25 research outputs found
Selected reactive oxygen species and antioxidant enzymes in common bean after Pseudomonas syringae pv. phaseolicola and Botrytis cinerea infection
Phaseolus vulgaris cv. Korona plants were
inoculated with the bacteria Pseudomonas syringae pv.
phaseolicola (Psp), necrotrophic fungus Botrytis cinerea
(Bc) or with both pathogens sequentially. The aim of the
experiment was to determine how plants cope with multiple
infection with pathogens having different attack strategy.
Possible suppression of the non-specific infection with
the necrotrophic fungus Bc by earlier Psp inoculation was
examined. Concentration of reactive oxygen species
(ROS), such as superoxide anion (O2
-) and H2O2 and
activities of antioxidant enzymes such as superoxide dismutase
(SOD), catalase (CAT) and peroxidase (POD) were
determined 6, 12, 24 and 48 h after inoculation. The
measurements were done for ROS cytosolic fraction and
enzymatic cytosolic or apoplastic fraction. Infection with
Psp caused significant increase in ROS levels since the
beginning of experiment. Activity of the apoplastic
enzymes also increased remarkably at the beginning of
experiment in contrast to the cytosolic ones. Cytosolic
SOD and guaiacol peroxidase (GPOD) activities achieved
the maximum values 48 h after treatment. Additional forms
of the examined enzymes after specific Psp infection were
identified; however, they were not present after single Bc
inoculation. Subsequent Bc infection resulted only in
changes of H2O2 and SOD that occurred to be especially
important during plant–pathogen interaction. Cultivar Korona
of common bean is considered to be resistant to Psp and mobilises its system upon infection with these bacteria.
We put forward a hypothesis that the extent of defence
reaction was so great that subsequent infection did not
trigger significant additional response
Anti-Apoptotic Machinery Protects the Necrotrophic Fungus Botrytis cinerea from Host-Induced Apoptotic-Like Cell Death during Plant Infection
Necrotrophic fungi are unable to occupy living plant cells. How such pathogens survive first contact with living host tissue and initiate infection is therefore unclear. Here, we show that the necrotrophic grey mold fungus Botrytis cinerea undergoes massive apoptotic-like programmed cell death (PCD) following germination on the host plant. Manipulation of an anti-apoptotic gene BcBIR1 modified fungal response to PCD-inducing conditions. As a consequence, strains with reduced sensitivity to PCD were hyper virulent, while strains in which PCD was over-stimulated showed reduced pathogenicity. Similarly, reduced levels of PCD in the fungus were recorded following infection of Arabidopsis mutants that show enhanced susceptibility to B. cinerea. When considered together, these results suggest that Botrytis PCD machinery is targeted by plant defense molecules, and that the fungal anti-apoptotic machinery is essential for overcoming this host-induced PCD and hence, for establishment of infection. As such, fungal PCD machinery represents a novel target for fungicides and antifungal drugs