David M. Cahill

Abscisic acid influences the susceptibility of Arabidopsis thaliana to Pseudomonas syringae pv. tomato and Peronospora parasitica

The phytohormone abscisic acid (ABA) plays a major role in the regulation of many physiological stresses although its role in pathogen-induced stress remains poorly understood. We examined the influence of ABA on interactions of Arabidopsis thaliana (L.) Heynh. (Arabidopsis) with a bacterial pathogen, Pseudomonas syringae pv. tomato and an Oomycete, Peronospora parasitica. Both addition of 100 μM ABA to plants and drought stress stimulated increased susceptibility of Arabidopsis to an avirulent isolate of P. syringae pv. tomato. In contrast, an ABA-deficient mutant of Arabidopsis, aba1-1, displayed reduced susceptibility to virulent isolates of P. parasitica. An ABA-insensitive mutant, abi1-1, that is impaired in ABA signal transduction did not alter in susceptibility to either P. syringae pv. tomato or P. parasitica. These results demonstrate that the concentration of endogenous ABA at the time of pathogen challenge is important for the development of susceptibility in Arabidopsis.

Suppression by ABA of salicylic acid and lignin accumulation and the expression of multiple genes, in Arabidopsis infected with Pseudomonas syringae pv. tomato

Abscisic acid (ABA) has been implicated in determining the outcome of interactions between many plants and their pathogens. We had previously shown that increased concentrations of ABA within leaves of Arabidopsis induced susceptibility towards an avirulent strain of Pseudomonas syringae pathovar (pv.) tomato. We now show that ABA induces susceptibility via suppression of the accumulation of components crucial for a resistance response. Lignin and salicylic acid concentrations in leaves were increased during a resistant interaction but reduced when plants were treated with ABA. The reduction in lignin and salicylic acid production was independent of the development of the hypersensitive response (HR), indicating that, in this host-pathogen system, HR is not required for resistance. Genome-wide gene expression analysis using microarrays showed that treatment with ABA suppressed the expression of many defence-related genes, including those important for phenylpropanoid biosynthesis and those encoding resistance-related proteins. Together, these results show that resistance induction in Arabidopsis to an avirulent strain of P. syringae pv. tomato is regulated by ABA.

Phytophthora cinnamomi and Australia's biodiversity : impacts, predictions and progress towards control

Phytophthora cinnamomi continues to cause devastating disease in Australian native vegetation and consequently the disease is listed by the Federal Government as a process that is threatening Australia’s biodiversity. Although several advances have been made in our understanding of how this soil-borne pathogen interacts with plants and of how we may tackle it in natural systems, our ability to control the disease is limited. The pathogen occurs widely across Australia but the severity of its impact is most evident within ecological communities of the south-west and south-east of the country. A regional impact summary for all states and territories shows the pathogen to be the cause of serious disease in numerous species, a significant number of which are rare and threatened. Many genera of endemic taxa have a high proportion of susceptible species including the iconic genera Banksia, Epacris and Xanthorrhoea. Long-term studies in Victoria have shown limited but probably unsustainable recovery of susceptible vegetation, given current management practices. Management of the disease in conservation reserves is reliant on hygiene, the use of chemicals and restriction of access, and has had only limited effectiveness and not provided complete control. The deleterious impacts of the disease on faunal habitat are reasonably well documented and demonstrate loss of individual animal species and changes in population structure and species abundance. Few plant species are known to be resistant to P. cinnamomi; however, investigations over several years have discovered the mechanisms by which some plants are able to survive infection, including the activation of defence-related genes and signalling pathways, the reinforcement of cell walls and accumulation of toxic metabolites. Manipulation of resistance and resistance-related mechanisms may provide avenues for protection against disease in otherwise susceptible species. Despite the advances made in Phytophthora research in Australia during the past 40 years, there is still much to be done to give land managers the resources to combat this disease. Recent State and Federal initiatives offer the prospect of a growing and broader awareness of the disease and its associated impacts. However, awareness must be translated into action as time is running out for the large number of susceptible, and potentially susceptible, species within vulnerable Australian ecological communities.

