ABSTRACT
Bacterial speck caused by pathogen Pseudomonas syringae pv.
tomato (P. s. tomato) is a devastating disease of tomato plants. Here we
show that inhibition of Ep5C gene expression, which encodes a secreted
cationic peroxidase, is sufficient to confer resistance against P. s.
tomato. The inhibition of Ep5C protein accumulation in antisense tomato
plants established resistance that was not accompanied by the
preactivation of known defense pathways. Therefore, Ep5C inhibition
represent a novel form of disease resistance based on a loss of a gene
function which is required in the plant for successful infection by a
compatible bacterial pathogen. Ep5C expression is rapidly induced by
H2O2, a reactive oxygen intermediate normally generated during the
course of a plant-pathogen interaction. The mechanisms controlling
plant resistance to necrotrophic fungal pathogens are poorly understood.
To identify novel plant components operating in pathogen-induced
signalling cascades, we initiated a large-scale screen using Arabidopsis
plants carrying the ß-glucoronidase reporter gene under the control of
the H2O2 –responsive Ep5C promoter. Here we report the identification
and characterization of a mutant, ocp3 (for overexpressor of cationic
peroxidase 3) in which the reporter construct is constitutively expressed.
Healthy ocp3 show increased accumulation of H2O2 and express
constitutively the GST1 and PDF1.2 marker genes, but not the salicylic
acid (SA)-dependent pathogenesis-related PR-1 gene. Strikingly, the
ocp3 mutant shows enhanced resistance to the necrotrophic pathogens
Botrytis cinerea and Plectosphaerella cucumerina . Conversely,
resistance to virulent forms of the biotrophic oomycete
Hyaloperonospora parasitica and the bacterial pathogen Pseudomonas
syringae pv. tomato DC3000 remains unaffected in ocp3 plants when
compared to wild-type plants. Consistently whit this, ocp3 plants are not
affected in SA metabolism and express normal levels of PR genes after
pathogen attack. To analyze signal transduction pathways where ocp3
operates, epistasis analyses between ocp3 and pad4, nahG, npr1, ein2
jin1 or coi1 were performed. These studies revealed that the resistance
signalling to necrotrophic infection in ocp3 is fully dependent on the
appropriate perception of jasmonic acid (JA) through COI1 and
independent of the SA or ethylene (ET) signalling pathways.
The OCP3 gene encodes a homeodomain transcription factor that is
constitutively expressed in healthy plants but repressed in response to
infection by necrotrophic fungis. Together, these results suggest that
OCP3 is an important factor for the COI1-dependent resistance of plants
to infection by necrotrophic pathogens.