INVESTIGADORES
DIAZ RICCI Juan Carlos
congresos y reuniones científicas
Título:
Molecular characterization of AsES-triggered defense response against Botrytis cinerea in Arabidopsis thaliana
Autor/es:
HAEL-CONRAD, V.; DÍAZ RICCI JC.; MÉTRAUX, JP.; SERRANO, M
Lugar:
Foz do Iguazú
Reunión:
Congreso; 11th International Congress of Plant Molecular Biology Iguazú Falls (Argentina - Brazil). 25-30 October.; 2015
Institución organizadora:
International Plant Molecular Biology
Resumen:
AsES is a novelextracellular elicitor protein produced by and purified from an avirulentisolate of the strawberry opportunist fungus pathogen Acremonium strictum.Foliar spray with AsES provided a total systemic protection against theanthracnose disease agent. Botrytis cinerea is an important fungalpathogen that causes pre- and post-harvest losses, for this reason newbio-technologies should emerge in the attempt to control it. AsES, undernational and international patent, could be an option. To help elucidating themode of action of this elicitor we determined its activity in thewell-described plant-pathogen interaction system Arabidopsis thaliana-B.cinerea. We show that when A. thaliana plants were treated with 60nM of AsES 48 hours prior to infection, symptoms (measured as lesion size) werereduced by approximately 50% with respect to mock-treated plants when evaluated48 hours post infection. It is noteworthy that fungus growth was not inhibitedin presence of AsES neither in vitro nor in planta. We furtherdemonstrate that the protection to B. cinerea after AsES treatment wasthe result of induced plant defenses, since AsES affects differentially mutantsimpaired in the response to salicylic acid (SA), jasmonic acid (JA) andethylene (ET). qRT-PCR analyzes suggest that SA acts at the beginning of theinteraction, and when becomes ineffective, JA pathway, and probably ET,emerges in the attempt to restrict the infection. These promising results makeit possible to exploit the full potential of A. thaliana and itsgenetics to understand the molecular mechanisms triggered by AsES against B.cinerea.