Closing the Circle on the Discovery of Genes Encoding Hrp Regulon Members and Type III Secretion System Effectors in the Genomes of Three Model Pseudomonas syringae Strains

Abstract

Pseudomonas syringae strains translocate large and distinct collections of effector proteins into plant cells via the type III secretion system (T3SS). Mutations in T3SS-encoding hrp genes are unable to elicit the hypersensitive response or pathogenesis in nonhost and host plants, respectively. Mutations in individual effectors lack strong phenotypes, which has impeded their discovery. P. syringae effectors are designated Hop (Hrp outer protein) or Avr (avirulence) proteins. Some Hop proteins are considered to be extracellular T3SS helpers acting at the plant-bacterium interface. Identification of complete sets of effectors and related proteins has been enabled by the application of bioinformatic and high-throughput experimental techniques to the complete genome sequences of three model strains: P. syringae pv. tomato DC3000, P. syringae pv. phaseolicola 1448A, and P. syringae pv. syringae B728a. Several recent papers, including three in this issue of Molecular Plant-Microbe Interactions, address the effector inventories of these strains. These studies establish that active effector genes in P. syringae are expressed by the HrpL alternative sigma factor and can be predicted on the basis of cis Hrp promoter sequences and N-terminal amino-acid patterns. Among the three strains analyzed, P. syringae pv. tomato DC3000 has the largest effector inventory and P. syringae pv. syringae B728a has the smallest. Each strain has several effector genes that appear inactive. Only five of the 46 effector families that are represented in these three strains have an active member in all of the strains. Web-based community resources for managing and sharing growing information on these complex effector arsenals should help future efforts to understand how effectors promote P. syringae virulence.

Pathogen exploitation of an abscisic acid- and jasmonate-inducible MAPK phosphatase and its interception by Arabidopsis immunity

“…S3 C and D). COR and pathogen-induced ABA may compensate for the virulence of Pto DC3000 lacking a functional HopAI1 effector, which inactivates MAPKs (40,41).…”

Antagonistic action of harpin proteins: HrpWea from Erwinia amylovora suppresses HrpNea-induced cell death in Arabidopsis thaliana

“…Collectively, harpins could be involved in the release of nutrients from the host cells or they could facilitate the delivery of other bacterial proteins in the host cell (Holeva et al, 2004;Lindeberg et al, 2006). Harpins are not homologous in primary sequence but have common physiochemical characteristics: they are heat-stable, glycine rich, do not possess cysteine, and above all, trigger a hypersensitive response (HR) cell death, requiring an active plant metabolism, in non-host plants (Wei et al, 1992;He et al, 1993;He et al, 1994;Arlat et al, 1994).…”

A Subset of Ubiquitin-Conjugating Enzymes Is Essential for Plant Immunity

“…Of the various MAMPs associated with Pst, flagellin plays a major role in causing immunityassociated transcriptional changes in tomato (Rosli et al, 2013). To suppress host immune responses, Pst uses a type III secretion system to deliver during the infection process around 30 sequence-diverse effectors into the host cell (Chang et al, 2005;Lindeberg et al, 2006). Many of the effectors have been found to suppress PTI (Li et al, 2005;He et al, 2006;Zhang et al, 2007;Guo et al, 2009).…”