Elisabeth Chevreau,4 and
1INRA, UMR217, LIPP, 16 rue Claude Bernard, 75231 Paris cedex 05, France; 2UPMC, Université Paris VI, UMR217, LIPP, 16 rue Claude Bernard, 75231 Paris cedex 05, France; 3AgroParisTech, UMR217, LIPP, 16 rue Claude Bernard, 75231 Paris cedex 05, France; 4UMR GenHort (INRA/ACO/UA), IFR149, 42 rue Georges Morel, 49071 Beaucouzé Cedex, France
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Accepted 7 January 2011.
Erwinia amylovora is responsible for fire blight of apple and pear trees. Its pathogenicity depends on a type III secretion system (T3SS) mediating the translocation of effectors into the plant cell. The DspA/E effector suppresses callose deposition on apple leaves. We found that E. amylovora and Pseudomonas syringae DC3000 tts mutants or peptide flg22 do not trigger callose deposition as strongly as the dspA/E mutant on apple leaves. This suggests that, on apple leaves, callose deposition is poorly elicited by pathogen-associated molecular patterns (PAMPs) such as flg22 or other PAMPs harbored by tts mutants and is mainly elicited by injected effectors or by the T3SS itself. Callose elicitation partly depends on HrpW because an hrpW-dspA/E mutant elicits lower callose deposition than a dspA/E mutant. Furthermore, an hrpN-dspA/E mutant does not trigger callose deposition, indicating that HrpN is required to trigger this plant defense reaction. We showed that HrpN plays a general role in the translocation process. Thus, the HrpN requirement for callose deposition may be explained by its role in translocation: HrpN could be involved in the translocation of other effectors inducing callose deposition. Furthermore, HrpN may also directly contribute to the elicitation process because we showed that purified HrpN induces callose deposition.
© 2011 The American Phytopathological Society