Link to home

DspA/E, a Type III Effector Essential for Erwinia amylovora Pathogenicity and Growth In Planta, Induces Cell Death in Host Apple and Nonhost Tobacco Plants

January 2006 , Volume 19 , Number  1
Pages  16 - 24

Tristan Boureau , 1 Hayat ElMaarouf-Bouteau , 1 Amélie Garnier , 1 Marie-Noëlle Brisset , 2 Claude Perino , 1 Igor Pucheu , 1 and Marie-Anne Barny 1

1Laboratoire des Interactions Plantes-Pathogènes, UMR217 INRA/INA-PG/Université Paris VI, 16 rue Claude Bernard, 75231 Paris Cedex 05, France; 2UMR PaVé INRA/INH/Université d'Angers, Centre INRA d'Angers, 42 rue Georges Morel, BP 60057-49071 Beaucouzé Cedex, France

Go to article:
Accepted 2 September 2005.

Erwinia amylovora is responsible for fire blight, a necrotic disease of apples and pears. E. amylovora relies on a type III secretion system (TTSS) to induce disease on hosts and hypersensitive response (HR) on nonhost plants. The DspA/E protein is essential for E. amylovora pathogenicity and is secreted via the TTSS in vitro. DspA/E belongs to a type III effector family that is conserved in several phytopathogenic bacteria. In E. amylovora, DspA/E has been implicated in the generation of an oxidative stress during disease and the suppression of callose deposition. We investigated the fate of DspA/E in planta. DspA/E delivered artificially to apple or tobacco cells by agroinfection induced necrotic symptoms, indicating that DspA/E was probably injected via the TTSS. We confirmed that DspA/E acts as a major cell-death inducer during disease and HR, because the dspA/E mutant is severely impaired in its ability to induce electrolyte leakage in apple and tobacco leaves. Expression of the defense marker gene PR1 was delayed when dspA/E was transiently expressed in tobacco, suggesting that DspA/E-mediated necrosis may be associated with an alteration of defense responses.

© 2006 The American Phytopathological Society