73 research outputs found
Alcohol dehydrogenase 1 of barley modulates susceptibility to the parasitic fungus Blumeria graminis f.sp. hordei
Plant primary energy metabolism is profoundly reorganized under biotic stress conditions and there is increasing evidence for a role for the fermentative pathway in biotic interactions. However, the mechanisms regulating metabolic reprogramming are not well understood despite its critical function in the biotic stress response. Here the function of alcohol dehydrogenase (ADH) in the interaction of barley with the parasitic fungus Blumeria graminis f.sp. hordei (Bgh) is addressed. Challenge of susceptible barley leaves with Bgh resulted in transcriptional activation of HvADH1 and an induction of ADH enzyme activity starting 24 h after infection and reaching a clear-cut effect 4 d after infection. This increase in ADH enzyme activity was not observed in the resistant near-isogenic mlo5 line. Moreover, an induction of ADH enzyme activity by Bgh was enhanced in the presence of sucrose in hydroponically grown seedlings. Transient knock-down or overexpression of HvADH1 in barley epidermal cells mediated a decrease or increase in the penetration success of Bgh, respectively. Inhibition of ADH activity by pyrazole resulted in a delay in symptoms. The pyrazole effect could be overcome by adding glucose to the incubation medium, pinpointing a nutritional effect of ADH in the barley–Bgh interaction. Taken together, misexpression of pathogen-inducible HvADH1 or variation of ADH activity modulates the pathogen response of barley to the biotrophic fungal parasite Bgh. In this way, ADH knock-down/inhibition results in reduced fungal success. The possibility is discussed that ADH activity supports biotrophy by maintaining glycolytic metabolism in pathogen-stressed barley
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
The Deubiquitinating Enzyme AMSH1 and the ESCRT-III Subunit VPS2.1 Are Required for Autophagic Degradation in Arabidopsis
A Bacterial Acetyltransferase Destroys Plant Microtubule Networks and Blocks Secretion
The eukaryotic cytoskeleton is essential for structural support and intracellular transport, and is therefore a common target of animal pathogens. However, no phytopathogenic effector has yet been demonstrated to specifically target the plant cytoskeleton. Here we show that the Pseudomonas syringae type III secreted effector HopZ1a interacts with tubulin and polymerized microtubules. We demonstrate that HopZ1a is an acetyltransferase activated by the eukaryotic co-factor phytic acid. Activated HopZ1a acetylates itself and tubulin. The conserved autoacetylation site of the YopJ / HopZ superfamily, K289, plays a critical role in both the avirulence and virulence function of HopZ1a. Furthermore, HopZ1a requires its acetyltransferase activity to cause a dramatic decrease in Arabidopsis thaliana microtubule networks, disrupt the plant secretory pathway and suppress cell wall-mediated defense. Together, this study supports the hypothesis that HopZ1a promotes virulence through cytoskeletal and secretory disruption
Yeast Bax Inhibitor, Bxi1p, Is an ER-Localized Protein That Links the Unfolded Protein Response and Programmed Cell Death in Saccharomyces cerevisiae
Bax inhibitor-1 (BI-1) is an anti-apoptotic gene whose expression is upregulated in a wide range of human cancers. Studies in both mammalian and plant cells suggest that the BI-1 protein resides in the endoplasmic reticulum and is involved in the unfolded protein response (UPR) that is triggered by ER stress. It is thought to act via a mechanism involving altered calcium dynamics. In this paper, we provide evidence that the Saccharomyces cerevisiae protein encoded by the open reading frame, YNL305C, is a bona fide homolog for BI-1. First, we confirm that yeast cells from two different strain backgrounds lacking YNL305C, which we have renamed BXI1, are more sensitive to heat-shock induced cell death than wildtype controls even though they have indistinguishable growth rates at 30°C. They are also more susceptible both to ethanol-induced and to glucose-induced programmed cell death. Significantly, we show that Bxi1p-GFP colocalizes with the ER localized protein Sec63p-RFP. We have also discovered that Δbxi1 cells are not only more sensitive to drugs that induce ER stress, but also have a decreased unfolded protein response as measured with a UPRE-lacZ reporter. Finally, we have discovered that deleting BXI1 diminishes the calcium signaling response in response to the accumulation of unfolded proteins in the ER as measured by a calcineurin-dependent CDRE-lacZ reporter. In toto, our data suggests that the Bxi1p, like its metazoan homologs, is an ER-localized protein that links the unfolded protein response and programmed cell death
The role of seven-transmembrane domain MLO proteins, heterotrimeric G-proteins, and monomeric RAC/ROPs in plant defense
Mechanistic and genetic overlap of barley host and non-host resistance to Blumeria graminis
Non-host resistance of barley to Blumeria graminis f.sp. tritici (Bgt), an inappropriate forma specialis of the grass powdery mildew fungus, is associated with formation of cell wall appositions (papillae) at sites of attempted fungal penetration and a hypersensitive cell death reaction (HR) of single attacked cells. Penetration resistance and HR are also typical features of race-non-specific and race-specific resistance of barley to the appropriate Blumeria graminis f.sp. hordei (Bgh), raising the question of whether genotypic differences in the cellular response of barley to Bgt are delectable. First, we analysed fungal penetration frequencies and HR in different barley accessions known to show altered non-host resistance. In genotypes with limited resistance to inappropriate cereal rust fungi, we concomitantly detected low penetration resistance to Bgt and significant differences of HR rates during attack from Bgt. Second, we tested barley mutants known to show altered host responses to Bgh. The rar1-mutation that suppresses many types of race-cultivar-specific resistances did not influence the non-host response of the Bgt-isolate used in this study. However, mutants of Ror1 and Ror2, two genes required for full race non-specific penetration resistance of mlo-barley to barley powdery mildew fungus, exhibited altered defence response to Bgt, including higher frequencies of fungal penetration. On these mutants, growth of the inappropriate fungus was arrested subsequent to penetration by HR. Together, the data show that barley defence response to the wheat powdery mildew fungus is determined by similar factors as race-specific and race-non-specific resistance to appropriate Bgh
Alternative Cell Death Mechanisms Determine Epidermal Resistance in Incompatible Barley-Ustilago Interactions
Respiratory Burst Oxidase Homologue A of barley contributes to penetration by the powdery mildew fungus Blumeria graminis f. sp. hordei
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