Format

Send to

Choose Destination
See comment in PubMed Commons below
Proc Natl Acad Sci U S A. 2005 Sep 6;102(36):12990-5. Epub 2005 Aug 25.

Flagellin induces innate immunity in nonhost interactions that is suppressed by Pseudomonas syringae effectors.

Author information

1
National Institute of Biological Sciences, Beijing 102206, China.

Abstract

Arabidopsis NONHOST1 (NHO1) is required for limiting the in planta growth of nonhost Pseudomonas bacteria but completely ineffective against the virulent bacterium Pseudomonas syringae pv. tomato DC3000. However, the molecular basis underlying this observation remains unknown. Here we show that NHO1 is transcriptionally activated by flagellin. The nonhost bacterium P. syringae pv. tabaci lacking flagellin is unable to induce NHO1, multiplies much better than does the wild-type bacterium, and causes disease symptoms on Arabidopsis. DC3000 also possesses flagellin that is potent in NHO1 induction, but this induction is rapidly suppressed by DC3000 in a type III secretion system-dependent manner. Direct expression of DC3000 effectors in protoplasts indicated that at least nine effectors, HopS1, HopAI1, HopAF1, HopT1-1, HopT1-2, HopAA1-1, HopF2, HopC1, and AvrPto, are capable of suppressing the flagellin-induced NHO1 expression. One of the effectors, HopAI1, is conserved in both animal and plant bacteria. When expressed in transgenic Arabidopsis plants, HopAI1 promotes growth of the nonpathogenic hrpL- mutant bacteria. In addition, the purified phytotoxin coronatine, a known virulence factor of P. syringae, suppresses the flagellin-induced NHO1 transcription. These results demonstrate that flagellin-induced defenses play an important role in nonhost resistance. A remarkable number of DC3000 virulence factors act in the plant cell by suppressing the species level defenses, and that contributes to the specialization of DC3000 on Arabidopsis.

PMID:
16123135
PMCID:
PMC1200263
DOI:
10.1073/pnas.0502425102
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center