Characterization of a Ralstonia solanacearum Operon Required for Polygalacturonate Degradation and Uptake of Galacturonic Acid

Abstract

The bacterial wilt pathogen Ralstonia solanacearum produces three extracellular polygalacturonases (PGs): PehA, PehB, and PehC. All three PGs hydrolyze pectin's polygalacturonic acid backbone, but each releases different reaction products. PehA and PehB contribute significantly to pathogen virulence, probably by facilitating root invasion and colonization. To determine the collective contribution of PGs to virulence and saprophytic survival, we cloned, characterized, and mutated the R. solanacearum pehC gene, which encodes a distinctive monogalacturonate-releasing exo-PG. The virulence of a pehC mutant on tomato was indistinguishable from that of its wild-type parent; thus, this exo-PG alone does not contribute significantly to wilt pathogenesis. Unexpectedly, a completely PG-deficient triple pehA/B/C mutant was slightly more virulent than a pehA/B mutant. PehC may degrade galacturonide elicitors of host defense, thereby protecting the pathogen from plant antimicrobial responses. A galacturonate transporter gene, exuT, is immediately downstream of pehC and the two genes are co-transcribed. It has been hypothesized that galacturonic acid released by PGs from plant cell walls nourishes bacteria during pathogenesis. To separate the pectolytic and nutrient-generating roles of the PGs, we made an exuT mutant, which still produces all three isozymes of PG but cannot uptake PG degradation products. This exuT mutant had wild-type virulence on tomato, demonstrating that metabolism of galacturonic acid does not contribute significantly to bacterial success inside the plant.

Ralstonia solanacearum Needs Flp Pili for Virulence on Potato

“…R. solanacearum possesses various virulence factors that act quantitatively to cause disease. In addition to extracellular polysaccharide I (Denny and Baek 1991;McGarvey et al 1999), cell wall-degrading enzymes (Gonzalez and Allen 2003;Liu et al 2005), and type III-secreted effectors (Cunnac et al 2004), flagellar-driven swimming and pilus-driven twitching motility are also necessary for virulence (Tans-Kersten et al 2001;Liu et al 2001). All of these virulence factors are controlled by a complex regulatory signal transduction pathway (Schell 2000;Hikichi et al 2007) that responds to both environmental signals and quorum sensing (Brito et al 1999).…”

A selC -Associated Genomic Island of the Extraintestinal Avian Pathogenic Escherichia coli Strain BEN2908 Is Involved in Carbohydrate Uptake and Virulence

“…The aec-36 product shares similarity (62% similar amino acids) with ExuT of E. coli K-12 MG1655, a major facilitator superfamily transporter of the anion:cation symporter family 14 (48). ExuT is involved in galacturonate uptake in E. coli and in other bacteria such as Erwinia chrysanthemi and Ralstonia solanacearum (26,45,63). Aec-36, like ExuT, is predicted to be an integral membrane protein.…”

Dissection of Bacterial Wilt on Medicago truncatula Revealed Two Type III Secretion System Effectors Acting on Root Infection Process and Disease Development

“…In addition to EPS I, R. solanacearum secretes plant cell wall-degrading enzymes through the type II secretion system (T2SS). Pectinolytic enzymes fragment pectin into oligomers, which act as substrates for the bacterial growth (Tans-Kersten et al, 1998); the breakdown of pectin enhances virulence by facilitating movements through pectin-rich regions such as vascular bundles (Gonzalez and Allen, 2003). Cellulytic enzymes also facilitate invasion of roots and/or penetration of xylem vessels by degrading cellulosic glucans in the cell wall (Liu et al, 2005).…”