The etiology of the selective neuronal death that occurs in Huntington's disease (HD) is unknown. Several lines of evidence implicate the involvement of energetic defects and oxidative damage in the disease process, including a recent study that demonstrated an interaction between huntingtin protein and the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Using spectrophotometric assays in postmortem brain tissue, we found evidence of impaired oxidative phosphorylation enzyme activities restricted to the basal ganglia in HD brain, while enzyme activities were unaltered in three regions relatively spared by HD pathology (frontal cortex, parietal cortex, and cerebellum). Citrate synthase-corrected complex II-III activity was markedly reduced in both HD caudate (-29%) and putamen (-67%), and complex IV activity was reduced in HD putamen (-62%). Complex I and GAPDH activities were unaltered in all regions examined. We also measured levels of the oxidative damage product 8-hydroxydeoxyguanosine (OH8dG) in nuclear DNA, and superoxide dismutase (SOD) activity. OH8dG levels were significantly increased in HD caudate. Cytosolic SOD activity was slightly reduced in HD parietal cortex and cerebellum, whereas particulate SOD activity was unaltered in these regions. These results further support a role for metabolic dysfunction and oxidative damage in the pathogenesis of HD.

Phytopathogen infection leads to changes in secondary metabolism based on the induction of defence programmes as well as to changes in primary metabolism which affect growth and development of the plant. Therefore, pathogen attack causes crop yield losses even in interactions which do not end up with disease or death of the plant. While the regulation of defence responses has been intensively studied for decades, less is known about the effects of pathogen infection on primary metabolism. Recently, interest in this research area has been growing, and aspects of photosynthesis, assimilate partitioning, and source-sink regulation in different types of plant-pathogen interactions have been investigated. Similarly, phytopathological studies take into consideration the physiological status of the infected tissues to elucidate the fine-tuned infection mechanisms. The aim of this review is to give a summary of recent advances in the mutual interrelation between primary metabolism and pathogen infection, as well as to indicate current developments in non-invasive techniques and important strategies of combining modern molecular and physiological techniques with phytopathology for future investigations.

12-oxo-phytodienoic acid and several phytoprostanes are cyclopentenone oxylipins that are formed via the enzymatic jasmonate pathway and a nonenzymatic, free radical-catalyzed pathway, respectively. Both types of cyclopentenone oxylipins induce the expression of genes related to detoxification, stress responses, and secondary metabolism, a profile clearly distinct from that of the cyclopentanone jasmonic acid. Microarray analyses revealed that 60% of the induction by phytoprostanes and 30% of the induction by 12-oxo-phytodienoic acid was dependent on the TGA transcription factors TGA2, TGA5, and TGA6. Moreover, treatment with phytoprostanes and 12-oxo-phytodienoic acid inhibited cell division and root growth, a property also shared by jasmonic acid. Besides being potent signals, cyclopentenones and other lipid peroxidation products are reactive electrophiles that can covalently bind to and damage proteins. To this end, we show that at least two of the induced detoxification enzymes efficiently metabolize cyclopentenones in vitro. Accumulation of two of these metabolites was detectable during Pseudomonas infection. The cyclopentenone oxylipin gene induction profile resembles the defense response induced by a variety of lipophilic xenobiotics. Hence, oxidized lipids may activate chemosensory mechanisms of a general broad-spectrum detoxification network involving TGA transcription factors.

In incompatible plant-pathogen interactions, disease resistance is generated by rapid activation of a multitude of plant defence reactions. Little is known about the dependency of these resistance responses on external factors. The plasticity of plant defence mechanisms in terms of light conditions is studied here. Interaction of Arabidopsis thaliana (L.) Heynh. with an avirulent strain of Pseudomonas syringae pv. maculicola in the dark resulted in increased apoplastic bacterial growth and therefore reduced local resistance as compared to an infection process in the presence of light. Several characteristic defence reactions, including activation of phenylalanine ammonia-lyase, accumulation of salicylic acid (SA), expression of the pathogenesis-related protein PR-1 and the development of a microscopically defined hypersensitive response, proved to be light dependent. In contrast, the extent of the oxidative burst, as estimated by induction of the protectant gene glutathione- S-transferase, was not weakened by the absence of light. Moreover, pathogen-induced accumulation of jasmonic acid, production of the phytoalexin camalexin and transcriptional induction of a pathogen-inducible myrosinase were even more pronounced in the dark. Apart from affecting local defence responses, light also influenced the establishment of systemic acquired resistance (SAR). SAR development in response to infection by avirulent bacteria was completely lost when the primary infection process occurred in the absence of light. SAR developed both under medium (70 micromol photons m(-2) s(-1)) and strong (500 micromol photons m(-2) s(-1)) light conditions but was in the latter case not associated with an accumulation of SA and PR-1 in systemic leaves, demonstrating that SAR can be executed independently from these molecular SAR markers. Our results are consistent with the notion that SA accumulation in infected primary leaves is necessary for induction of systemic resistance and indicate that defence mechanisms different from SA signalling and PR-protein action exist in systemic tissue to confer resistance during SAR.