MEDIATOR25 Acts as an Integrative Hub for the Regulation of Jasmonate-Responsive Gene Expression in Arabidopsis

The PHYTOCHROME AND FLOWERING TIME1 gene encoding the MEDIATOR25 (MED25) subunit of the eukaryotic Mediator complex is a positive regulator of jasmonate (JA)-responsive gene expression in Arabidopsis (Arabidopsis thaliana). Based on the function of the Mediator complex as a bridge between DNA-bound transcriptional activators and the RNA polymerase II complex, MED25 has been hypothesized to function in association with transcriptional regulators of the JA pathway. However, it is currently not known mechanistically how MED25 functions to regulate JA-responsive gene expression. In this study, we show that MED25 physically interacts with several key transcriptional regulators of the JA signaling pathway, including the APETALA2 (AP2)/ETHYLENE RESPONSE FACTOR (ERF) transcription factors OCTADECANOID-RESPONSIVE ARABIDOPSIS AP2/ERF59 and ERF1 as well as the master regulator MYC2. Physical interaction detected between MED25 and four group IX AP2/ERF transcription factors was shown to require the activator interaction domain of MED25 as well as the recently discovered Conserved Motif IX-1/EDLL transcription activation motif of MED25-interacting AP2/ERFs. Using transcriptional activation experiments, we also show that OCTADECANOID-RESPONSIVE ARABIDOPSIS AP2/ERF59- and ERF1-dependent activation of PLANT DEFENSIN1.2 as well as MYC2-dependent activation of VEGETATIVE STORAGE PROTEIN1 requires a functional MED25. In addition, MED25 is required for MYC2-dependent repression of pathogen defense genes. These results suggest an important role for MED25 as an integrative hub within the Mediator complex during the regulation of JA-associated gene expression.

Diverse roles of the Mediator complex in plants

Since its original discovery in yeast, the Mediator complex has been identified in a wide range of organisms across the eukaryotic kingdom. Despite being experimentally purified from a number of fungal and metazoan organisms, it was not until 2007, thirteen years after its initial discovery, that the Mediator complex was successfully isolated from plants. With a number of papers now beginning to emerge on the plant Mediator complex, this review aims to provide an overview of the diverse functions that have been identified for individual plant Mediator subunits. In addition to demonstrating roles in plant development, flowering, hormone signaling and biotic and abiotic stress tolerance; recent findings have revealed novel functions for plant Mediator subunits, including mRNA, miRNA and rRNA processing, as well as controlling DNA and protein stability. These diverse activities have expanded the known functions of the Mediator complex and demonstrate a variety of new insights that have been gained from investigations into the plant Mediator complex. Future directions for research into this multi-functional protein complex will be discussed.

Influence of abscisic acid and the abscisic acid biosynthesis inhibitor, norflurazon, on interactions between Phytophthora sojae and soybean (Glycine max)

A comparison was made of the effects of abscisic acid (ABA) and the ABA biosynthesis inhibitor, norflurazon on the interaction between soybean leaves and Phytophthora sojae. Inoculation of leaves of cv. Harosoy resulted in a compatible interaction typified by the presence of spreading, water soaked lesions with ill-defined margins while inoculation of cv. Haro 1272 resulted in an incompatible interaction with lesions restricted to the inoculation site. Activity of phenylalanine ammonia lyase (PAL) slowly increased in the compatible interaction but in the incompatible interaction there was a rapid rise in activity within 8 h after inoculation. When Haro 1272 plants were treated with ABA the normally incompatible interaction with race 1 was changed to what resembled a compatible interaction and activity of PAL was reduced to control levels. There was no visible effect on the compatible combination. In contrast when plants of cv. Harosoy were treated with norflurazon the normally compatible interaction with race 1 was changed to that which resembled an incompatible interaction and PAL activity increased to high levels rapidly. There was no effect of norflurazon on the incompatible interaction of cv. Haro 1272 with race 1. Stomata on leaves of cv. Harosoy treated with norflurazon closed within 2 h of inoculation resembling the response of stomata in normal incompatible interactions but not compatible interactions where stomata remained open. On leaves of cv. Harosoy treated with norflurazon at sites 3 and 20 mm from the inoculation point stomata also closed. These results extend and confirm the idea that ABA is a molecule that may regulate the outcome of the interaction between soybeans and P. sojae.

Modelling habitat suitability of the swamp antechinus (Antechinus minimus maritimus) in the coastal heathlands of southern Victoria, Australia

Abstract In recent years, predictive habitat distribution models, derived by combining multivariate statistical analyses with Geographic Information System (GIS) technology, have been recognised for their utility in conservation planning. The size and spatial arrangement of suitable habitat can influence the long-term persistence of some faunal species. In southwestern Victoria, Australia, populations of the rare swamp antechinus (Antechinus minimus maritimus) are threatened by further fragmentation of suitable habitat. In the current study, a spatially explicit habitat suitability model was developed for A. minimus that incorporated a measure of vegetation structure. Models were generated using logistic regression with species presence or absence as the dependent variable and landscape variables, extracted from both GIS data layers and multi-spectral digital imagery, as the predictors. The most parsimonious model, based on the Akaike Information Criterion, was spatially extrapolated in the GIS. Probability of species presence was used as an index of habitat suitability. A negative association between A. minimus presence and both elevation and habitat complexity was evidenced, suggesting a preference for relatively low altitudes and a vegetation structure of low vertical complexity. The predictive performance of the selected model was shown to be high (91%), indicating a good fit of the model to the data. The proportion of the study area predicted as suitable habitat for A. minimus (Probability of occurrence ⩾0.5) was 11.7%. Habitat suitability maps not only provide baseline information about the spatial arrangement of potentially suitable habitat for a species, but they also help to refine the search for other populations, making them an important conservation tool.

