (3): 393. SSRN1017832.[dead link]][Maykuth, Andrew (January 10, 1986). “Genetic wonders to come: Some see boon, others calamity”. The Philadelphia Inquirer. Retrieved February 11, 2007.] Once approval was granted, both test fields were attacked by activist groups the night before the tests occurred: “The world’s first trial site attracted the world’s first field trasher”.[“GM crops: A bitter harvest?”. BBC News. June 14, 2002. Retrieved April 4, 2016.] The BBC quoted Andy Caffrey from Earth First!: “When I first heard that a company in Berkley was planning to release these bacteria Frostban in my community, I literally felt a knife go into me. Here once again, for a buck, science, technology and corporations were going to invade my body with new bacteria that hadn’t existed on the planet before. It had already been invaded by smog, by radiation, by toxic chemicals in my food, and I just wasn’t going to take it anymore.”[“GM crops: A bitter harvest?”. BBC News. June 14, 2002. Retrieved April 4, 2016.]

Rifkin’s successful legal challenge forced the Reagan Administration to more quickly develop an overarching regulatory policy to guide federal decision-making about agricultural biotechnology. In 1986, the Office of Science and Technology Policy issued the Coordinated Framework for Regulation of Biotechnology, which continues to govern US regulatory decisions.[Bratspies, Rebecca (2007). “Some Thoughts on the American Approach to Regulating Genetically Modified Organisms” (PDF). Kansas Journal of Law and Public Policy. 16 (3): 393. SSRN1017832.[dead link]] The controversy drove many biotech companies away from use of genetically engineering microorganisms in agriculture.[Baskin, Yvonne (1987). “Testing The Future”. Alicia Patterson Foundation. Retrieved February 11, 2007.]

Genetic engineering

Genomics

Based on a comparative genomic and phylogenomic analysis of 494 complete genomes from the entire Pseudomonas genus, P. syringae does not form a monophyletic species in the strict sense, but a wider evolutionary group (34 genomes in total, organized into 3 subgroups) that includes other species as well. The core proteome of the P. syringae group comprised 2944 proteins, whereas the protein count and GC content of the strains of this group ranged between 4973 and 6026 (average: 5465) and between 58 and 59.3% (average: 58.6%), respectively.

Disease cycle

Pseudomonas syringae overwinters on infected plant tissues such as regions of necrosis or gummosis (sap oozing from wounds on the tree) but can also overwinter in healthy looking plant tissues. In the spring, water from rain or other sources will wash the bacteria onto leaves/blossoms where it will grow and survive throughout the summer. This is the epiphyte phase of P. syringae’s life cycle where it will multiply and spread but will not cause a disease. Once it enters the plant through a leaf’s stomata or necrotic spots on either leaves or woody tissue then the disease will start. The pathogen will then exploit and grow in intercellular space causing the leaf spots and cankers. P. syringae can also survive in temperatures slightly below freezing. These below freezing temperatures increase the severity of infection within trees like sour cherry, apricot, and peach.

Epidemiology

Diseases caused by P. syringae tend to be favoured by wet, cool conditions—optimum temperatures for disease tend to be around 12–25 °C (54–77 °F), although this can vary according to the pathovar involved. The bacteria tend to be seed-borne, and are dispersed between plants by rain splash.

  • Hirano, S S; Upper, C D (1990). “Population Biology and Epidemiology of Pseudomonas Syringae”. Annual Review of Phytopathology. 28: 155–77. doi:10.1146/annurev.py.28.090190.001103.

Although it is a plant pathogen, it can also live as a saprotroph in the phyllosphere when conditions are not favourable for disease. Some saprotrophic strains of P. syringae have been used as biocontrol agents against postharvest rots.

From Wikipedia, the free encyclopedia (Redirected from Saprotroph)

Mycelial cord made up of a collection of hyphae; an essential part in the process of saprotrophic nutrition, it is used for the intake of organic matter through its cell wall. The network of hyphae is referred to as a mycelium, which is fundamental to fungal nutrition.

Saprotrophic nutrition or lysotrophic nutrition is a process of chemoheterotrophic extracellular digestion involved in the processing of decayed (dead or waste) organic matter. It occurs in saprotrophs, and is most often associated with fungi (for example Mucor) and soil bacteria. Saprotrophic microscopic fungi are sometimes called saprobes. Saprotrophic plants or bacterial flora are called saprophytes (sapro- ‘rotten material’ + -phyte ‘plant’), although it is now believed[citation needed] that all plants previously thought to be saprotrophic are in fact parasites of microscopic fungi or other plants. The process is most often facilitated through the active transport of such materials through endocytosis within the internal mycelium and its constituent hyphae.

Various word roots relating to decayed matter (detritus, sapro-), eating and nutrition (-vore, -phage), and plants or life forms (-phyte, -obe) produce various terms, such as detritivore, detritophage, saprotroph, saprophyte, saprophage, and saprobe; their meanings overlap, although technical distinctions (based on physiologic mechanisms) narrow the senses. For example, usage distinctions can be made based on macroscopic swallowing of detritus (as an earthworm does) versus microscopic lysis of detritus (as a mushroom does).

Process

As matter decomposes within a medium in which a saprotroph is residing, the saprotroph breaks such matter down into its composites.

  • Clegg & Mackean (2006, p. 296), fig 14.16—Diagram detailing the re-absorption of substrates within the hypha.

These products are re-absorbed into the hypha through the cell wall by endocytosis and passed on throughout the mycelium complex. This facilitates the passage of such materials throughout the organism and allows for growth and, if necessary, repair.

