THE HRPN PROTEIN OF THE PLANT PATHOGEN ERWINIA AMYLOVORA, WHICH PARTICIPATES TO TYPE III SECRETION TRANSLOCATION, TRIGGERS CALLOSE DEPOSITION ON APPLE LEAVES

Pathogenicity of the plant pathogen Erwinia amylovora relies on a functional type III secretion system (T3SS) which allows translocation of a number of effectors into the plant cell.
Injected effectors manipulate plant cell metabolism to allow successful bacterial colonization.
Among those, the DspA/E effector efficiently suppresses plant basal defense such as callose deposition.
Surprisingly, an E. amylovora tts mutant is unable to trigger callose deposition indicating that this plant basal defense response is triggered either by another type III effector (T3E) or by the T3SS apparatus itself.
Genetic analysis indicates that the T3E HrpN, which is involved in DspA/E translocation, is required to trigger callose deposition.
The purified HrpN protein induces a faint callose accumulation.
HrpN could be injected into the plant cell as shown by analysis of translocation of HrpN1-200::CyaA fusion.
Translocation of HrpN1-200-CyaA or HrpW1-200-CyaA fusions is impaired in a hrpN mutant background indicating that the involvement of HrpN in the translocation process is not restricted to DspA/E translocation.

XII International Workshop on Fire Blight

T. Boureau, S. Siamer, S. Gaubert, C. Perino, A. Degrave, M. Fagard, M.-A. Barny

Erwinia amylovora, translocation, HrpN, callose

https://doi.org/10.17660/ActaHortic.2011.896.24