The bacterial disease of ash (Fraxinus excelsior), caused by Pseudomonas syringae subsp. savastanoi pv. fraxini III. Pathogenesis

Janse, J.

doi:10.1111/j.1439-0329.1982.tb01472.x

Cited by 10 publications

(8 citation statements)

References 17 publications

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“…Unlimited bacterial invasion and indeterminate growth of the knots were constrained by the eventual formation of periderm around bacterial cavities and at the surface of the knots. Previous studies on the anatomy of host–pathogen interactions of P. savastanoi on ash ( Janse 1982), olive ( Surico 1977) and oleander ( Wilson 1965) reported similar findings with respect to initial establishment of the bacterium, colonization of host tissues, formation of bacterial cavities, hypertrophy and hyperplasic activity around bacterial cavities, and periderm formation. However, on oleander ( Wilson 1965) and olive ( Surico 1977) differentiation of vascular tissues in the knots occurred during the first 15 days of knot formation, in contrast to buckthorn, where vascular tissues were formed 55 days after inoculation.…”

Section: Discussionsupporting

confidence: 59%

“…However, on oleander ( Wilson 1965) and olive ( Surico 1977) differentiation of vascular tissues in the knots occurred during the first 15 days of knot formation, in contrast to buckthorn, where vascular tissues were formed 55 days after inoculation. On ash, growth of the knot was limited and did not show differentiation of vascular elements ( Janse 1982). Successive degradation of host cell wall components by P. savastanoi on buckthorn suggests activities of different bacterial enzymes ( Temsah et al.…”

Section: Discussionmentioning

confidence: 99%

“…The objectives of this study were to monitor and record disease symptoms and anatomical changes in inoculated young stem tissues of buckthorn. Anatomical changes in buckthorn tissues, caused by P. savastanoi , were compared with those reported on ash ( Janse 1982), olive ( Surico 1977), and oleander ( Wilson 1965) by strains of the same pathogen, originating from the respective hosts.…”

Section: Introductionmentioning

confidence: 99%

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Anatomical observations of Pseudomonas savastanoi on Rhamnus alaternus

Temsah¹,

Hanna²,

Saad³

2007

Forest Pathology

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Buckthorn (Rhamnus alaternus) was recently reported as a new host of Pseudomonas savastanoi. The main symptom on buckthorn is the formation of knots on stems, branches and occasionally on leaves. Knot formation and anatomical changes in host tissues induced by P. savastanoi were studied macroscopically and by light microscopy. Inoculation of buckthorn shoots with P. savastanoi initiated small green swellings that developed into normal size knots. The pathogen invades intercellular spaces of parenchyma tissues degrading cell walls and resulting in extensive cavities filled with bacterial cells. Many host cells contiguous to such cavities were plasmolysed and necrotic. Depending on the depth of the inoculation wound, parenchyma, cambium, ray parenchyma, and pith cells close to bacterial cavities enlarge and proliferate forming the fully grown knots. At later stages of knot development, the cambium appears dispersed in the knot and forms unoriented vascular tissues. Periderm surrounds bacterial cavities and outer layers of knots. These findings on buckthorn are compared with those reported to be caused by the same pathogen on ash, oleander and olive.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Anatomical observations of Pseudomonas savastanoi on Rhamnus alaternus

Temsah¹,

Hanna²,

Saad³

2007

Forest Pathology

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“…At present, the role of auxins in symptom development on ash is still unknown but, as already suggested (Surico & Iacobellis, 1992), they might be responsible for the formation of the wart‐like excrescences. The extensive periderm formation in diseased ash tissues also suggests this effect (Janse, 1982b). The availability of mutants either lacking the ability to produce auxins or whose auxin‐producing ability had changed might allow the role of auxin to be confirmed.…”

Section: Discussionmentioning

confidence: 99%

Characterization of Pseudomonas syringae ssp. savastanoi strains isolated from ash