  • Clegg & Mackean (2006, p. 296) states the purpose of saprotrophs and their internal nutrition, as well as the main two types of fungi that are most often referred to, as well as describes, visually, the process of saprotrophic nutrition through a diagram of hyphae, referring to the Rhizobium on damp, stale whole-meal bread or rotting fruit.

Conditions

In order for a saprotrophic organism to facilitate optimal growth and repair, favourable conditions and nutrients must be present.

  • Clegg & Mackean (2006, p. 296), fig 14.17—A diagram explaining the optimal conditions needed for successful growth and repair.

Optimal conditions refers to several conditions which optimise the growth of saprotrophic organisms, such as;

  1. Presence of water: 80–90% of the mass of the fungi is water, and the fungi require excess water for absorption due to the evaporation of internally retained water.
  2. Presence of oxygen: Very few saprotrophic organisms can endure anaerobic conditions as evidenced by their growth above media such as water or soil.
  3. Neutral-acidic pH: The condition of neutral or mildly acidic conditions under pH 7 are required. 
  4. Low-medium temperature: The majority of saprotrophic organisms require temperatures between 1 °C and 35 °C (33.8 °F and 95 °F), with optimum growth occurring at 25 °C (77 °F).

The majority of nutrients taken in by such organisms must be able to provide carbon, proteins, vitamins and, in some cases, ions. Due to the carbon composition of the majority of organisms, dead and organic matter provide rich sources of disaccharides and polysaccharides such as maltose and starch, and of the monosaccharide glucose.

  • Clegg & Mackean (2006, p. 296) states the purpose of saprotrophs and their internal nutrition, as well as the main two types of fungi that are most often referred to, as well as describes, visually, the process of saprotrophic nutrition through a diagram of hyphae, referring to the Rhizobium on damp, stale whole-meal bread or rotting fruit.

In terms of nitrogen-rich sources, saprotrophs require combined protein for the creation of proteins, which is facilitated by the absorption of amino acids, and usually taken from rich soil. Although both ions and vitamins are rare, thiamine or ions such as potassium, phosphorus, and magnesium aid the growth of the mycelium.

  • Clegg & Mackean (2006, p. 296) states the purpose of saprotrophs and their internal nutrition, as well as the main two types of fungi that are most often referred to, as well as describes, visually, the process of saprotrophic nutrition through a diagram of hyphae, referring to the Rhizobium on damp, stale whole-meal bread or rotting fruit.
  • Further reading
    • Clegg, C. J.; Mackean, D. G. (2006). Advanced Biology: Principles and Applications (2nd ed.). Hodder Publishing.
    • Zmitrovich, I. V.; Wasser, S. P.; Ţura, D. (2014). “Wood-inhabiting fungi” (PDF). In Misra, J. K.; Tewari, J. P.; Deshmukh, S. K.; Vágvölgyi, C. (eds.). Fungi from Different Substrates. N. Y.: CRC Press, Taylor and Francis group. pp. 17–74.
Ecology: Modelling ecosystems: Trophic components
Ecology: Modelling ecosystems: Other components

Categories: 

Mechanisms of pathogenicity

The mechanisms of P. syringae pathogenicity can be separated into several categories: ability to invade a plant, ability to overcome host resistance, biofilm formation, and production of proteins with ice-nucleating properties.

  • Ichinose, Yuki; Taguchi, Fumiko; Mukaihara, Takafumi (2013). “Pathogenicity and virulence factors of Pseudomonas syringae”. J Gen Plant Pathol. 79 (5): 285–296. doi:10.1007/s10327-013-0452-8. S2CID 17519705.

Ability to invade plants

Planktonic P. syringae is able to enter plants using its flagella and pili to swim towards a target host. It enters the plant via wounds of natural opening sites, as it is not able to breach the plant cell wall. An example of this is the partnership with the leaf-mining fly Scaptomyza flava, which creates holes in leaves during oviposition that the pathogen can take advantage of. The role of taxis in P. syringae has not been well-studied, but the bacteria are thought to use chemical signals released by the plant to find their host and cause infection.

Overcoming host resistance

Effectors

Pseudomonas syringae isolates carry a range of virulence factors called type III secretion system (T3SS) effector proteins. These proteins primarily function to cause disease symptoms and manipulate the host’s immune response to facilitate infection. The major family of T3SS effectors in P. syringae is the hrp gene cluster, coding for the Hrp secretion apparatus.

  • Ichinose, Yuki; Taguchi, Fumiko; Mukaihara, Takafumi (2013). “Pathogenicity and virulence factors of Pseudomonas syringae”. J Gen Plant Pathol. 79 (5): 285–296. doi:10.1007/s10327-013-0452-8. S2CID 17519705.
Hop effectors

HopZ1s are type III effectors which interfere with the Glycine max 2-hydroxyisoflavanone dehydratase (GmHID1). HopZ1b degrades daidzein after production, reducing concentrations and thus reducing the immunity it provides the plant.

Elicitors

Pst DC3000 produces a PsINF1, the INF1 in P. syringae. Hosts respond with autophagy upon detection of this elicitor. Liu et al. 2005 finds this to be the only alternative to mass hypersensitivity leading to mass programmed cell death.

Phytotoxins

The pathogens also produce phytotoxins which injure the plant and can suppress the host immune system. One such phytotoxin is coronatine, found in pathovars Pto and Pgl.

  • Ichinose, Yuki; Taguchi, Fumiko; Mukaihara, Takafumi (2013). “Pathogenicity and virulence factors of Pseudomonas syringae”. J Gen Plant Pathol. 79 (5): 285–296. doi:10.1007/s10327-013-0452-8. S2CID 17519705.

