Pathogenicity of and plant immunity to soft rot pectobacteria

Abstract

Soft rot pectobacteria are broad host range enterobacterial pathogens that cause disease on a variety of plant species including the major crop potato. Pectobacteria are aggressive necrotrophs that harbor a large arsenal of plant cell wall-degrading enzymes as their primary virulence determinants. These enzymes together with additional virulence factors are employed to macerate the host tissue and promote host cell death to provide nutrients for the pathogens. In contrast to (hemi)biotrophs such as Pseudomonas, type III secretion systems (T3SS) and T3 effectors do not appear central to pathogenesis of pectobacteria. Indeed, recent genomic analysis of several Pectobacterium species including the emerging pathogen Pectobacterium wasabiae has shown that many strains lack the entire T3SS as well as the T3 effectors. Instead, this analysis has indicated the presence of novel virulence determinants. Resistance to broad host range pectobacteria is complex and does not appear to involve single resistance genes. Instead, activation of plant innate immunity systems including both SA (salicylic acid) and JA (jasmonic acid)/ET (ethylene)-mediated defenses appears to play a central role in attenuation of Pectobacterium virulence. These defenses are triggered by detection of pathogen-associated molecular patterns (PAMPs) or recognition of modified-self such as damage-associated molecular patterns (DAMPs) and result in enhancement of basal immunity (PAMP/DAMP-triggered immunity or pattern-triggered immunity, PTI). In particular plant cell wall fragments released by the action of the degradative enzymes secreted by pectobacteria are major players in enhanced immunity toward these pathogens. Most notably bacterial pectin-degrading enzymes release oligogalacturonide (OG) fragments recognized as DAMPs activating innate immune responses. Recent progress in understanding OG recognition and signaling allows novel genetic screens for OG-insensitive mutants and will provide new insights into plant defense strategies against necrotrophs such as pectobacteria.

Lactobacillus plantarum Exopolysaccharides Induce Resistance against Tomato Bacterial Spot

“…Though, in some cases, these hormones can occur and act synergistically, e.g., when present in low concentrations in healthy tissues, performing nonspecific immune response (Fu & Dong, 2013). For example, Davidsson et al (2013) described that the simultaneous activation of salicylate and jasmonate pathways appear to be crucial for the attenuation of virulence of Pectobacterium spp. In our study, considering that Xanthomonas is a hemibiotrophic pathogen, initially forming an association with living cells of the host, thereafter killing the plant cell to use the nutrients from this process (Chan & Goodwin, 1999), the use of an inducer capable of stimulate both pathways, as we observed for EPS, can be an attractive way for control this bacterial disease.…”

Intervention of Phytohormone Pathways by Pathogen Effectors

“…Thus, in addition to MAMPs, detection of damage-associated molecular patterns (e.g., elicitors released from host cells in response to cellular damage) probably plays a major role for cellular defense against necrotrophs (Mengiste, 2012). Interestingly, the type III secretion system, which is essential for effector delivery and the pathogenicity of hemibiotrophic bacteria such as Pseudomonas syringae (Büttner and He, 2009;Xin and He, 2013), does not seem to be required for the virulence of necrotrophic bacteria such as Pectobacteria that cause soft rot disease in many plant species (Davidsson et al, 2013).…”

Rapid Communication. Monitoring the occurrence of bacteria in stored cabbage heads

“…Th e bacteria mainly attack the fl eshy storage organs of their hosts (Bhat et al 2010). Soft rot pathogens are transmitted by contact with infected plants or by their persistence on postharvest residues (Davidsson et al 2013). Infection can also be spread by insects (Nadarasah et al 2011).…”