1998

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Isolates of Pseudomonas syringae ssp. savastanoi from ash were examined for their ability to produce phytohormones in culture and for pathogenicity, in comparison with isolates from olive and oleander. Nineteen out of 20 ash isolates produced low levels of indole-3-acetic acid and its methyl ester but no cytokinins. In contrast, the remaining isolate, NCPPB3474, accumulated high levels of auxins and cytokinins in culture, comparable to those of olive and oleander strains. Hybridization of DNA preparations with tryptophan mono-oxygenase (iaaM) and isopentenyl transferase (ipt) gene-containing probes showed sequences of DNA homologous to both probes only in isolate NCPPB3474, and in which the iaaM and ipt genes were located on the chromosome and on a plasmid of about 80 kb, respectively. When assayed for pathogenicity on ash, olive and oleander, 19 of the 20 ash isolates caused disease only on ash but NCPPB3474 caused knots on both ash and olive. Oleander isolates infected all three hosts whereas those from olive caused symptoms only on olive and ash. All the cultures were able to multiply in host plant tissues, but the growth rates and final population densities were correlated to the plant species inoculated and the host origin of the isolates. In particular, the highest population densities were reached by isolates capable of causing symptoms on the inoculated host. The phytohormone production shown by ash, olive and oleander isolates of P. syringae ssp. savastanoi was in accordance with the type of symptoms: cankers accompanied by wart-like excrescences on ash and knots on olive and oleander. Furthermore, the pathogenic features of these isolates and, in particular, their growth patterns in the different host tissues, support previous evidence on the existence of three distinct pathovars in P. syringae ssp. savastanoi.

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“…Lenticels and leaf scars are the main infection points for Neonectria spp., which cause canker in apple and other tree species (Flack & Swinburne 1977). In ash, however, literature has often considered bark wounds and openings to be the entry point for fungal and bacterial cankers (Flack & Swinburne 1977, Janse 1981, Janse 1982 but lenticels have never been considered in this context. Our work shows that many known pathogens can use lenticels as entry points to infect ash shoot bark.…”

Section: Discussionmentioning

confidence: 99%

Lenticel infection in Fraxinus excelsior shoots in the context of ash dieback

Nemesio‐Gorriz¹,

McGuinness²,

Grant³

et al. 2019

iForest

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Biogeosciences and Forestry Biogeosciences and Forestry Lenticel infection in Fraxinus excelsior shoots in the context of ash dieback Miguel Nemesio-Gorriz (1) , Brian McGuinness (2) , Jim Grant (3) , Luke Dowd (4) , Gerry C Douglas (1) Common ash (Faxinus excelsior L.) in Europe is declining on a continental scale due to the action of Hymenoscyphus fraxineus, an invasive forest pathogen that causes ash dieback disease leading to the collapse and eventual death of ash trees through shoot infection in the crown and through stem collar infection. This study confirms for the first time lenticels as entry points for pathogens to enter shoot bark. Results show the impact of lenticel infection at a very early stage of invasion by H. fraxineus in a F. excelsior provenance trial and its correlation values with other factors such as shoot dieback, canker-like lesions and bud burst. No significant provenance effects were observed for incidence of shoot dieback, lenticel necrosis or canker-like lesions on shoots, but provenance effects were significant for bud burst phenology. The strongest correlation was observed between lenticel necrosis and canker-like lesions on the lenticels of shoots. Boheremia spp. were most frequently isolated from necrotic ash lenticels and confirmed by ITS sequencing, but also species of Diaporthe, Epicoccum, Aspergillus, Neonectria, Didymella and Hymenoscyphus fraxineus. Finally, lenticel density was similar in sets of ash genotypes that were characterized as having a high and low susceptibility to ash dieback.

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The bacterial disease of ash (Fraxinus excelsior), caused by Pseudomonas syringae subsp. savastanoi pv. fraxini III. Pathogenesis

Cited by 10 publications

References 17 publications

Anatomical observations of Pseudomonas savastanoi on Rhamnus alaternus

Anatomical observations of Pseudomonas savastanoi on Rhamnus alaternus

Characterization of Pseudomonas syringae ssp. savastanoi strains isolated from ash

Lenticel infection in Fraxinus excelsior shoots in the context of ash dieback

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