No description available.

A plant's response to pathogen infection is tailored dependent on infection strategy. Successful plant pathogens employ various infection strategies to avoid or reduce plant defense responses for the establishment of host compatibility. Autophagy is a non-selective degradation pathway conserved in eukaryotic organisms, which has been implicated in the regulation of cell survival or cell death, depending on cell type and stimulus. In <i>Arabidopsis thaliana</i>, an autophagic response has been reported to be activated during nutrient deprivation. Cellular contents, such as cytoplasm and organelles, are sequestered into double-membraned autophagosomes and delivered to the vacuole for degradation; degradative products, such as amino acids, are released back into the cell and reutilized to maintain cellular function. In this study, the response of the autophagy pathway was investigated in <i>A. thaliana</i> leaf tissues upon biotrophic <i>Erysiphe cichoracearum</i> and hemibiotrophic <i>Colletotrichum higginsianum</i> infections. Expression of some autophagy genes was induced in <i>A. thaliana</i> at 9 days post infection with <i>E. cichoracearum</i> and, 3 and 5 days post infection with <i>C. higginsianum</i>. Using a transgenic <i>A. thaliana</i> plant line over expressing autophagosome associated protein autophagy-8e (<i>ATG8e</i>) conjugated to green fluorescent protein (GFP) (<i>ATG8e-GFP</i>), confocal analysis revealed that autophagosomes specifically accumulated at the infection sites during <i>E. cichoracearum</i> and <i>C. higginsianum</i> invasions. These results indicate that the plant autophagic pathway responds to an interaction between <i>A. thaliana</i> and fungal pathogens. None of the defense signaling molecules including salicylic acid, jasmonic acid, ethylene, hydrogen peroxide and nitric oxide consistently triggered expression of autophagy genes. The insensitivity to defense signaling molecules and the delayed induction of autophagy genes compared to expression of pathogenesis-related genes suggest that the activation of this pathway does not contribute to host resistance responses during the infection process. In <i>A. thaliana</i> mutants, <i>atg4a/b, atg5-1, atg9-1</i> and <i>atg9-6</i> deficient for the autophagic response, virulence of <i>E. cichoracearum</i> was retarded whereas pathogenesis of <i>C. higginsianum</i> was accelerated. Taken together, these data suggest that the autophagy pathway is a potential host susceptibility factor for pathogen infection, possibly involved in establishing/facilitating biotrophy in <i>A. thaliana</i>.

A plant's response to pathogen infection is tailored dependent on infection strategy. Successful plant pathogens employ various infection strategies to avoid or reduce plant defense responses for the establishment of host compatibility. Autophagy is a non-selective degradation pathway conserved in eukaryotic organisms, which has been implicated in the regulation of cell survival or cell death, depending on cell type and stimulus. In <i>Arabidopsis thaliana</i>, an autophagic response has been reported to be activated during nutrient deprivation. Cellular contents, such as cytoplasm and organelles, are sequestered into double-membraned autophagosomes and delivered to the vacuole for degradation; degradative products, such as amino acids, are released back into the cell and reutilized to maintain cellular function. In this study, the response of the autophagy pathway was investigated in <i>A. thaliana</i> leaf tissues upon biotrophic <i>Erysiphe cichoracearum</i> and hemibiotrophic <i>Colletotrichum higginsianum</i> infections. Expression of some autophagy genes was induced in <i>A. thaliana</i> at 9 days post infection with <i>E. cichoracearum</i> and, 3 and 5 days post infection with <i>C. higginsianum</i>. Using a transgenic <i>A. thaliana</i> plant line over expressing autophagosome associated protein autophagy-8e (<i>ATG8e</i>) conjugated to green fluorescent protein (GFP) (<i>ATG8e-GFP</i>), confocal analysis revealed that autophagosomes specifically accumulated at the infection sites during <i>E. cichoracearum</i> and <i>C. higginsianum</i> invasions. These results indicate that the plant autophagic pathway responds to an interaction between <i>A. thaliana</i> and fungal pathogens. None of the defense signaling molecules including salicylic acid, jasmonic acid, ethylene, hydrogen peroxide and nitric oxide consistently triggered expression of autophagy genes. The insensitivity to defense signaling molecules and the delayed induction of autophagy genes compared to expression of pathogenesis-related genes suggest that the activation of this pathway does not contribute to host resistance responses during the infection process. In <i>A. thaliana</i> mutants, <i>atg4a/b, atg5-1, atg9-1</i> and <i>atg9-6</i> deficient for the autophagic response, virulence of <i>E. cichoracearum</i> was retarded whereas pathogenesis of <i>C. higginsianum</i> was accelerated. Taken together, these data suggest that the autophagy pathway is a potential host susceptibility factor for pathogen infection, possibly involved in establishing/facilitating biotrophy in <i>A. thaliana</i>.

Thesis (Ph. D.)--University of Washington, 2001. / Vita. Includes bibliographical references (leaves 115-138).

Thesis (Ph. D.)--University of Queensland, 2002. / Includes bibliographical references.