Coronatine (COR) is a toxin produced by the bacterium Pseudomonas syringae. It is involved in causing stomata to re-open after they close in response to pathogen-associated molecular patterns, as well as interfering with the responses mediated by salicylic acid after the infection has begun. It consists of coronafacic acid (CFA), which is an analog of methyl jasmonic acid (MeJA), and coronamic acid (CMA), joined by an amide bond between the acid group of CFA and the amino group of CMA.

Biofilm formation

Pseudomonas syringae produces polysaccharides which allow it to adhere to the surface of plant cells. It also releases quorum sensing molecules, which allows it to sense the presence of other bacterial cells nearby. If these molecules pass a threshold level, the bacteria change their pattern of gene expression to form a biofilm and begin expression of virulence-related genes. The bacteria secrete highly viscous compounds such as polysaccharides and DNA to create a protective environment in which to grow.

  • Ichinose, Yuki; Taguchi, Fumiko; Mukaihara, Takafumi (2013). “Pathogenicity and virulence factors of Pseudomonas syringae”. J Gen Plant Pathol. 79 (5): 285–296. doi:10.1007/s10327-013-0452-8. S2CID 17519705.

Ice-nucleating properties

Pseudomonas syringae—more than any mineral or other organism—is responsible for the surface frost damage in plants exposed to the environment. For plants without antifreeze proteins, frost damage usually occurs between −4 and −12 °C (25 and 10 °F) as the water in plant tissue can remain in a supercooled liquid state. P. syringae can cause water to freeze at temperatures as high as −1.8 °C (28.8 °F), but strains causing ice nucleation at lower temperatures (down to −8 °C (18 °F)) are more common. The freezing causes injuries in the epithelia and makes the nutrients in the underlying plant tissues available to the bacteria.[citation needed]

Pseudomonas syringae has ina (ice nucleation-active) genes that make INA proteins which translocate to the outer bacterial membrane on the surface of the bacteria, where the proteins act as nuclei for ice formation. Artificial strains of P. syringae known as ice-minus bacteria have been created to reduce frost damage.[citation needed]

  • Fall, Ray; Wolber, Paul K. (1995). “Biochemistry of Bacterial Ice Nuclei”. In Lee, Richard E.; Warren, Gareth J.; Gusta, L. V. (eds.). Biological Ice Nucleation and Its Applications. St. Paul, Minnesota: American Phytopathological Society. pp. 63–83. ISBN 978-0-89054-172-2.

Pseudomonas syringae has been found in the center of hailstones, suggesting the bacterium may play a role in Earth’s hydrological cycle.

Management

Currently there is not a 100% effective way to eradicate P. syringae from a field. The most common way to control this pathogen is to spray bactericides with copper compounds or other heavy metals that can be combined with fungicides or other pest control chemicals. Chemical treatments with fixed copper such as Bordeaux, copper hydroxide, and cupric sulfate are used to stop the spread of P. syringae by killing the bacteria while it is in the epiphyte stage on leaves, or woody parts of trees – however resistant P. syringae strains do exist. Spraying antibiotics such as streptomycin and organic bactericides is another way to control P. syringae but is less common than the methods listed above.

New research has shown that adding ammonium (NH4+) nutrition to tomato plants can cause a metabolic change leading to resistance against Pseudomonas syringae. This “ammonium syndrome” causes nutrient imbalances in the plant and therefore triggers a defense response against the pathogen.

  • González-Hernández, Ana Isabel; Fernández-Crespo, Emma; Scalschi, Loredana; Hajirezaei, Mohammad-Reza; von Wirén, Nicolaus; García-Agustín, Pilar; Camañes, Gemma (August 2019). “Ammonium mediated changes in carbon and nitrogen metabolisms induce resistance against Pseudomonas syringae in tomato plants”. Journal of Plant Physiology. 239: 28–37. doi:10.1016/j.jplph.2019.05.009. PMID 31177028. S2CID 182543294.

Strict hygiene practices used in orchards along with pruning in early spring and summer were proven to make the trees more resistant to P. syringae. Cauterizing cankers found on orchard trees can save the tree’s life by stopping the infection from spreading.

Breeding plants for resistance is another somewhat effective way to avoid P. syringae. It has been successful in the cherry rootstock with Pseudomonas syringae pv. syringae, but so far, no other species are 100% resistant to this pathogen. Resistance breeding is a slow process, especially in trees. Unfortunately, P. syringae bacteria can adapt genetically to infect resistant plants, and the process for resistance breeding has to start over again.

A combination treatment of bacteriophage and carvacrol shows promise in control of both the planktonic and biofilm forms.

Pathovars

Following ribotype analysis, incorporation of several pathovars of P. syringae into other species was proposed (see P. amygdali, ‘P. tomato’, P. coronafaciens, P. avellanae, ‘P. helianthi’, P. tremae, P. cannabina, and P. viridiflava).

According to this schema, the remaining pathovars are:

However, many of the strains for which new species groupings were proposed continue to be referred to in the scientific literature as pathovars of P. syringae, including pathovars tomato, phaseolicola, and maculicola. Pseudomonas savastanoi was once considered a pathovar or subspecies of P. syringae, and in many places continues to be referred to as P. s. pv. savastanoi, although as a result of DNA-relatedness studies, it has been instated as a new species.[33] It has three host-specific pathovars: P. s. fraxini (which causes ash canker), P. s. nerii (which attacks oleander), and P. s. oleae (which causes olive knot).

