Suppression of Bean Defense Responses by Pseudomonas syringae.

Abstract

We have developed a model system to examine suppression of defense responses in bean by the compatible bacterium Pseudomonas syringae pv phaseolicola. Previously, we have shown that there is a general mechanism for the induction of the bean defense genes phenylalanine ammonia-lyase (PAL), chalcone synthase (CHS), chalcone isomerase (CHI), and chitinase (CHT) by incompatible, compatible, and nonpathogenic bacteria. Here, we show that bean plants infiltrated with isolates of P. s. phaseolicola failed to produce transcripts for PAL, CHS, or CHI up to 120 hr after infiltration and CHT transcript accumulation was significantly delayed when compared to the incompatible P. syringae strains. Infiltration of bean plants with 108 cells per mL of P. s. phaseolicola NPS3121 8 hr prior to infiltration with an equal concentration of incompatible P. s. pv tabaci Pt11528 significantly reduced the typical profile of defense transcript accumulation when compared to plants infiltrated with Pt11528 alone. A corresponding suppression of phytoalexin accumulation was also observed. NPS3121 also suppressed PAL, CHS, CHI, and CHT transcript accumulation and phytoalexin production induced by Escherichia coli DH5[alpha] or the elicitor glutathione. Heat-killed NPS3121 cells or cells treated with protein synthesis inhibitors lost the suppressor activity. Taken together, these experiments suggest that NPS3121 has an active mechanism to suppress the accumulation of defense transcripts and phytoalexin biosynthesis in bean.

Regulation of Cell Wall-Bound Invertase in Pepper Leaves by Xanthomonas campestris pv. vesicatoria Type Three Effectors

“…In a very early study, Jakobek and colleagues showed that Pseudomonas syringae pv. phaseolicola has evolved strategies to suppress the expression of defense genes such as phenylalanine ammonia-lyase, chalcone synthase, chalcone isomerase and the production of phytoalexins in bean [53]. In addition, microscopic studies revealed that localized cell wall modification and associated papillae formation were caused by Xcv hrp- mutants but not by the wild type strain [54].…”

Specific Threonine Phosphorylation of a Host Target by Two Unrelated Type III Effectors Activates a Host Innate Immune Receptor in Plants

“…Although they can trigger immune receptor function, pathogen-encoded effector proteins, including bacterial T3Es, have evolved to promote virulence (Jakobek et al, 1993). Once delivered, effector proteins are trafficked to various sub-cellular locations (Nomura et al, 2005).…”

The Pseudomonas syringae type III‐secreted protein HopPtoD2 possesses protein tyrosine phosphatase activity and suppresses programmed cell death in plants

“…The actions and targets of P. syringae effectors that promote pathogenicity remain elusive (Staskawicz et al ., 2001). However, there were early indications that P. syringae could suppress the induction of defence related transcripts during infections on host plants (Jakobek et al ., 1993). Recent studies show that several P. syringae effectors contain biologically active cysteine protease catalytic triads similar to those found in YopJ and YopT from animal pathogenic Yersinia species (Orth et al ., 2000; Shao et al ., 2002).…”