The aim of this PhD was to investigate major gaps in our understanding of how mycorrhizal fungi and aphids interact via their effects on plants, and how these interactions regulate emission of plant volatiles and consequently aphid and parasitoid host location. A series of experiments was designed using broad bean (Vicia faba L.), pea aphids (Acyrthosiphon pisum) and their parasitoid wasp, Aphidius ervi and mixed or single spore cultures of AM fungi as a model system. This PhD has determined that arbuscular mycorrhizal fungi are more important drivers of above-ground ecological interactions than ever considered before. They have key roles in specialist aphid host location and in influencing their development. The antagonistic effect of aphids on functioning of mycorrhizal association suggests that the interactions operate in both directions. However, if plants were supplied with phosphorus the aphids did not affect mycorrhizal colonisation suggesting that at sufficient phosphorus availability plants can tolerate the effect of aphids on mycorrhizal colonisation. This demonstrates how dynamic the multi-trophic systems are and that their outcomes are also influenced by soil nutrient availability, with implications for agricultural practices. This PhD has discovered that underground signals carried through common mycelial networks warn neighbouring plants of aphid attack. This signalling allows plants that receive the signal to initiate their defence system by changing their profiles of volatiles emissions and repel aphids and attract their parasitoids so that they may prevent the attack. Because the signal transfer is rapid it incurs the greatest fitness benefit for the receiving plant and potentially also for the donor of the signal and for the fungi. We now need to determine the wider ecosystem implications of this phenomenon, how the signalling is regulated in nature and in agroecosystems and what the fitness consequences are for each component organism.

Incompatible plant/pathogen interactions are often manifested as the hypersensitive response (HR), characterised by host cell death and rapid tissue collapse at the site of attempted infection. A key early response during the HR is the generation of reactive oxygen species (ROS), such as the superoxide anion ( 0; -) and hydrogen peroxide (H20 2), in an oxidative burst. The ROS produced during the oxidative burst have been implicated as cellular signalling molecules for the induction of defences responses including hypersensitive cell death. Increasing evidence exist that the free radical, nitric oxide (NO) also acts as a signalling molecule in plants during plant/pathogen interactions. The generation of NO in response to bacterial challenge, and the potential signalling pathways involved in H20 2- and NO-induced defence responses in Arabidopsis were therefore investigated Arabidopsis suspension cultures were found to generate elevated levels of NO and undergo cell death analogous to HR seen in planta, in response to challenge by avirulent bacteria. Using NO donors, elevated levels of NO were found to be sufficient to induce cell death independently of ROS, but not the expression of the defence-related genes PAL or GST. The NO-induced cell death was sensitive to inhibitors of RNA processing and protein synthesis, suggesting that NO-induced cell death is a form of programmed cell death (PCD), requiring the expression of at least one gene. However, the source of NO production by Arabidopsis remains to be elucidated, but appears to be independent of nitric oxide synthase-like activity. Pharmacological studies using specific inhibitors of mammalian mitogen activated protein kinase (MAPK) signalling cascades, and guanylate cyclase, the enzyme responsible for the production of second messenger cyclic guanosine monophosphate (cGMP), suggest that a MAPK signalling cascade acts downstream or independently of the oxidative burst to initiate H20 2-induced defence responses, while NO-induced cell death requires the production of cGMP in Arabidopsis. A number of studies have attempted to establish whether PCD induced during the HR in plants is similar to apoptotic cell death of anin1al cells. The key executioners of apoptosis in animal cells are caspases. NO was found to induce caspase-like activity in Arabidopsis cells, while a specific inhibitor of caspase-l blocked harpin-, H20 2- and NO-induced cell death. A characteristic of apoptosis is chromatin condensation and DNA fragmentation into nucleosomal fragments. Chromatin condensation was observed in Arabidopsis cells treated with the NO donor Roussin's black salt, but no DNA fragmentation was found in DNA extracted from cells treated with harpin, H20 2 or NO. In addition, random DNA degradation indicative of necrosis was found in DNA extracted from cells following avirulent bacterial challenge.

Pathogens are one of the prevalent stresses to plants. Resistance mediated by the resistance genes is efficient mechanism for evading the pathogens. To understand the influence of various biotic and abiotic factors on resistance gene promoters, plants having N gene promoter fused with reporter genes were developed. Experiments with tobacco plants revealed that on tobacco mosaic virus infection, the N protein may increase in the cells. Also, extreme temperature may result in decrease in the N protein. The salicylic acid produced during the development of systemic acquired resistance does not hinder the N promoter function. Hence, it can be concluded that the promoter region of resistance genes can be influenced by many biotic and abiotic factors. In the tobacco plants lacking the N gene, infection with tobacco mosaic virus leads to generation of systemic recombination signal. Experiments suggest that this signal can lead to better tolerance of the pathogen in next generation. Also, in the plants which received systemic recombination signal, the resistance gene loci are hypermethylated and the frequency of rearrangement in these loci increases. Hence, the signal results in higher tolerance to pathogen and increased genetic variability in resistance genes. / xvi, 147 leaves : ill. (some col.) ; 29 cm.

No description available.

No description available.