Etiology of basal kernel blight of barley caused by<i>Pseudomonas syringae</i>pv.<i>syringae</i>

Martinez-Miller, C.; Braun, A. S.; Siemsen, Susan; Sands, David C.

doi:10.1080/07060669709501057

Cited by 3 publications

(1 citation statement)

References 14 publications

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“…Bacterial diseases of barley have been described, although the mechanisms of resistance have not been studied in detail [ 12 , 13 ]. Apparently, there is no race-specific resistance to bacterial pathogens: thus, only PAMP-triggered immunity is operational, even though cultivar-dependent differences in infection rates have been reported for bacterial kernel blight caused by Pseudomonas syringae [ 14 ]. Significant over-production of salicylic acid (SA) upon P. syringae infection in barley suggests that barley resistance to non-host bacterial pathogens is achieved through a SA-mediated defense pathway [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Differential disease resistance response in the barley necrotic mutant nec1

et al. 2011

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BackgroundAlthough ion fluxes are considered to be an integral part of signal transduction during responses to pathogens, only a few ion channels are known to participate in the plant response to infection. CNGC4 is a disease resistance-related cyclic nucleotide-gated ion channel. Arabidopsis thaliana CNGC4 mutants hlm1 and dnd2 display an impaired hypersensitive response (HR), retarded growth, a constitutively active salicylic acid (SA)-mediated pathogenesis-related response and elevated resistance against bacterial pathogens. Barley CNGC4 shares 67% aa identity with AtCNGC4. The barley mutant nec1 comprising of a frame-shift mutation of CNGC4 displays a necrotic phenotype and constitutively over-expresses PR-1, yet it is not known what effect the nec1 mutation has on barley resistance against different types of pathogens.Resultsnec1 mutant accumulated high amount of SA and hydrogen peroxide compared to parental cv. Parkland. Experiments investigating nec1 disease resistance demonstrated positive effect of nec1 mutation on non-host resistance against Pseudomonas syringae pv. tomato (Pst) at high inoculum density, whereas at normal Pst inoculum concentration nec1 resistance did not differ from wt. In contrast to augmented P. syringae resistance, penetration resistance against biotrophic fungus Blumeria graminis f. sp. hordei (Bgh), the causal agent of powdery mildew, was not altered in nec1. The nec1 mutant significantly over-expressed race non-specific Bgh resistance-related genes BI-1 and MLO. Induction of BI-1 and MLO suggested putative involvement of nec1 in race non-specific Bgh resistance, therefore the effect of nec1on mlo-5-mediated Bgh resistance was assessed. The nec1/mlo-5 double mutant was as resistant to Bgh as Nec1/mlo-5 plants, suggesting that nec1 did not impair mlo-5 race non-specific Bgh resistance.ConclusionsTogether, the results suggest that nec1 mutation alters activation of systemic acquired resistance-related physiological markers and non-host resistance in barley, while not changing rapid localized response during compatible interaction with host pathogen. Increased resistance of nec1 against non-host pathogen Pst suggests that nec1 mutation may affect certain aspects of barley disease resistance, while it remains to be determined, if the effect on disease resistance is a direct response to changes in SA signaling.

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Section: Introductionmentioning

confidence: 99%

Differential disease resistance response in the barley necrotic mutant nec1

et al. 2011

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Pseudomonas syringae pv. syringae (bacterial canker or blast (stone and pome fruits))

Balestra¹

2022

CABI Compendium

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Biological Control of Pseudomonas syringae pv. syringae, the Causal Agent of Basal Kernel Blight of Barley, by Antagonistic Pantoea agglomerans

Braun-Kiewnick¹,

Jacobsen²,

Sands³

2000

Phytopathology®

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Strains of Pantoea agglomerans (synanamorph Erwinia herbicola) suppressed the development of basal kernel blight of barley, caused by Pseudomonas syringae pv. syringae, when applied to heads prior to the Pseudomonas syringae pv. syringae infection window at the soft dough stage of kernel development. Field experiments in 1994 and 1995 revealed 45 to 74% kernel blight disease reduction, whereas glasshouse studies resulted in 50 to 100% disease control depending on the isolate used and barley cultivar screened. The efficacy of biocontrol strains was affected by time and rate of application. Percentage of kernels infected decreased significantly when P. agglomerans was applied before pathogen inoculation, but not when coinoculated. A single P. agglomerans application 3 days prior to the pathogen inoculation was sufficient to provide control since populations of about 10(7) CFU per kernel were established consistently, while Pseudomonas syringae pv. syringae populations dropped 100-fold to 2.0 x 10(4) CFU per kernel. An application to the flag leaf at EC 49 (before heading) also reduced kernel infection percentages significantly. Basal blight decreased with increasing concentrations (10(3) to 10(7) CFU/ml) of P. agglomerans, with 10(7) CFU/ml providing the best control. For long-term preservation and marketability, the survival of bacterial antagonists in several wettable powder formulations was tested. Over all formulations tested, the survival declined between 10- to >100-fold over a period of 1.5 years (r = -0.7; P = 0.000). Although not significant, storage of most formulations at 4 degrees C was better for viability (90 to 93% survival) than was storage at 22 degrees C (73 to 79%). However, long-term preservation had no adverse effect on biocontrol efficacy.

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Etiology of basal kernel blight of barley caused byPseudomonas syringaepv.syringae

Cited by 3 publications

References 14 publications

Differential disease resistance response in the barley necrotic mutant nec1

Differential disease resistance response in the barley necrotic mutant nec1

Pseudomonas syringae pv. syringae (bacterial canker or blast (stone and pome fruits))

Biological Control of Pseudomonas syringae pv. syringae, the Causal Agent of Basal Kernel Blight of Barley, by Antagonistic Pantoea agglomerans

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