Determinants of host specificity

A combination of the pathogen’s effector genes and the plant’s resistance genes is thought to determine which species a particular pathovar can infect. Plants can develop resistance to a pathovar by recognising pathogen-associated molecular patterns (PAMPs) and launching an immune response. These PAMPs are necessary for the microbe to function, so cannot be lost, but the pathogen may find ways to suppress this immune response, leading to an evolutionary arms race between the pathogen and the host.

Pseudomonas syringae as a model system

Owing to early availability of genome sequences for P. syringae pv. tomato strain DC3000, P. syringae pv. syringae strain B728a, and P. syringae pv. phaseolicola strain 1448A, together with the ability of selected strains to cause disease on well-characterized host plants such as Arabidopsis thaliana, Nicotiana benthamiana, and tomato, P. syringae has come to represent an important model system for experimental characterization of the molecular dynamics of plant-pathogen interactions. The P. syringae experimental system has been a source of pioneering evidence for the important role of pathogen gene products in suppressing plant defense. The nomenclature system developed for P. syringae effectors has been adopted by researchers characterizing effector repertoires in other bacteria, and methods used for bioinformatic effector identification have been adapted for other organisms. In addition, researchers working with P. syringae have played an integral role in the Plant-Associated Microbe Gene Ontology working group, aimed at developing gene ontology terms that capture biological processes occurring during the interactions between organisms, and using the terms for annotation of gene products.

Pseudomonas syringae pv. tomato strain DC3000 and Arabidopsis thaliana

As mentioned above, the genome of P. syringae pv. tomato DC3000 has been sequenced, and approximately 40 Hop (Hrp Outer Protein) effectors – pathogenic proteins that attenuate the host cell – have been identified. These 40 effectors are not recognized by A. thaliana thus making P. syringae pv. tomato DC3000 virulent against it – that is, P. syringae pv. tomato DC3000 is able to infect A. thaliana – thus A. thaliana is susceptible to this pathogen.[citation needed]

Many gene-for-gene relationships have been identified using the two model organisms, P. syringae pv. tomato strain DC3000 and Arabidopsis. The gene-for-gene relationship describes the recognition of pathogenic avirulence (avr) genes by host resistance genes (R-genes). P. syringae pv. tomato DC3000 is a useful tool for studying avr: R-gene interactions in A. thaliana because it can be transformed with avr genes from other bacterial pathogens, and furthermore, because none of the endogenous hops genes is recognized by A. thaliana, any observed avr recognition identified using this model can be attributed to recognition of the introduced avr by A. thaliana. The transformation of P. syringae pv. tomato DC3000 with effectors from other pathogens have led to the identification of many R-genes in Arabidopsis to further advance knowledge of plant pathogen interactions.

Examples of avr genes in P. syringae DC3000 and A. thaliana R-genes that recognize them

Avr geneA. thaliana R-gene
AvrBRPM1
AvrRpm1RPM1
AvrRpt2RPS2
AvrRps4RPS4
AvrRps6RPS6
AvrPphB *RPS5/RESISTANCE TO PSEUDOMONAS SYRINGAE 5 (see also Arabidopsis thaliana § RPS5) *
* Weigel, Detlef; Nordborg, Magnus (23 November 2015). “Population Genomics for Understanding Adaptation in Wild Plant Species”. Annual Review of Genetics. Annual Reviews. 49 (1): 315–338. doi:10.1146/annurev-genet-120213-092110. ISSN 0066-4197. PMID 26436459.
Pottinger, Sarah E.; Innes, Roger W. (25 August 2020). “RPS5-Mediated Disease Resistance: Fundamental Insights and Translational Applications”. Annual Review of Phytopathology. Annual Reviews. 58 (1): 139–160. doi:10.1146/annurev-phyto-010820-012733. ISSN 0066-4286. PMID 32284014. S2CID 215757180.
Wang, Yan; Tyler, Brett M.; Wang, Yuanchao (8 September 2019). “Defense and Counterdefense During Plant-Pathogenic Oomycete Infection”. Annual Review of Microbiology. Annual Reviews. 73 (1): 667–696. doi:10.1146/annurev-micro-020518-120022. ISSN 0066-4227. PMID 31226025. S2CID 195259901.

The Dynamin-related protein 2b/drp2b gene in A. thaliana is not directly an immunity gene, but by helping move external material into the intracellular network is indirectly related, and some mutants increase susceptibility.

Pseudomonas syringae pv. tomato strain DC3000, its derivatives, and its tomato host

As its name suggests, P. syringae pv. tomato DC3000 (Pst DC3000) is virulent to tomato (Solanum lycopersicum). However, the tomato cultivar Rio Grande-PtoR (RG-PtoR), harboring the resistance gene Pto, recognizes key effectors secreted by Pst DC3000, making it resistant to the bacteria. Studying the interactions between the Pto-expressing tomato lines and Pst DC3000 and its pathovars is a powerful system for understanding plant-microbe interactions.

Like other plants, the tomato has a two-tier pathogen defense system. The first and more universal line of plant defense, pattern-triggered immunity (PTI), is activated when plant pattern recognition receptors (PRRs) on the cell surface bind to pathogen-associated molecular patterns (PAMPs). The other branch of plant immunity, effector-triggered immunity (ETI), is triggered when intracellular (Nucleotide-binding site, Leucine-rich repeat) NB-LRR proteins bind to an effector, a molecule specific to a particular pathogen. ETI is generally more severe than PTI, and when a threshold of defense activation is reached, it can trigger a hypersensitive response (HR), which is purposeful death of host tissue to prevent the spread of infection. Two key effectors secreted by Pst DC3000 are AvrPto and AvrPtoB, which initiate ETI by binding the Pto/Prf receptor complex in Pto-expressing tomato lines like RG-PtoR.

