Cumplo un rol de Investigador Asociado.
Which are the molecular and physiological mechanisms involved in priming and defense activation in cherry plants upon Pss infection?
Are these mechanisms differentially activated between susceptible and resistance cherry varieties?
Do susceptible and resistance cherry varieties present a differential priming under different PRIs exposure?
Even more, the increasing of aridity and drought in the North of the country, the advancing desert toward the South and a
reduction in water resources in the central zone of Chile, are expected along the XXI century. In this scenario of climate change, other question arises: Which are the molecular and physiological mechanisms involved in priming and defense activation in cherry plants upon Pss infection combined with water deficit?
Through this proposal, we intend to answer to these questions, in order to establish the basis for optimize the control of the bacterial canker in cherry fruit tree, by strategies that provide for the use of resistance inductors.
We propose two hypotheses: a) Cherry cultivars with differential susceptibility to bacterial canker, caused by Pseudomonas syringae pv. syringae, present genetic differences in the molecular machinery of plant immunity; b) Pseudomonas syringae pv. syringae infection is enhanced by water restriction due to an alteration of the molecular machinery of plant immunity.
The aims of this proposal is to obtain a better understanding of the plant-pathogen molecular interactions of sweet cherry bacterial canker in relationship with water deficit, using mainly omics strategies.