Peroxisomes are the cellular location of many antioxidants and are themselves significant producers of reactive oxygen species. In this report we demonstrate the induction of peroxisome biogenesis genes in both plant and animal cells by the universal stress signal molecule hydrogen peroxide. Using PEX1–LUC transgenic plants, rapid local and systemic induction of PEX1–luciferase could be demonstrated in vivo in response to physiological levels of hydrogen peroxide. PEX1–luciferase was also induced in response to wounding and to infection with an avirulent pathogen. We propose a model in which various stress situations that lead to the production of hydrogen peroxide can be ameliorated by elaboration of the peroxisome compartment to assist in restoration of the cellular redox balance.

SummaryThe phytohormone abscisic acid (ABA) inhibits the germination of many seeds, including Arabidopsis, but the mechanism for this is not known. In cereals, ABA inhibits the expression of genes involved in storage reserve mobilization. We have found that in Arabidopsis ABA decreases transcription from the promoters of marker genes for b-oxidation and the glyoxylate cycle, essential pathways for the conversion of storage lipid (triacylglycerol) into sucrose. Thirty per cent of stored lipid is broken down over 6 days following imbibition of ABA-treated seed. Sucrose levels in ABA-treated seeds, rather than decreasing as under normal growth conditions, actually double during the 3 days following imbibition. This sucrose is derived from triacylglycerol as demonstrated by two mutants disrupted in the conversion of triacylglycerol into sucrose, kat2 and icl1, which do not accumulate sucrose in the presence of ABA. We conclude that the ABA block on germination is not a consequence of inhibition of storage lipid mobilization. Two independent programmes appear to operate, one that is blocked by ABA, governing developmental growth resulting in germination; and a second that governs storage lipid mobilization which is largely ABA-independent.

RNA interference (RNAi) is a powerful tool for the analysis of gene function in model organisms such as the nematode Caenorhabditis elegans. Recent demonstrations of RNAi in plant parasitic nematodes provide a stimulus to explore the potential of using RNAi to investigate disruption of gene function in Meloidogyne incognita, one of the most important nematode pests of global agriculture. We have used RNAi to examine the importance of dual oxidases (peroxidase and NADPH oxidase), a class of enzyme associated with extracellular matrix cross-linking in C. elegans. RNAi uptake by M. incognita juveniles is highly efficient. In planta infection data show that a single 4-h preinfection treatment with double-stranded RNA derived from the peroxidase region of a dual oxidase gene has effects on gene expression that are phenotypically observable 35 days postinfection. This RNAi effect results in a reduction in egg numbers at 35 days of up to 70%. The in vitro feeding strategy provides a powerful tool for identifying functionally important genes, including those that are potential targets for the development of new agrochemicals or transgenic resistance strategies.

The PEX11 family of peroxisome membrane proteins have been shown to be involved in regulation of peroxisome size and number in plant, animals, and yeast cells. We and others have previously suggested that peroxisome proliferation as a result of abiotic stress may be important in plant stress responses, and recently it was reported that several rice PEX11 genes were up regulated in response to abiotic stress. We sought to test the hypothesis that promoting peroxisome proliferation in Arabidopsis thaliana by over expression of one PEX11 family member, PEX11e, would give increased resistance to salt stress. We could demonstrate up regulation of PEX11e by salt stress and increased peroxisome number by both PEX11e over expression and salt stress, however our experiments failed to find a correlation between PEX11e over expression and increased peroxisome metabolic activity or resistance to salt stress. This suggests that although peroxisome proliferation may be a consequence of salt stress, it does not affect the ability of Arabidopsis plants to tolerate saline conditions.

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The expression of three genes that encode proteins involved in peroxisome biogenesis, beta-oxidation and the glyoxylate cycle was studied in Arabidopsis plants by fusing their promoter regions to the reporter gene luciferase. Malate synthase showed an extremely restricted pattern of expression, being detected only in young seedlings and the root tips of older plants. PEX1 and 3-ketoacyl thiolase (PED1) were expressed in roots, mature leaves, stems and flowers. However, only thiolase was up-regulated by starvation. Immunoblotting confirmed that neither malate synthase nor the other unique glyoxylate cycle enzyme isocitrate lyase are expressed in senescent leaves. These results indicate that, in contrast to cucumber, pumpkin and barley, the glyoxylate cycle does not play a role in the recycling of carbon from the turnover of membrane lipids during senescence and starvation in Arabidopsis.

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Peroxisomes participate in many biological functions including detoxification of reactive oxygen species and biosynthesis of oxylipin signalling molecules. Peroxisome protein and enzyme activities have been reported to change in response to salt stress. To investigate the relationship between peroxisomes and salt stress the level of expression of three peroxisome-associated genes, thiolase ( PED1 ), PEX10 and PEX1 was analysed by quantitative real-time polymerase chain reaction. The steady-state transcript level of all three genes was increased by salt and ABA treatment, and was blocked in the abi1-1 mutant. Salt-dependent increase of transcript for all three genes also required the JAR1 gene as it was prevented in the jar1-1 mutant. Expression of thiolase, and to a lesser extent PEX1 , was increased in the jar1-1 mutant in the absence of salt, suggesting jasmonate may negatively regulate these genes in the absence of salt stress. PEX1 was up-regulated in the ethylene over-producer eto1-1 and salt had an additive effect on PEX1 transcript level, but salt induction may be inhibited in the ethylene-insensitive line etr1-1 . Consistent with this, PEX1 was also up-regulated in transgenic plants over-expressing the ethylene response element binding factors AtERF1 and AtERF5.