Plant responses to UV radiation and links to pathogen resistance

Increased incident ultraviolet (UV) radiation due to ozone depletion has heightened interest in plant responses to UV because solar UV wavelengths can reduce plant genome stability, growth, and productivity. These detrimental effects result from damage to cell components including nucleic acids, proteins, and membrane lipids. As obligate phototrophs, plants must counter the onslaught of cellular damage due to prolonged exposure to sunlight. They do so by attenuating the UV dose received through accumulation of UV-absorbing secondary metabolites, neutralizing reactive oxygen species produced by UV, monomerizing UV-induced pyrimidine dimers by photoreactivation, extracting UV photoproducts from DNA via nucleotide excision repair, and perhaps transiently tolerating the presence of DNA lesions via replicative bypass of the damage. The signaling mechanisms controlling these responses suggest that UV exposure also may be beneficial to plants by increasing cellular immunity to pathogens. Indeed, pathogen resistance can be enhanced by UV treatment, and recent experiments suggest DNA damage and its processing may have a role.

Analysis of global host gene expression during the primary phase of the Arabidopsis thaliana–Plasmodiophora brassicae interaction

Microarray analysis was used to investigate changes in host gene expression during the primary stages of the interaction between the susceptible plant Arabidopsis thaliana (L.) Heynh ecotype Col-0 and the biotrophic pathogen Plasmodiophora brassicae Woronin. Analyses were conducted at 4, 7 and 10 days after inoculation (DAI) and revealed significant induction or suppression of a relatively low number of genes in a range of functional categories. At 4 DAI, there was induced expression of several genes known to be critical for pathogen recognition and signal transduction in other resistant host-pathogen interactions. As the pathogen further colonised root tissue and progressed through the primary plasmodium stage to production of zoosporangia at 7 and 10 DAI, respectively, fewer genes showed changes in expression. The microarray results were validated by examining a subset of induced genes at 4 DAI by quantitative real-time reverse transcriptase PCR (RT-qPCR) analysis all of which correlated positively with the microarray data. The two A. thaliana mutants jar1 and coiI tested were found to be susceptible to P. brassicae. The involvement of defence-related hormones in the interaction was further investigated and the findings indicate that addition of salicylic acid can suppress clubroot disease in A. thaliana plants.

UV-Induced DNA Damage Promotes Resistance to the Biotrophic Pathogen Hyaloperonospora parasitica in Arabidopsis

Plant innate immunity to pathogenic microorganisms is activated in response to recognition of extracellular or intracellular pathogen molecules by transmembrane receptors or resistance proteins, respectively. The defense signaling pathways share components with those involved in plant responses to UV radiation, which can induce expression of plant genes important for pathogen resistance. Such intriguing links suggest that UV treatment might activate resistance to pathogens in normally susceptible host plants. Here, we demonstrate that pre-inoculative UV (254 nm) irradiation of Arabidopsis (Arabidopsis thaliana) susceptible to infection by the biotrophic oomycete Hyaloperonospora parasitica, the causative agent of downy mildew, induces dose- and time-dependent resistance to the pathogen detectable up to 7 d after UV exposure. Limiting repair of UV photoproducts by postirradiation incubation in the dark, or mutational inactivation of cyclobutane pyrimidine dimer photolyase, (6-4) photoproduct photolyase, or nucleotide excision repair increased the magnitude of UV-induced pathogen resistance. In the absence of treatment with 254-nm UV, plant nucleotide excision repair mutants also defective for cyclobutane pyrimidine dimer or (6-4) photoproduct photolyase displayed resistance to H. parasitica, partially attributable to short wavelength UV-B (280–320 nm) radiation emitted by incubator lights. These results indicate UV irradiation can initiate the development of resistance to H. parasitica in plants normally susceptible to the pathogen and point to a key role for UV-induced DNA damage. They also suggest UV treatment can circumvent the requirement for recognition of H. parasitica molecules by Arabidopsis proteins to activate an immune response.