Search

Victorin, the host-selective toxin produced by the fungus Cochliobolus victoriae, induces programmed cell death ( PCD) in victorin-sensitive oat lines with characteristic features of animal apoptosis, such as mitochondrial permeability transition, chromatin condensation, nuclear DNA laddering and rRNA/ mRNA degradation. In this study, we characterized a calcium-binding protein, namely AsALG-2, which might have a role in the victorin-induced PCD. AsALG-2 is homologous to the Apoptosis- Linked Gene ALG-2 identified in mammalian cells. Northern blot analysis revealed that the accumulation of AsALG-2 transcripts increased during victorin-induced PCD, but not during necrotic cell death. Salicylic acid, chitosan and chitin strongly activated the expression of general defence response genes, such as PR-10; however, neither induced cell death nor the accumulation of AsALG-2 mRNA. Pharmacological studies indicated that victorin-induced DNA laddering and AsALG-2 expression were regulated through similar pathways. The calcium channel blocker, nifedipine, moderately inhibited the accumulation of AsALG-2 mRNA during cell death. Trifluoperazine (calmodulin antagonist) and K252a (serine-threonine kinase inhibitor) reduced the victorin-induced phytoalexin accumulation, but did not prevent the victorin-induced DNA laddering or accumulation of AsALG-2 mRNA. Taken together, our investigations suggest that there is a calcium-mediated signalling pathway in animal and plant PCD in common. [ABSTRACT FROM AUTHOR]

Here we report that rRNA and mRNA are specifically degraded in oat ( Avena sativa L.) cells during apoptotic cell death induced by victorin, a host-selective toxin produced by Cochliobolus victoriae. Northern analysis indicated that rRNA species from the cytosol, mitochondria and chloroplasts were all degraded via specific degradation intermediates during victorin-induced apoptotic cell death but, in contrast, they were randomly digested in necrotic cell death induced by 30 mm CuSO4 and heat shock. This indicates that specific rRNA cleavage could be controlled by an intrinsic program. We also observed specific cleavage of mRNA of housekeeping genes such as actin and ubiquitin during victorin-induced cell death. Interestingly, no victorin-induced mRNA degradation was detected with stress-responding genes such as PR-1, PR-10 and GPx throughout the experimental period. The RNA degradation mostly, but not always, occurred in parallel with DNA laddering, but pharmacological studies indicated that these processes are regulated by different signaling pathways with some overlapping upstream signals. [ABSTRACT FROM AUTHOR]

Reactive oxygen species (ROS) are thought to be involved in various forms of programmed cell death (PCD) in animal and plant cells. PCD, along with the production of ROS, occurs during plant–pathogen interactions. Here we show that victorin, a host-specific toxin produced by Cochliobolus victoriae, which causes victoria blight of oats, induces two phases of intracellular ROS production in victorin-sensitive oat mesophyll cells. The initial production of ROS is restricted at mitochondria and not accompanied with cellular oxidative damage. Later production of ROS is dispersed into cells concomitant with lipid peroxidation, chloroplast dysfunction, and cell death. Superoxide dismutase can clearly suppress the initial ROS production and delay the progression of cell death. These data indicate that the initial ROS production may be involved in the cell death induction process, and the later ROS production may play important roles in events leading to cellular disruption. [ABSTRACT FROM AUTHOR]

We examined whether PWT4, an avirulence gene of Avena isolates of Magnaporthe oryzae toward wheat, corresponded to Rwt4, a resistance gene identified in wheat cultivar Norin 4, in a one-to-one manner. Twelve wheat cultivars were inoculated with 65X1, an F1 culture with PWT4 derived from a cross between an Avena isolate (Br58) and a Triticum isolate (Br48). Three wheat cultivars (Norin 26, Shin-chunaga, Cheyenne) were resistant and therefore selected as possible carriers of Rwt4. The three cultivars were then inoculated with a population derived from a backcross of 61M2 carrying PWT4 with Br48 carrying pwt4. Segregation analyses revealed that PWT4 operates against the three cultivars. If PWT4 corresponds to Rwt4 in a one-to-one manner, all three cultivars should carry Rwt4. To test if this is the case, the three cultivars were crossed with Chinese Spring (a noncarrier of Rwt4) and Norin 4. When F2 seedlings from Chinese Spring × Norin 26, Chinese Spring × Shin-chunaga, and Chinese Spring × Cheyenne were inoculated with 61M2, resistant and susceptible seedlings segregated in a 3 : 1 ratio. On the other hand, crosses between the three cultivars and Norin 4 yielded no susceptible F2 seedlings. These results indicate that all three cultivars carry Rwt4. Considering all results, we concluded that PWT4 corresponds to Rwt4 in a one-to-one manner. An inoculation test with Chinese Spring–Cheyenne chromosome substitution lines indicated that Rwt4 is located on chromosome 1D. [ABSTRACT FROM AUTHOR]

Summary Apoptotic cell response in oats is induced by victorin, a host-selective toxin secreted by Cochliobolus victoriae and thought to exert toxicity by inhibiting mitochondrial glycine decarboxylase (GDC) in Pc-2/Vb oats. We examined the role of mitochondria, especially the organelle-derived production of reactive oxygen species (ROS), in the induction of apoptotic cell death. Cytofluorimetric analysis showed that victorin caused mitochondrial ΔΨm breakdown and mitochondrial oxidative burst. Ultrastructural analysis using a cytochemical assay based on the reaction of H2 O2 with CeCl3 detected H2 O2 eruption at permeability transition pore-like sites on the mitochondrial membrane in oat cells treated with victorin. ROS generation preceded the apoptotic cell responses seen in chromatin condensation and DNA laddering. Both aminoacetonitrile (a specific GDC inhibitor) and antimycin A (a mitochondrial complex III inhibitor) also induced mitochondrial H2 O2 eruption, and led to the apoptotic response in oat cells. ROS scavengers such as N -acetyl-l-cysteine and catalase suppressed the mitochondrial oxidative burst and delayed chromatin condensation and DNA laddering in the victorin- or antimycin A-treated leaves. These findings indicate possible involvement of mitochondria, especially mitochondrial-derived ROS generation, as an important regulator in controlling apoptotic cell death in oats. [ABSTRACT FROM AUTHOR]

Transcriptionally active Ty1-copia LTR-retrotransposons were found in oat using RT-PCR for amplifying the reverse transcriptase domain. Sequence analysis of the RT-PCR clones suggested that oat LTR-retrotransposons consist of at least seven groups, which were tentatively designated as Oatrt1 to Oatrt7. A full length copy of Oatrt1 was isolated from an oat genomic library, and was designated OARE-1. OARE-1 was 8,665 bp long and a member of the BARE-1 subgroup. The oat genome carried it in multiple copies (at least 10,000 copies / a hexaploid genome). The expression of OARE-1 was intensively induced by wounding, UV light, jasmonic acid and salicylic acid, and its pattern was very similar to that of the PAL (phenylalanin ammonia lyase) gene. Furthermore, OARE-1 was highly activated by infection with an incompatible race of the crown rust fungus, Puccinia coronata. These results suggest that OARE-1 is highly sensitive to various abiotic and biotic stimuli leading to plant defense responses. [ABSTRACT FROM PUBLISHER]