Pst DC3000 has been modified to create the mutant strain Pst DC3000∆avrPto∆avrPtoB (Pst DC3000∆∆), which expresses neither AvrPto nor AvrPtoB. By infecting RG-PtoR with Pst DC3000∆∆, ETI to the pathogen is not triggered due to the absence of the main effectors recognized by the Pto/Prf complex. In the lab this is highly valuable, as using Pst DC3000∆∆ allows researchers to study the function of PTI-candidate genes in RG-PtoR, which would otherwise be masked by ETI.

Another useful DC3000 derivative is Pst DC3000∆avrPto∆avrPtoB∆fliC (Pst DC3000∆∆∆). Like Pst DC3000∆∆, this strain does not express AvrPto and AvrPtoB, but it also has an additional knock-out for fliC, the gene encoding flagellin, whose fragments serve as main PAMPs required for tomato PTI. By comparing plants within the same line that have been infected with either Pst DC3000∆∆ or Pst DC3000∆∆∆, researchers can determine if genes of interest are important to the flagellin recognition pathway of PTI.

By treating CRISPR-induced tomato knockout mutants (in a RG-PtoR background) with Pst DC3000, Pst DC3000∆avrPto∆avrPtoB, or Pst DC3000∆avrPto∆avrPtoB∆fliC has led to the characterization of key components of the tomato immune system and continues to be used to further the field of tomato pathology.

Importance

Pseudomonas syringae has impacted many crop and orchard industries with its various pathovars.

P. s. pv. actinidiae

Mesarich et al. 2017 provides several libraries for transposon insertion sequencing of mutants of P. s. a.

The kiwifruit industry in New Zealand has suffered catastrophic losses since their first known outbreak in 2007 from P. syringae pv. actinidiae. New Zealand is second to Italy in the total volume of kiwifruit exports making an annual revenue of $NZ 1 billion, making it the most economically valuable export in the country. In 2014 the loss of exports alone was as high as NZ$930 million. Growers had to pay for treatments, and removal of infected vines along with suffering the loss of capital value in their orchards. For some, the orchard values went from NZ$450,000/ha to $70,000/ha after the outbreak, which is the price of bare land. The total loss of equity for the country of New Zealand was as high as NZ$2 billion.

Between 2010 and 2012 over 2,000 hectares (4,900 acres) of Italian kiwi orchards either were killed by P. syringae pv. actinidiae or were killed to contain the disease. The financial consequences for growers and their suppliers were severe, as were the economic consequences more widely.

See also

External links

Wikimedia Commons has media related to Pseudomonas syringae.

Wikispecies has information related to Pseudomonas syringae.

Taxon identifiersWikidata: Q311202Wikispecies: Pseudomonas syringae BacDive: 13024CoL: 4P3SSEoL: 6374832 EPPO: PSDMSXGBIF: 3223236iNaturalist: 337405 IRMNG: 11223972ITIS: 965302LPSN: pseudomonas.html#syringae NCBI: 317NZOR: caa46401-76ac-468c-86b6-1d5a030bb666PPE: pseudomonas-syringae

Categories: 

Crown gall

Agrobacterium radiobacter attaching itself to a carrot cell

Agrobacterium tumefaciens

Agrobacterium radiobacter (more commonly known as Agrobacterium tumefaciens) is the causal agent of crown gall disease (the formation of tumours) in over 140 species of eudicots. It is a rod-shaped, Gram-negative soil bacterium. Symptoms are caused by the insertion of a small segment of DNA (known as the T-DNA, for ‘transfer DNA’, not to be confused with tRNA that transfers amino acids during protein synthesis), from a plasmid into the plant cell, which is incorporated at a semi-random location into the plant genome. Plant genomes can be engineered by use of Agrobacterium for the delivery of sequences hosted in T-DNA binary vectors.

Agrobacterium tumefaciens
Scientific classification
Domain:Bacteria
Phylum:Pseudomonadota
Class:Alphaproteobacteria
Order:Hyphomicrobiales
Family:Rhizobiaceae
Genus:Agrobacterium
Species:A. radiobacter
Binomial name
Agrobacterium radiobacter
(Beijerinck and van Delden 1902)
Conn 1942 (Approved Lists 1980)
Type strain
ATCC 23308[1]
B6
CFBP 2413
HAMBI 1811
ICMP 5856
LMG 187
NCPPB 2437
Synonyms
Bacillus radiobacter 
Beijerinck and van Delden 1902
Bacterium tumefaciens 
Smith and Townsend 1907
Beijerinckia fluminensis 
Döbereiner and Ruschel 1958
(Approved Lists 1980)
Pseudomonas tumefaciens
 (Smith and Townsend 1907)
Duggar 1909
Phytomonas tumefaciens 
(Smith and Townsend 1907)
Bergey et al. 1923
Polymonas tumefaciens 
(Smith and Townsend 1900)
Lieske 1928
Agrobacterium tumefaciens 
(Smith and Townsend 1907)
Conn 1942
Rhizobium radiobacter 
(Beijerinck and van Delden 1902)
Young et al. 2001

Agrobacterium tumefaciens is an Alphaproteobacterium of the family Rhizobiaceae, which includes the nitrogen-fixing legume symbionts. Unlike the nitrogen-fixing symbionts, tumor-producing Agrobacterium species are pathogenic and do not benefit the plant. The wide variety of plants affected by Agrobacterium makes it of great concern to the agriculture industry. Economically, A. tumefaciens is a serious pathogen of walnuts, grape vines, stone fruits, nut trees, sugar beets, horse radish, and rhubarb, and the persistent nature of the tumors or galls caused by the disease make it particularly harmful for perennial crops.

