Origin of the Polysaccharide Component of Ooze from Plants Infected with Erwinia amylovora

Bennett, Robert A.; Billing, Eve

doi:10.1099/00221287-116-2-341

Cited by 25 publications

(28 citation statements)

References 8 publications

(11 reference statements)

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“…The asparagine-sorbitol-minimal salts medium of Bennett & Billing (1980) was modified for bulk culture of the bacteria to contain (1-l): sorbitol, 20 g; asparagine, 4 g; K2HP04, 2 g; MgSO,. 7H20, 0.2 g; nicotinic acid, 0.2 g; thiamin.…”

Section: Methodsmentioning

confidence: 99%

“…Goodman et al (1974) suggested that EPS was a host-specific wilting toxin, a view which is now questioned (Beer et al, 1983; Van-Alfen & McMillan, 1982). Bennett & Billing (1980) established that EPS contained galactose with lesser amounts of glucose, uronic acid and mannose, but its structure has never been satisfactorily described (see Goodman, 1983). Bennett (1980) isolated an avirulent capsulate strain (P66), thus establishing that EPS could not be the sole determinant of virulence.…”

Section: Introductionmentioning

confidence: 99%

“…Although the mechanism by which the disease is established and progresses is not known, all virulent strains are capsulate and produce an extracellular polysaccharide (EPS) which has the same chemical composition whether produced in the plant host or in artificial culture media containing sorbitol (Bennett & Billing, 1980;Ayers et al, 1979;Slade & Tiffin, 1978). Goodman et al (1974) suggested that EPS was a host-specific wilting toxin, a view which is now questioned (Beer et al, 1983; Van-Alfen & McMillan, 1982).…”

Section: Introductionmentioning

confidence: 99%

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Composition of Lipopolysaccharides from Four Strains of Erwinia amylovora

et al. 1986

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The lipopolysaccharides (LPSs) from four isolates of Erwinia amylovora were examined. One isolate was virulent and capsulate, and it produced extracellular polysaccharide (EPS). Three were avirulent, of which one was capsulate and produced EPS; the remainder were noncapsulate and did not produce EPS. LPS was recovered from the cells and from the culture medium. Material extracted from the cells using phenol-water was indistinguishable from LPS extracted with phenol-chloroform-light petroleum. Acid hydrolysis released lipid A which contained in all cases glucosamine, phosphate and the fatty acids 12 : 0, 14 : 0 and 3-OH 14 : 0. The carbohydrate released by mild acid hydrolysis was resolved by gel permeation chromatography into three components I, a partially included species identified as core substituted with a short sidechain of fucose, galactose and glucose; 11, an unsubstituted core oligosaccharide containing heptose, glucose, uronic acid, amino compounds and 3-deoxy-2-octulosonic acid (KDO) ; I11 ; a totally-included low M, fraction containing KDO, phosphate and amino compounds. The sidechain component was missing from LPS of one of the noncapsulate strains that did not produce EPS. This strain is believed to lack UDP-glucose-4-epimerase, a key enzyme in the biosynthesis of galactose. Galactose (with glucose and uronic acid) is known also to be a component of EPS. Defects in galactose synthesis may therefore affect the assembly of LPS as well as EPS.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Composition of Lipopolysaccharides from Four Strains of Erwinia amylovora

et al. 1986

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“…Under favorable climatic conditions, drops of ooze consisting of bacteria embedded in exopolysaccharides (EPS) are produced from infected tissues. In vitro, E. amylovora produces these same EPS, which are either tightly bound to the cell to form a capsule or run freely on the medium to constitute the slime (2,7,53). To date, EPS are the only components known to be involved in the pathogenicity of this bacterium (5,6); however their role is still controversial (4,25,27,31,46,52).…”

mentioning

confidence: 99%

Bacteriophage Mu as a genetic tool to study Erwinia amylovora pathogenicity and hypersensitive reaction on tobacco

1990

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Erwinia amylovora 1430 was shown to be sensitive to Mu G(-) particles. Infection resulted either in lytic development or in lysogenic derivatives with insertion of the Mu genome at many sites in the bacterial chromosome. We used the Mu d1Bx::Tn9 (lac Apr Cmr) derivative, called Mu dX, to identify mutants affected in pathogenicity and in their ability to induce a hypersensitive reaction (HR) on tobacco plants. Inoculation of 1,400 lysogenic derivatives on apple root calli led to the identification of 12 mutants in three classes: (i) class 1 mutants were nonpathogenic and unable to induce an HR on tobacco plants; (ii) class 2 mutants were nonpathogenic but retained the ability to induce an HR; and (iii) class 3 mutants showed attenuated virulence. Of the 12 mutants, 8 had a single insertion of the Mu dX prophage. For class 1 and 2 mutants, reversion to pathogenicity was concomitant with the loss of the Mu dX prophage. Furthermore, revertants from the class 1 mutants also recovered the ability to induce an HR on tobacco plants. Five of the six class 3 mutants were impaired in exopolysaccharide production. No changes of the envelope structure (lipopolysaccharide and outer membrane proteins) were correlated with differences in pathogenicity. One class 3 mutant did not produce any functional siderophore, suggesting that iron uptake could be involved in pathogenicity.

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“…The presence of D-fucose is reminiscent of the presence of D-6-deoxyhexoses in the lipopolysaccharide of other bacterial plant pathogens, and has been commented on before [2]. Glucose and galactose are also components of the extracellular polysaccharide produced by E. amylovora [18], but it appears probable that here the sugars are linked in a different pattern [19].…”

Section: Periodate Oxidation and Smith Degradationmentioning

confidence: 99%