The species P. savastanoi is a member of the Pseudomonas syringae complex and includes four pathovars causing knots or excrescences in woody hosts. These are P. savastanoi pv. savastanoi (Psv), pv. nerii (Psn), pv. fraxini (Psf) and pv. retacarpa (Psr), comprising isolates from olive (Olea europaea), oleander (Nerium oleander), ash (Fraxinus excelsior) and Spanish broom (Retama sphaerocarpa), respectively (Gardan et al., 1992a; Bull et al., 2010). Additionally, DNA-DNA hybridization studies formally classified the causative agents of bacterial brown spot of soybeans and halo blight disease of beans into the species P. savastanoi (i.e., P. savastanoi pv. glycinea and P. savastanoi pv. phaseolicola, respectively) (Gardan et al., 1992a). However, it is now clear that P. savastanoi belongs to a larger phylogenetic group, which should be called P. amygdali when elevated to the species rank, comprising 25 pathovars and four additional Pseudomonas species, and that pathovars Psv, Psn, Psf, and Psr are phylogenetically closer to other pathovars infecting trees than to pv. glycinea and pv. phaseolicola (Gardan et al., 1999; Nowell et al., 2014; Baltrus et al., 2017). Remarkably, this phylogenetic group ... is the only one from the P. syringae complex containing bacteria causing tumors in woody hosts, namely Psv, Psn, Psr, P. meliae, P. tremae and P. syringae pathovars cerasicola, daphniphylli, dendropanacis, myricae, and rhaphiolepidis (Lamichhane et al., 2014).

While artificial infections with Psv, Psn, and Psr strains cause knots, Psf isolates induce cankers accompanied by wart-like excrescences in both ash and olive. Psv strains induce knot formation in olive and ash but not in oleander, whereas Psn strains can infect all three hosts. In contrast, the host range of Psr isolates is restricted to Spanish broom (Janse, 1982; Iacobellis et al., 1998; Ramos et al., 2012). Knot formation by P. savastanoi has also been described in several other hosts, including jasmine (Gardan et al., 1992b), privet (Gardan et al., 1992b), mock privet (Gardan et al., 1992b), forsythia (Bradbury, 1986), buckthorn (Temsah et al., 2007a), fontanesia (Mirik et al., 2011), pomegranate (Bozkurt et al., 2014), myrtle (Goumas et al., 2000; Temsah et al., 2007b; Cinelli et al., 2014) and dipladenia (Putnam et al., 2010; Eltlbany et al., 2012; Pirc et al., 2014; Caballo-Ponce and Ramos, 2016). Although these P. savastanoi hosts are classified in several plant families, over 50% of them belong to the Oleaceae family. Lack of accurate cross-pathogenicity tests for most of these strains preclude their classification within any of the four well-established P. savastanoi pathovars causing diseases in woody hosts

Knot induction by P. savastanoi in woody hosts is characterized by the formation of hypertrophic and hyperplastic overgrowths on the trunks, stems and branches; however, this symptomatology is rarely observed on the leaves and fruits ...

Psv lives epiphytically on the surface of leaves and stems and reaches the highest cell populations in warm, rainy months (Ercolani, 1978; Quesada et al., 2007). However, these bacteria are able to switch from an epiphytic to an endopathogenic lifestyle after penetration into plant tissues through wounds generated by climatic conditions or agricultural practices. As a pathogen, P. savastanoi induces hypertrophy and hyperplasia of plant tissues, generally leading to the generation of knots, an exception occurs in ash infections by Psf strains, which induce the formation of small protuberances (i.e., cankers or excrescences). A histological examination of the knots induced by P. savastanoi infections in different hosts reveals strong similarities among olive (Surico, 1977; Temsah et al., 2008; Rodríguez-Moreno et al., 2009), oleander (Wilson, 1965; Temsah et al., 2010), buckthorn (Temsah et al., 2007a), and myrtle (Temsah et al., 2007b).

During the early stages of an infection, bacteria are localized in the intercellular spaces of the cortical parenchyma and in the vascular tissues damaged by the wound, where bacterial pectolytic and hemicellulolytic enzymatic activities cause cell wall degradation of adjacent plant cells, resulting in the plasmolysis of host cells and the generation of internal cavities. Bacterial cells colonize these cavities and multiply, while lignin deposits appear as a defense mechanism in the cell walls of plasmolyzed cells. Adjacent to them, the parenchymal cells of the cortex and vascular system show hypertrophic and hyperplastic activities initiated by coenocytic divisions, resulting in multinucleated cells. Additionally, in oleander infections, tyloses develop in the xylem vessels, hampering bacterial movement

Subsequent enlargement of the internal cavities and hyperplastic tissues result in the formation of an incipient multilobed knot. Additionally, the parenchyma cells adjacent to the bacterial cavities have been shown to differentiate into xylem elements, which are connected with the primary vascular cylinder in olive infections (Rodríguez-Moreno et al., 2009). Taking into account that neovascularization is essential for the growth of plant and animal tumors (Ullrich and Aloni, 2000), the existence of this network of vascular tissues might facilitate the supply of water and nutrients necessary for the knots to reach their final size. The existence of a vascular connection between plant galls and the vascular system of the host plant has also been reported in A. tumefaciens-induced crown galls (Aloni et al., 1995).

During later stages of knot development, the hypertrophied tissue is composed of groups of disorganized cells, except for those being part of the xylem vessels generated during the infection. Psv cells have been visualized inside olive knots forming small groups and microcolonies, which remain attached to the surface of hypertrophied host cells and to each other by an extracellular matrix ...

In addition, the pressure generated by continuous hyperplastic activity causes the appearance of fissures in the knot tissues. The enlargement of these fissures produces breakage of the periderm and exposure of the internal cavities filled with bacteria to the environment, which contributes to pathogen spread.