Agrobacterium tumefaciens grows optimally at 28 °C (82 °F). The doubling time can range from 2.5–4h depending on the media, culture format, and level of aeration. At temperatures above 30 °C (86 °F), A. tumefaciens begins to experience heat shock which is likely to result in errors in cell division.

Conjugation

To be virulent, the bacterium contains a tumour-inducing plasmid (Ti plasmid or pTi) 200 kbp long, which contains the T-DNA and all the genes necessary to transfer it to the plant cell. Many strains of A. tumefaciens do not contain a pTi.

Since the Ti plasmid is essential to cause disease, prepenetration events in the rhizosphere occur to promote bacterial conjugation – exchange of plasmids amongst bacteria. In the presence of opines, A. tumefaciens produces a diffusible conjugation signal called 30C8HSL or the Agrobacterium autoinducer[citation needed]. This activates the transcription factor TraR, positively regulating the transcription of genes required for conjugation[citation needed].

Infection methods

Agrobacterium tumefaciens infects the plant through its Ti plasmid. The Ti plasmid integrates a segment of its DNA, known as T-DNA, into the chromosomal DNA of its host plant cells. A. tumefaciens has flagella that allow it to swim through the soil towards photoassimilates that accumulate in the rhizosphere around roots. Some strains may chemotactically move towards chemical exudates from plants, such as acetosyringone and sugars, which indicate the presence of a wound in the plant through which the bacteria may enter. Phenolic compounds are recognised by the VirA protein, a transmembrane protein encoded in the virA gene on the Ti plasmid. Sugars are recognised by the chvE protein, a chromosomal gene-encoded protein located in the periplasmic space.

At least 25 vir genes on the Ti plasmid are necessary for tumor induction[citation needed]. In addition to their perception role, virA and chvE induce other vir genes. The VirA protein has autokinase activity: it phosphorylates itself on a histidine residue. Then the VirA protein phosphorylates the VirG protein on its aspartate residue. The virG protein is a cytoplasmic protein produced from the virG Ti plasmid gene. It is a transcription factor, inducing the transcription of the vir operons. The ChvE protein regulates the second mechanism of the vir genes’ activation. It increases VirA protein sensitivity to phenolic compounds.

Attachment is a two-step process. Following an initial weak and reversible attachment, the bacteria synthesize cellulose fibrils that anchor them to the wounded plant cell to which they were attracted. Four main genes are involved in this process: chvA, chvB, pscA, and att. The products of the first three genes apparently are involved in the actual synthesis of the cellulose fibrils. These fibrils also anchor the bacteria to each other, helping to form a microcolony.[citation needed]

VirC, the most important virulent protein, is a necessary step in the recombination of illegitimate recolonization. It selects the section of the DNA in the host plant that will be replaced and it cuts into this strand of DNA.[citation needed]

After production of cellulose fibrils, a calcium-dependent outer membrane protein called rhicadhesin is produced, which also aids in sticking the bacteria to the cell wall. Homologues of this protein can be found in other rhizobia. Currently, there are several reports on standardisation of protocol for the Agrobacterium-mediated transformation. The effect of different parameters such as infection time, acetosyringone, DTT, and cysteine have been studied in soybean (Glycine max).

Possible plant compounds that initiate Agrobacterium to infect plant cells:

Formation of the T-pilus

To transfer the T-DNA into the plant cell, A. tumefaciens uses a type IV secretion mechanism, involving the production of a T-pilus. When acetosyringone and other substances are detected, a signal transduction event activates the expression of 11 genes within the VirB operon which are responsible for the formation of the T-pilus.

The pro-pilin is formed first. This is a polypeptide of 121 amino acids which requires processing by the removal of 47 residues to form a T-pilus subunit. The subunit was though to be circularized by the formation of a peptide bond between the two ends of the polypeptide. However, high-resolution structure of the T-pilus revealed no cyclization of the pilin, with the overall organization of the pilin subunits being highly similar to those of other conjugative pili, such as F-pilus.

Products of the other VirB genes are used to transfer the subunits across the plasma membrane. Yeast two-hybrid studies provide evidence that VirB6, VirB7, VirB8, VirB9 and VirB10 may all encode components of the transporter. An ATPase for the active transport of the subunits would also be required.

Transfer of T-DNA into the plant cell

A: Agrobacterium tumefaciens
B: Agrobacterium genome
C: Ti Plasmid: a: T-DNA, b: Vir genes, c: Replication origin, d: Opines catabolism genes
D: Plant cell
E: Mitochondria
F: Chloroplast
G: Nucleus

The T-DNA must be cut out of the circular plasmid. This is typically done by the Vir genes within the helper plasmid. A VirD1/D2 complex nicks the DNA at the left and right border sequences. The VirD2 protein is covalently attached to the 5′ end. VirD2 contains a motif that leads to the nucleoprotein complex being targeted to the type IV secretion system (T4SS). The structure of the T-pilus showed that the central channel of the pilus is too narrow to allow the transfer of the folded VirD2, suggesting that VirD2 must be partially unfolded during the conjugation process.

