Global Genomic Analysis of Pseudomonas savastanoi pv. savastanoi Plasmids

Abstract

Pseudomonas savastanoi pv. savastanoi strains harbor native plasmids belonging to the pPT23A plasmid family (PFPs) which are detected in all pathovars of the related species Pseudomonas syringae examined and contribute to the ecological and pathogenic fitness of their host. However, there is a general lack of information about the gene content of P. savastanoi pv. savastanoi plasmids and their role in the interaction of this pathogen with olive plants. We designed a DNA macroarray containing 135 plasmid-borne P. syringae genes to conduct a global genetic analysis of 32 plasmids obtained from 10 P. savastanoi pv. savastanoi strains. Hybridization results revealed that the number of PFPs per strain varied from one to four. Additionally, most strains contained at least one plasmid (designated non-PFP) that did not hybridize to the repA gene of pPT23A. Only three PFPs contained genes involved in the biosynthesis of the virulence factor indole-3-acetic acid (iaaM, iaaH, and iaaL). In contrast, ptz, a gene involved in the biosynthesis of cytokinins, was found in five PFPs and one non-PFP. Genes encoding a type IV secretion system (T4SS), type IVA, were found in both PFPs and non-PFPs; however, type IVB genes were found only on PFPs. Nine plasmids encoded both T4SSs, whereas seven other plasmids carried none of these genes. Most PFPs and non-PFPs hybridized to at least one putative type III secretion system effector gene and to a variety of additional genes encoding known P. syringae virulence factors and one or more insertion sequence transposase genes. These results indicate that non-PFPs may contribute to the virulence and fitness of the P. savastanoi pv. savastanoi host. The overall gene content of P. savastanoi pv. savastanoi plasmids, with their repeated information, mosaic arrangement, and insertion sequences, suggests a possible role in adaptation to a changing environment.Pseudomonas syringae strains and related pathogens, such as Pseudomonas savastanoi strains, infect a wide range of herbaceous and woody plants causing diverse symptoms, such as leaf spots and blights, soft rots of fruits, wilts, overgrowths, scabs, and cankers (18,23). During the last decade, research on diseases caused by pseudomonads in herbaceous plants has progressed rapidly, and the application of molecular genetics and genome and plasmid sequencing (4,13,22,31,36,39) has provided new insights into determinants of pathogenicity and virulence. However, there is a general lack of knowledge on virulence and pathogenicity determinants specific for infection of woody plants. Clear examples of this are the pathogens P. savastanoi pathovars nerii, fraxini, and savastanoi, which cause knots and galls on members of the various genera of the family Oleaceae and oleander (14). Symptoms on infected trees include hyperplasia formation on stems and branches and occasionally on leaves and fruit (23). At present, the only P. savastanoi determinants known to be involved in knot development are production of the phytohormones indole-3-acetic acid (IAA) an...

Pseudomonas savastanoi pv. savastanoi Contains Two iaaL Paralogs, One of Which Exhibits a Variable Number of a Trinucleotide (TAC) Tandem Repeat

“…The IAA operon and the iaaL gene reside on a plasmid (pIAA) in P. savastanoi strains isolated from oleander galls (5,7,8,14); however, the direction of iaaL transcription has been determined to be opposite to IAA operon transcription (14). In contrast, most olive isolates have been reported to carry all three IAA genes on the chromosome (5,8,32). In a recent study, P. savastanoi pv.…”

“…Recently, a global genomic analysis of P. savastanoi pv. savastanoi plasmids allowed the identification of several putative virulence factors in the olive pathogen, including several type III secretion system protein effectors and a variety of genes encoding known Pseudomonas syringae virulence factors (32).…”

Epidemiology and Control of Plant Diseases Caused by Phytopathogenic Bacteria: The Case of Olive Knot Disease Caused by Pseudomonas savastanoi pv. savastanoi

“…Tumor development is dependent on bacterial production of phytohormones indoleacetic acid and cytokinins (Comai & Kosuge, 1980;Iacobellis et al, 1994;Rodríguez-Moreno et al, 2008;Smidt & Kosuge, 1978;Surico et al, 1985). Besides, recent results have revealed that Psv strains contain two copies of all the genes involved in indoleacetic acid synthesis (Matas et al, 2009;Pérez-Martínez et al, 2008). It has been reported that olive knots are also dependent on the hrp/hrc genes (Sisto et al, 2004), which encode the biosynthesis of a functional Type III Secretion System (TTSS).…”

“…It has been reported that olive knots are also dependent on the hrp/hrc genes (Sisto et al, 2004), which encode the biosynthesis of a functional Type III Secretion System (TTSS). Recently, remarkable progress has been made in research into several aspects of the host-pathogen interaction of the causal agent of olive knot (Pérez-Martínez et al, 2008;Matas, 2010;Pérez-Martínez et al, 2010). Several putative virulence factors in Psv have been identified, including TTSS protein effectors and a variety of genes encoding known P. syringae virulence determinants (Pérez-Martínez et al, 2008).…”

“…Recently, remarkable progress has been made in research into several aspects of the host-pathogen interaction of the causal agent of olive knot (Pérez-Martínez et al, 2008;Matas, 2010;Pérez-Martínez et al, 2010). Several putative virulence factors in Psv have been identified, including TTSS protein effectors and a variety of genes encoding known P. syringae virulence determinants (Pérez-Martínez et al, 2008). Analyses of TTSS protein effectors of Psv have recently shed light on the role of TTSS in pathogenicity and host range (Matas, 2010;Pérez-Martínez et al, 2010).…”