Reactive oxygen species (ROS) are key players in the regulation of plant development, stress responses, and programmed cell death. Previous studies indicated that depending on the type of ROS (hydrogen peroxide, superoxide, or singlet oxygen) or its subcellular production site (plastidic, cytosolic, peroxisomal, or apoplastic), a different physiological, biochemical, and molecular response is provoked. We used transcriptome data generated from ROS-related microarray experiments to assess the specificity of ROS-driven transcript expression. Data sets obtained by exogenous application of oxidative stress-causing agents (methyl viologen, Alternaria alternata toxin, 3-aminotriazole, and ozone) and from a mutant (fluorescent) and transgenic plants, in which the activity of an individual antioxidant enzyme was perturbed (catalase, cytosolic ascorbate peroxidase, and copper/ zinc superoxide dismutase), were compared. In total, the abundance of nearly 26,000 transcripts of Arabidopsis (Arabidopsis thaliana) was monitored in response to different ROS. Overall, 8,056, 5,312, and 3,925 transcripts showed at least a 3-, 4-, or 5-fold change in expression, respectively. In addition to marker transcripts that were specifically regulated by hydrogen peroxide, superoxide, or singlet oxygen, several transcripts were identified as general oxidative stress response markers because their steady-state levels were at least 5-fold elevated in most experiments. We also assessed the expression characteristics of all annotated transcription factors and inferred new candidate regulatory transcripts that could be responsible for orchestrating the specific transcriptomic signatures triggered by different ROS. Our analysis provides a framework that will assist future efforts to address the impact of ROS signals within environmental stress conditions and elucidate the molecular mechanisms of the oxidative stress response in plants.

Hydrogen peroxide plays a central role in launching the defense response during stress in plants. To establish a molecular profile provoked by a sustained increase in hydrogen peroxide levels, catalase-deficient tobacco plants (CAT1AS) were exposed to high light (HL) intensities over a detailed time course. The expression kinetics of >14,000 genes were monitored by using transcript profiling technology based on cDNA-amplified fragment length polymorphism. Clustering and sequence analysis of 713 differentially expressed transcript fragments revealed a transcriptional response that mimicked that reported during both biotic and abiotic stresses, including the up-regulation of genes involved in the hypersensitive response, vesicular transport, posttranscriptional processes, biosynthesis of ethylene and jasmonic acid, proteolysis, mitochondrial metabolism, and cell death, and was accompanied by a very rapid up-regulation of several signal transduction components. Expression profiling corroborated by functional experiments showed that HL induced photoinhibition in CAT1AS plants and that a short-term HL exposure of CAT1AS plants triggered an increased tolerance against a subsequent severe oxidative stress.

Tolerance against oxidative stress generated by high light intensities or the catalase inhibitor aminotriazole (AT) was induced in intact tobacco plants by spraying them with hydrogen peroxide (H2O2). Stress tolerance was concomitant with an enhanced antioxidant status as reflected by higher activity and/or protein levels of catalase, ascorbate peroxidase, guaiacol peroxidases, and glutathione peroxidase, as well as an increased glutathione pool. The induced stress tolerance was dependent on the dose of H2O2 applied. Moderate doses of H2O2 enhanced the antioxidant status and induced stress tolerance, while higher concentrations caused oxidative stress and symptoms resembling a hypersensitive response. In stress-tolerant plants, induction of catalase was 1.5-fold, that of ascorbate peroxidase and glutathione peroxidase was 2-fold, and that of guaiacol peroxidases was approximately 3-fold. Stress resistance was monitored by measuring levels of malondialdehyde, an indicator of lipid peroxidation. The levels of malondialdehyde in all H2O2-treated plants exposed to subsequent high light or AT stress were similar to those of unstressed plants, whereas lipid peroxidation in H2O2-untreated plants stressed with either high light or AT was 1.5- or 2-fold higher, respectively. Although all stress factors caused increases in the levels of reduced glutathione, its levels were much higher in all H2O2-pretreated plants. Moreover, significant accumulation of oxidized glutathione was observed only in plants that were not pretreated with H2O2. Extending the AT stress period from 1 to 7 days resulted in death of tobacco plants that were not pretreated with H2O2, while all H2O2-pretreated plants remained little affected by the prolonged treatment. Thus, activation of the plant antioxidant system by H2O2 plays an important role in the induced tolerance against oxidative stress.

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An extensive microarray analysis of AAL-toxin-induced cell death in Arabidopsis thaliana brings new insights into the complexity of programmed cell death in plants Gechev, T.S.; Gadjev, I.Z.; Hille, J. Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. Abstract. A T-DNA knockout of the Arabidopsis homologue of the tomato disease resistance gene Asc was obtained. The asc gene renders plants sensitive to programmed cell death (PCD) triggered by the fungal AAL toxin. To obtain more insights into the nature of AALtoxin-induced cell death and to identify genes of potential importance for PCD, we carried out transcription profiling of AAL-toxin-induced cell death in this knockout with an oligonucleotide array representing 21,500 Arabidopsis genes. Genes responsive to reactive oxygen species (ROS) and ethylene were among the earliest to be upregulated, suggesting that an oxidative burst and production of ethylene played a role in the activation of the cell death. This notion was corroborated by induction of several genes encoding ROS-generating proteins, including a respiratory burst oxidase and germin oxalate oxi- CMLS, Cell. Mol. Life Sci. 61 (2004) 1185 -1197 1420-682X/04/101185-13 DOI 10.1007/s00018-004-4067-2 © Birkhäuser Verlag, Basel, 2004 CMLS Cellular and Molecular Life Sciences dase. Cytochemical studies confirmed the oxidative burst and, in addition, showed synthesis of callose, a feature of the hypersensitive response. A diverse group of transcription factors was also induced. These events were followed by repression of most of the auxin-regulated genes known to be involved in growth and developmental responses. All photosynthesis-related genes were repressed. Blocking the synthesis of ethylene or NO significantly compromised cell death. In addition, we identified a heterogeneous group of early-induced genes, some of them never before associated with PCD. The group of earlyinduced genes included a number of proteases that were previously implicated in developmentally regulated types of PCD, suggesting a more principal role for these proteases in the PCD process. These findings provide new insights into the molecular mechanisms of plant PCD.

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In recent decades, advances in the life sciences have created an unprecedentedly detailed picture of heredity and the formation of the phenotype where clusters of simplistic reductionist and deterministic views and interpretations have begun to lose ground to more complex and holistic notions. The developments in gene regulation and epigenetics have become a vivid emblem of the ongoing ‘softening’ of heredity. Despite this headway, the outlook and rhetoric widely popular in the twentieth century favoring the ‘gene’ in the ‘gene↔genetic plasticity↔phenotype↔environment’ tetrad have not been successfully tackled but continue to exist in parallel with a new, equally monochromatic, viewpoint championing genetic plasticity. An examination of epigenetics and its presentation in the public sphere, open to a conversation with the social disciplines and philosophy, could address this dichotomy and contribute to the discourse. This article outlines key biological aspects of epigenetics and discusses the language, presentation and wider resonance of this field of life science research.

This year (2014) marks the 270th anniversary of Jean-Baptiste de Lamarck's birth, which presents a good occasion to reflect on the wide-reaching, although largely ignored, legacy of the French naturalist and its modern-day renaissance. A discussion is provided of the broad and controversial influence of Lamarckian thought on science, politics and art, with a focus on Lamarck's curious recent comeback to the public and academic eyes in relation to the burgeoning discipline of epigenetics.