In the cytoplasm of the recipient cell, the T-DNA complex becomes coated with VirE2 proteins, which are exported through the T4SS independently from the T-DNA complex. Nuclear localization signals, or NLSs, located on the VirE2 and VirD2, are recognised by the importin alpha protein, which then associates with importin beta and the nuclear pore complex to transfer the T-DNA into the nucleus. VIP1 also appears to be an important protein in the process, possibly acting as an adapter to bring the VirE2 to the importin. Once inside the nucleus, VIP2 may target the T-DNA to areas of chromatin that are being actively transcribed, so that the T-DNA can integrate into the host genome.

Genes in the T-DNA

Hormones

To cause gall formation, the T-DNA encodes genes for the production of auxin or indole-3-acetic acid via the IAM pathway. This biosynthetic pathway is not used in many plants for the production of auxin, so it means the plant has no molecular means of regulating it and auxin will be produced constitutively. Genes for the production of cytokinins are also expressed. This stimulates cell proliferation and gall formation.

Opines

The T-DNA contains genes for encoding enzymes that cause the plant to create specialized amino acid derivatives which the bacteria can metabolize, called opines. Opines are a class of chemicals that serve as a source of nitrogen for A. tumefaciens, but not for most other organisms. The specific type of opine produced by A. tumefaciens C58 infected plants is nopaline (Escobar et al., 2003).

Two nopaline type Ti plasmids, pTi-SAKURA and pTiC58, were fully sequenced. “A. fabrum” C58, the first fully sequenced pathovar, was first isolated from a cherry tree crown gall. The genome was simultaneously sequenced by Goodner et al. and Wood et al. in 2001. The genome of A. tumefaciens C58 consists of a circular chromosome, two plasmids, and a linear chromosome. The presence of a covalently bonded circular chromosome is common to Bacteria, with few exceptions. However, the presence of both a single circular chromosome and single linear chromosome is unique to a group in this genus. The two plasmids are pTiC58, responsible for the processes involved in virulence, and pAtC58,[2] once dubbed the “cryptic” plasmid.

The pAtC58 plasmid has been shown to be involved in the metabolism of opines and to conjugate with other bacteria in the absence of the pTiC58 plasmid. If the Ti plasmid is removed, the tumor growth that is the means of classifying this species of bacteria does not occur.

Biotechnological uses

Transformed plant tissue cultures

The Asilomar Conference (Berg et al. 1975) established widespread agreement that recombinant techniques were insufficiently understood and needed to be tightly controlled. The DNA transmission capabilities of Agrobacterium have been vastly explored in biotechnology as a means of inserting foreign genes into plants. Shortly after Asilomar, Marc Van Montagu and Jeff Schell, (University of Ghent and Plant Genetic Systems, Belgium) discovered the gene transfer mechanism between Agrobacterium and plants, which resulted in the development of methods to alter the bacterium into an efficient delivery system for genetic engineering in plants. The plasmid T-DNA that is transferred to the plant is an ideal vehicle for genetic engineering. This is done by cloning a desired gene sequence into T-DNA binary vectors that will be used to deliver a sequence of interest into eukaryotic cells. Soon it was widely agreed that Asilomar like protections were needed in plant technologies as well. This process has been performed using firefly luciferase gene to produce glowing plants.[citation needed] This luminescence has been a useful device in the study of plant chloroplast function and as a reporter gene. It is also possible to transform Arabidopsis thaliana by dipping flowers into a broth of Agrobacterium: the seed produced will be transgenic. Under laboratory conditions, the T-DNA has also been transferred to human cells, demonstrating the diversity of insertion application.

The mechanism by which Agrobacterium inserts materials into the host cell is by a type IV secretion system which is very similar to mechanisms used by pathogens to insert materials (usually proteins) into human cells by type III secretion. It also employs a type of signaling conserved in many Gram-negative bacteria called quorum sensing[citation needed]. This makes Agrobacterium an important topic of medical research, as well[citation needed].

Natural genetic transformation

Natural genetic transformation in bacteria is a sexual process involving the transfer of DNA from one cell to another through the intervening medium, and the integration of the donor sequence into the recipient genome by homologous recombination. A. tumefaciens can undergo natural transformation in soil without any specific physical or chemical treatment.

Disease cycle

A drawing of the disease cycle of Agrobacterium tumefaciens.

Agrobacterium tumefaciens overwinters in infested soils. Agrobacterium species live predominantly saprophytic lifestyles, so its common even for plant-parasitic species of this genus to survive in the soil for lengthy periods of time, even without host plant presence. When there is a host plant present, however, the bacteria enter the plant tissue via recent wounds or natural openings of roots or stems near the ground. These wounds may be caused by cultural practices, grafting, insects, etc. Once the bacteria have entered the plant, they occur intercellularly and stimulate surrounding tissue to proliferate due to cell transformation. Agrobacterium performs this control by inserting the plasmid T-DNA into the plant’s genome. See above for more details about the process of plasmid DNA insertion into the host genome. Excess growth of the plant tissue leads to gall formation on the stem and roots. These tumors exert significant pressure on the surrounding plant tissue, which causes this tissue to become crushed and/or distorted. The crushed vessels lead to reduced water flow in the xylem. Young tumors are soft and therefore vulnerable to secondary invasion by insects and saprophytic microorganisms. This secondary invasion causes the breakdown of the peripheral cell layers as well as tumor discoloration due to decay. Breakdown of the soft tissue leads to release of the Agrobacterium tumefaciens into the soil allowing it to restart the disease process with a new host plant.

