Arabidopsis ocp3 mutant reveals a mechanism linking ABA and JA to pathogen-induced callose deposition.

In the present study, we evaluated the role of the defense-related gene OCP3 in callose deposition as a response to two necrotrophic fungal pathogens, Botrytis cinerea and Plectosphaerella cucumerina. ocp3 plants exhibited accelerated and intensified callose deposition in response to fungal infection associated with enhanced disease resistance to the two pathogens. A series of double mutant analyses showed potentiation of callose deposition and the heightened disease resistance phenotype in ocp3 plants required the plant hormone abscisic acid (ABA) and the PMR4 gene encoding a callose synthase. This finding was congruent with an observation that ocp3 plants exhibited increased ABA accumulation, and ABA was rapidly synthesized following fungal infection in wild-type plants. Furthermore, we determined that potentiation of callose deposition in ocp3 plants, including enhanced disease resistance, also required jasmonic acid (JA) recognition though a COI1 receptor, however JA was not required for basal callose deposition following fungal infection. In addition, potentiation of callose deposition in ocp3 plants appeared to follow a different mechanism than that proposed for callose β-amino-butyric acid (BABA)-induced resistance and priming, because ocp3 plants responded to BABA-induced priming for callose deposition and induced resistance of a magnitude similar to that observed in wild-type plants. Our results point to a model in which OCP3 represents a specific control point for callose deposition regulated by JA yet ultimately requiring ABA. These results provide new insights into the mechanism of callose deposition regulation in response to pathogen attack; however the complexities of the processes remain poorly understood.

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