PecS Is a Global Regulator of the Symptomatic Phase in the Phytopathogenic Bacterium Erwinia chrysanthemi 3937

Abstract

Pathogenicity of the enterobacterium Erwinia chrysanthemi (Dickeya dadantii), the causative agent of soft-rot disease in many plants, is a complex process involving several factors whose production is subject to temporal regulation during infection. PecS is a transcriptional regulator that controls production of various virulence factors. Here, we used microarray analysis to define the PecS regulon and demonstrated that PecS notably regulates a wide range of genes that could be linked to pathogenicity and to a group of genes concerned with evading host defenses. Among the targets are the genes encoding plant cell wall-degrading enzymes and secretion systems and the genes involved in flagellar biosynthesis, biosurfactant production, and the oxidative stress response, as well as genes encoding toxin-like factors such as NipE and hemolysin-coregulated proteins. In vitro experiments demonstrated that PecS interacts with the regulatory regions of five new targets: an oxidative stress response gene (ahpC), a biosurfactant synthesis gene (rhlA), and genes encoding exported proteins related to other plant-associated bacterial proteins (nipE, virK, and avrL). The pecS mutant provokes symptoms more rapidly and with more efficiency than the wild-type strain, indicating that PecS plays a critical role in the switch from the asymptomatic phase to the symptomatic phase. Based on this, we propose that the temporal regulation of the different groups of genes required for the asymptomatic phase and the symptomatic phase is, in part, the result of a gradual modulation of PecS activity triggered during infection in response to changes in environmental conditions emerging from the interaction between both partners.

The Role of Secretion Systems and Small Molecules in Soft-Rot Enterobacteriaceae Pathogenicity

“…In Pectobacterium, the T1SS is upregulated by plant extracts and acylhomoserine lactone (AHL), and controlled by GacAS (97,98). In Dickeya, this system is controlled by PecS (59,104) cand GacAS (85). Metalloproteases may play two roles in virulence; they may attack plant cell wall proteins or may degrade enzymes secreted by the pathogen to affect their activity.…”

“…Metalloproteases secreted through the Prt T1SS contribute to SRE virulence (59). In Pectobacterium, the T1SS is upregulated by plant extracts and acylhomoserine lactone (AHL), and controlled by GacAS (97,98).…”

Inactivation of pecS restores the virulence of mutants devoid of osmoregulated periplasmic glucans in the phytopathogenic bacterium Dickeya dadantii

“…The sigma factor s 28 , encoded by the fliA gene, is required for expression of the flagella apparatus genes (including the fliC gene) encoding flagellin. Expression of the fliA gene is repressed by PecS and activated by FlhC 2 D 2 (Hommais et al, 2008) encoded by the master operon flhDC, requiring OPGs for expression (Bontemps-Gallo et al, 2013). Thus, restoration of motility may be one of the factors required for restoration of virulence in strains devoid of OPGs.…”

“…As was observed for the RcsCDB phosphorelay, several cellular functions are controlled by both this regulator and OPGs. Among the numerous genes of the PecS regulon are PCWDE genes, oxidative stress response genes such as the antioxidant blue pigment indigoidine, and motility genes (Hommais et al, 2008;Rouanet et al, 2004). No inducer is known to inactivate the PecS transcriptional repressor.…”

Streptomyces coelicolor Encodes a Urate-Responsive Transcriptional Regulator with Homology to PecS from Plant Pathogens

“…However, PecS from Agrobacterium tumefaciens (Rhizobium radiobacter) and MftR from Burkholderia thailandensis regulate expression of a predicted membrane transporter (8,9). R. radiobacter PecS and PecM (the membrane transporter) are homologous to proteins previously described in the plant pathogen Erwinia chrysanthemi (Dickeya dadantii) (3,(11)(12)(13). D. dadantii pecM, which is also regulated by PecS, was shown to encode a transporter involved in indigoidine excretion (11).…”