Host Range Determinants of Pseudomonas savastanoi Pathovars of Woody Hosts Revealed by Comparative Genomics and Cross-Pathogenicity Tests

Abstract

system proteins, the phytotoxine phevamine A, a siderophore, c-di-GMP-related proteins, methyl chemotaxis proteins, and a broad collection of transcriptional regulators and transporters of eight different superfamilies. Our combination of pathogenicity analyses and genomics tools allowed us to correctly assign strains to pathovars and to propose a repertoire of host range-related genes in the P. syringae complex.

Pseudomonas savastanoi pv. mandevillae pv. nov., a Clonal Pathogen Causing an Emerging, Devastating Disease of the Ornamental Plant Mandevilla spp.

“…This perceived homogeneity contrasts with the variability previously observed for the four P. savastanoi pathovars from woody hosts: although they correspond to well-defined genetic lineages, they show a degree of variability in intrapathovar virulence gene repertoires, plasmid profile, virulence, arbitrarily-primed PCR, real-time PCR and high-resolution melting analysis (Pérez-Martínez et al 2008;Tegli et al 2010;Gori et al 2012;Moretti et al 2017;Moreno-Pérez et al 2020), among other characteristics. Nevertheless, and because dipladenias are reproduced vegetatively, we cannot discount the possibility that the small number of dipladenia isolates characterized so far belong to a particular clonal lineage that was dispersed with plant material, rather than being representative of their variability as a whole.…”

Genes ptz and idi, Coding for Cytokinin Biosynthesis Enzymes, Are Essential for Tumorigenesis and In Planta Growth by P. syringae pv. savastanoi NCPPB 3335

“…Furthermore, P. savastanoi strains isolated from Myrtus lacking gene ptz and producing undetectable amounts of CKs successfully invaded the host tissues and moved systemically, apparently unaffected by host defenses, such as the synthesis of tannins and the lignin deposits around the inoculation sites ( Schiff et al., 2019 ). Thus, the role of CKs in the ability of P. savastanoi to multiply and survive in plant tissues might be strain- and/or host-dependent and could be influenced by other virulence factors varying among strains ( Moreno-Pérez et al., 2020 ). An attractive possibility is that genes involved in CKs biosynthesis in Psv, including idi , might be regulating the expression of other virulence genes, as has been shown for certain Psv virulence genes upon exogenous IAA treatment ( Aragón et al., 2014 ).…”

“…We have to stress that there are strains of diverse pathovars of the P. syringae complex that contain genes iaaMH , ptz and/or produce high amounts of IAA or CKs, but that do not induce tumors in their common plant hosts ( Glickmann et al., 1998 ; Cinelli et al., 2014 ). These strains, therefore, might lack some of the numerous genes needed for tumorigenesis (such as genes for type III secretion system effectors, for Na + /Ca 2+ exchange or for the metabolism of phenolics) or to not produce an adequate balance of phytohormones ( Caballo-Ponce et al., 2017a ; Moretti et al., 2019 ; Moreno-Pérez et al., 2020 ).…”

“…photiniae deposited in the NCBI, even though this pathovar produces leaf spots ( Goto, 1983 ) and is not reported to induce tumors. These discrepancies might be due to one or more of these reasons: 1) that there is variability in the distribution of these genes among all the tumorigenic bacteria, being absent in a small proportion of strains, as occurs in pathovars nerii and savastanoi ( Cinelli et al., 2014 ; Moreno-Pérez et al., 2020 ); in particular, the three genomes currently available for P. amygdali are for strain NCPPB 2607, which was shown to produce negligible amounts of CKs in culture ( Iacobellis et al., 1990 ) and that might therefore naturally lack ptz ; 2) that the genes remained in the non-assembled reads, which is possible given that these genes are often surrounded by repeated sequences and their exclusion from the assembly has already been reported for other draft genomes ( Moreno-Pérez et al., 2020 ); 3) that the sequenced strain has been misidentified, which is somewhat common among sequenced strains of the P. syringae complex ( Gomila et al., 2017 ) and likely has occurred with the P. tremae strain, which belongs to PG3 and should have clustered close to the other strains ( Gardan et al., 1999 ; Gomila et al., 2017 ); 4) that CKs perform diverse functions contributing to bacterial fitness and not necessarily related to the elicitation of tumors ( Spallek et al., 2018 ), perhaps explaining the presence of genes ptz and idi in many non-tumorigenic bacteria ( Supplementary Figure S2 ); and 5) that the contribution of ptz and idi to tumor development could be fulfilled by the activity of other gene(s) in certain bacterial phytopathogens.…”

“…Evidence for the independent loss of ptz and/or idi comes from their patchy distribution among diverse pathovars, including P. syringae pvs. nerii and savastanoi ( Iacobellis et al., 1998 ; Cinelli et al., 2014 ; Moreno-Pérez et al., 2020 ). The DNA fragment containing the linked ptz and idi is currently present in, at least, strains of P. syringae pv.…”