Pseudomonas savastanoi pv. savastanoi: some like it knot
Version of Record online: 17 JUL 2012
© 2012 THE AUTHORS. MOLECULAR PLANT PATHOLOGY © 2012 BSPP AND BLACKWELL PUBLISHING LTD
Molecular Plant Pathology
Volume 13, Issue 9, pages 998–1009, December 2012
How to Cite
Ramos, C., Matas, I. M., Bardaji, L., Aragón, I. M. and Murillo, J. (2012), Pseudomonas savastanoi pv. savastanoi: some like it knot. Molecular Plant Pathology, 13: 998–1009. doi: 10.1111/j.1364-3703.2012.00816.x
- Issue online: 24 OCT 2012
- Version of Record online: 17 JUL 2012
- Spanish Plan Nacional I+D+i. Grant Numbers: AGL2008-05311-C02-01, AGL2008-05311-C02-02, AGL2011-30343-C02-01, AGL2011-30343-C02-02
- Fondo Europeo de Desarrollo Regional (FEDER)
- Junta de Andalucía. Grant Number: P08-CVI-03475
- Ramón Areces Foundation
Pseudomonas savastanoi pv. savastanoi is the causal agent of olive (Olea europaea) knot disease and an unorthodox member of the P. syringae complex, causing aerial tumours instead of the foliar necroses and cankers characteristic of most members of this complex. Olive knot is present wherever olive is grown; although losses are difficult to assess, it is assumed that olive knot is one of the most important diseases of the olive crop. The last century witnessed a large number of scientific articles describing the biology, epidemiology and control of this pathogen. However, most P. savastanoi pv. savastanoi strains are highly recalcitrant to genetic manipulation, which has effectively prevented the pathogen from benefitting from the scientific progress in molecular biology that has elevated the foliar pathogens of the P. syringae complex to supermodels. A number of studies in recent years have made significant advances in the biology, ecology and genetics of P. savastanoi pv. savastanoi, paving the way for the molecular dissection of its interaction with other nonpathogenic bacteria and their woody hosts. The selection of a genetically pliable model strain was soon followed by the development of rapid methods for virulence assessment with micropropagated olive plants and the analysis of cellular interactions with the plant host. The generation of a draft genome of strain NCPPB 3335 and the closed sequence of its three native plasmids has allowed for functional and comparative genomic analyses for the identification of its pathogenicity gene complement. This includes 34 putative type III effector genes and genomic regions, shared with other pathogens of woody hosts, which encode metabolic pathways associated with the degradation of lignin-derived compounds. Now, the time is right to explore the molecular basis of the P. savastanoi pv. savastanoi–olive interaction and to obtain insights into why some pathovars like it necrotic and why some like it knot.
Pseudomonas syringae pv. savastanoi.
Kingdom Bacteria; Phylum Proteobacteria; Class Gammaproteobacteria; Family Pseudomonadaceae; Genus Pseudomonas; included in genomospecies 2 together with at least P. amygdali, P. ficuserectae, P. meliae and 16 other pathovars from the P. syringae complex (aesculi, ciccaronei, dendropanacis, eriobotryae, glycinea, hibisci, mellea, mori, myricae, phaseolicola, photiniae, sesami, tabaci, ulmi and certain strains of lachrymans and morsprunorum); when a formal proposal is made for the unification of these bacteria, the species name P. amygdali would take priority over P. savastanoi.
Gram-negative rods, 0.4–0.8 × 1.0–3.0 μm, aerobic. Motile by one to four polar flagella, rather slow growing, optimal temperatures for growth of 25–30 °C; oxidase negative, arginine dihydrolase negative; elicits the hypersensitive response on tobacco; most isolates are fluorescent and levan negative, although some isolates are nonfluorescent and levan positive.
P. savastanoi pv. savastanoi causes tumours in cultivated and wild olive and ash (Fraxinus excelsior). Although strains from olive have been reported to infect oleander (Nerium oleander), this is generally not the case; however, strains of P. savastanoi pv. nerii can infect olive. Pathovars fraxini and nerii are differentiated from pathovar savastanoi mostly in their host range, and were not formally recognized until 1996. Literature before about 1996 generally names strains of the three pathovars as P. syringae ssp. savastanoi or P. savastanoi ssp. savastanoi, contributing to confusion on the host range and biological properties.
Symptoms of infected trees include hyperplastic growths (tumorous galls or knots) on the stems and branches of the host plant and, occasionally, on leaves and fruits.
The pathogen can survive and multiply on aerial plant surfaces, as well as in knots, from where it can be dispersed by rain, wind, insects and human activities, entering the plant through wounds. Populations are very unevenly distributed in the plant, and suffer drastic fluctuations throughout the year, with maximum numbers of bacteria occurring during rainy and warm months. Populations of P. savastanoi pv. savastanoi are normally associated with nonpathogenic bacteria, both epiphytically and endophytically, and have been demonstrated to form mutualistic consortia with Erwinia toletana and Pantoea agglomerans, which could result in increased bacterial populations and disease symptoms.
Based on preventive measures, mostly sanitary and cultural practices. Integrated control programmes benefit from regular applications of copper formulations, which should be maintained for at least a few years for maximum benefit. Olive cultivars vary in their susceptibility to olive knot, but there are no known cultivars with full resistance to the pathogen.