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|標題:||Plant Innate Immunity Induced by Flagellin Suppresses the Hypersensitive Response in Non-Host Plants Elicited by Pseudomonas syringae pv. averrhoi||作者:||Wei, Chia-Fong
|Project:||Plos one, Volume 7, Issue 7||摘要:||
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 PtaDfliC, PA5DfliC 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 PA5DfliC. PA5Dfgt1 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 PA5DfliC 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.
|Appears in Collections:||生物科技學研究所|
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