Plant Innate Immunity Induced by Flagellin Suppresses the Hypersensitive Response in Non-Host Plants Elicited by Pseudomonas syringae pv. averrhoi

Abstract

A new pathogen, Pseudomonas syringae pv. averrhoi (Pav), which causes bacterial spot disease on carambola was identified in Taiwan in 1997. Many strains of this pathovar have been isolated from different locations and several varieties of hosts. Some of these strains, such as HL1, are nonmotile and elicit a strong hypersensitive response (HR) in nonhost tobacco leaves, while other strains, such as PA5, are motile and elicit a weak HR. Based on the image from a transmission electron microscope, the results showed that HL1 is flagellum-deficient and PA5 has normal flagella. Here we cloned and analyzed the fliC gene and glycosylation island from Pav HL1 and PA5. The amino acid sequences of FliC from HL1 and PA5 are identical to P. s. pvs. tabaci (Pta), glycinea and phaseolicola and share very high similarity with other pathovars of P. syringae . In contrast to the flagellin mutant PtaΔ fliC , PA5Δ fliC grows as well as wild type in the host plant, but it elicits stronger HR than wild type does in non-host plants. Furthermore, the purified Pav flagellin, but not the divergent flagellin from Agrobacterium tumefaciens , is able to impair the HR induced by PA5Δ fliC . PA5Δ fgt1 possessing nonglycosylated flagella behaved as its wild type in both bacterial growth in host and HR elicitation. Flagellin was infiltrated into tobacco leaves either simultaneously with flagellum-deficient HL1 or prior to the inoculation of wild type HL1, and both treatments impaired the HR induced by HL1. Moreover, the HR elicited by PA5 and PA5Δ fliC was enhanced by the addition of cycloheximide, suggesting that the flagellin is one of the PAMPs (pathogen-associated molecular patterns) contributed to induce the PAMP-triggered immunity (PTI). Taken together, the results shown in this study reveal that flagellin in Pav is capable of suppressing HR via PTI induction during an incompatible interaction.

Allelic variation in two distinct Pseudomonas syringae flagellin epitopes modulates the strength of plant immune responses but not bacterial motility

“…Intriguingly, although the various fliC alleles did not affect bacterial growth in the Pto DC3000∆ fliC background, they did lead to significant differences in the development of leaf necrosis (Fig. b,c), suggesting that in planta expression of FliC protein can interfere with symptom development, which was recently demonstrated (Wei et al ., ), in an allele‐dependent manner.…”

Identification of the Flagellin Glycosylation System in Burkholderia cenocepacia and the Contribution of Glycosylated Flagellin to Evasion of Human Innate Immune Responses

“…In contrast, lack of flagellin glycosylation does not affect the pathogenicity of starfruit pathogen P. syringae pv. averrhoi (66), whereas glycosylated flagellin of Acidovorax avenae elicits a strong immune response in cultured rice cells (67).…”

The pathogenicity factor HrpF interacts with HrpA and HrpG to modulate type III secretion system (T3SS) function and t3ss expression in Pseudomonas syringae pv. averrhoi

“…Tobacco leaves were infiltrated with bacteria at 1 × 10 8 CFU/mL or by serial titration for HR elicitation and ion leakage experiments, and the ionic conductivity was measured as an indicator of membrane damage during the onset of HR (Goodman, ) at 7 or 24 hpi by a conductivity meter (Radiometer analytical IONcheck 30, Lyon, France), as described by Wei et al . ().…”