Disease management

Crown gall disease caused by Agrobacterium tumefaciens can be controlled by using various methods. The best way to control this disease is to take preventative measures, such as sterilizing pruning tools so as to avoid infecting new plants. Performing mandatory inspections of nursery stock and rejecting infected plants as well as not planting susceptible plants in infected fields are also valuable practices. Avoiding wounding the crowns/roots of the plants during cultivation is important for preventing disease. In horticultural techniques in which multiple plants are joined to grow as one, such as budding and grafting these techniques lead to plant wounds. Wounds are the primary location of bacterial entry into the host plant. Therefore, it is advisable to perform these techniques during times of the year when Agrobacteria are not active. Control of root-chewing insects is also helpful to reduce levels of infection, since these insects cause wounds (aka bacterial entryways) in the plant roots. It is recommended that infected plant material be burned rather than placed in a compost pile due to the bacteria’s ability to live in the soil for many years.

Biological control methods are also utilized in managing this disease. During the 1970s and 1980s, a common practice for treating germinated seeds, seedlings, and rootstock was to soak them in a suspension of K84. K84 is composed of A. radiobacter, which is a species related to A. tumefaciens but is not pathogenic. K84 produces a bacteriocin (agrocin 84) which is an antibiotic specific against related bacteria, including A. tumefaciens. This method, which was successful at controlling the disease on a commercial scale, had the risk of K84 transferring its resistance gene to the pathogenic Agrobacteria. Thus, in the 1990s, the use of a genetically engineering strain of K84, known as K-1026, was created. This strain is just as successful in controlling crown gall as K84 without the caveat of resistance gene transfer.

Environment

Crown gall of sunflower
Crown gall of sunflower caused by A. tumefaciens

Host, environment, and pathogen are extremely important concepts in regards to plant pathology. Agrobacteria have the widest host range of any plant pathogen, so the main factor to take into consideration in the case of crown gall is environment. There are various conditions and factors that make for a conducive environment for A. tumefaciens when infecting its various hosts. The bacterium can’t penetrate the host plant without an entry point such as a wound. Factors leading to wounds in plants include cultural practices, grafting, freezing injury, growth cracks, soil insects, and other animals in the environment causing damage to the plant. Consequently, in exceptionally harsh winters, it is common to have an increased incidence of crown gall due to the weather-related damage. Along with this, there are methods of mediating infection of the host plant. For example, nematodes can act as a vector to introduce Agrobacterium into plant roots. More specifically, the root parasitic nematodes damage the plant cell, creating a wound for the bacteria to enter through. Finally, temperature is a factor when considering A. tumefaciens infection. The optimal temperature for crown gall formation due to this bacterium is 22 °C (72 °F) because of the thermosensitivity of T-DNA transfer. Tumor formation is significantly reduced at higher temperature conditions.

See also

Note

  1. This is contested: Velazquez E, Flores-Felix JD, Sanchez-Juanes F, Igual JM, Peix A (2020). “Strain ATCC 4720T is the authentic type strain of Agrobacterium tumefaciens, which is not a later heterotypic synonym of Agrobacterium radiobacter“. Int J Syst Evol Microbiol. 70 (9): 5172–5176. doi:10.1099/ijsem.0.004443. PMID 32915125.
  2. “At plasmid” when talking about related plasmids

Further reading

External links

Taxon identifiersWikidata: Q131472 Wikispecies: Agrobacterium tumefaciens BioLib: 645737 EPPO: AGRBTUGBIF: 3220726i Naturalist: 485613 IRMNG: 10032681ITIS: 967928 LPSN: agrobacterium.html#tumefaciens NCBI: 358 NZOR: 6e52f4ce-0a9a-4b88-a231-1b5652e4782d PPE: agrobacterium-tumefaciensu Bio: 5337471

Categories: 

Fungal diseases

Fungal diseases
AnthracnosePiggotia coryli
= Monostichella coryli
= Gloeosporium coryli
= Labrella coryli
Armillaria root diseaseArmillaria spp.
Borro secCryptosporiopsis tarraconensis
Cytospora cankerCytospora spp.
Eastern filbert blightAnisogramma anomala
Kernel moldsMycosphaerella punctiformis [teleomorph]
Ramularia sp. [anamorph]
Phomopsis spp.
Septoria ostryae
Kernel spotNematospora coryli
Leaf blisterTaphrina coryli
Leaf spotsAnguillosporella vermiformis
Asteroma coryli
Cercospora corylina
Cercospora coryli
Mamianiella coryli
Monochaetia coryli
Mycosphaerella punctiformis [teleomorph]
Ramularia sp. [anamorph]
Phyllosticta coryli
Ramularia coryli
Septoria ostryae
Sphaceloma coryli
Nectria cankerNectria ditissima
Texas root rotPhymatotrichopsis omnivora
Powdery mildewMicrosphaera coryli
Microsphaera ellisii
Microsphaera hommae
Microsphaera verruculosa
Phyllactinia guttata
= Phyllactinia suffulta
RustPucciniastrum coryli

Viral diseases

Viral diseases
Hazelnut mosaicgenus Ilarvirus, Apple mosaic virus (ApMV)
genus Ilarvirus, Prunus necrotic ringspot virus (PNRSV)
genus Ilarvirus, Tulare apple mosaic virus (TAMV)

Phytoplasmal and spiroplasmal diseases

Phytoplasmal and spiroplasmal diseases
Filbert Stuntunknown, suspect a phytoplasma
Hazelnut Yellowsphytoplasma

Miscellaneous diseases and disorders

Miscellaneous diseases and disorders
Blanksempty nut shells, cause unknown
Brown Stainbrown liquefied portions of shell and kernel, cause unknown
Catkin Blastdeformed catkins, cause unknown
Sun Scaldhigh temperature
Wet Feetsaturated soil conditions for extended periods.

References

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