11 research outputs found
The redox-sensitive transcription factor Rap2.4a controls nuclear expression of 2-Cys peroxiredoxin A and other chloroplast antioxidant enzymes
Shaikhali J, Heiber I, Seidel T, et al. The redox-sensitive transcription factor Rap2.4a controls nuclear expression of 2-Cys peroxiredoxin A and other chloroplast antioxidant enzymes. BMC Plant Biology. 2008;8(1):48
Deterministic pushdown automata can compress some normal sequences
In this paper, we give a deterministic pushdown transducer and a normal sequence of digits compressed by it. This solves positively a question left open in a previous paper by V. Becher, P. A. Heiber and the first author
Redox regulation and antioxidative defence in Arabidopsis leaves viewed from a systems biology perspective
Wormuth D, Heiber I, Shaikali J, Kandlbinder A, Baier M, Dietz K-J. Redox regulation and antioxidative defence in Arabidopsis leaves viewed from a systems biology perspective. JOURNAL OF BIOTECHNOLOGY. 2007;129(2):229-248.Redox regulation is a central control element in cell metabolism. It is employed to adjust photosynthesis and the antioxidant defence system of leaves to the prevailing environment. During recent years progress has been made in describing the redox-dependent alterations in metabolism, the thiol/disulfide proteome, the redox-dependent and cross-talking signalling pathways and the target genes of redox regulation. Some transcription factors have been identified as proteins that perform thiol/disulfide transitions linked to the redox-regulation of specific plant promoters. In addition first mathematical models have been designed to simulate antioxidant defence and predict its response. Taken together, a profound experimental data set has been generated which allows to approach a systems biology type of understanding of antioxidant defence in photosynthesising cells in the near future. Since oxidative stress is likely to limit plant growth under stress, such a systematic understanding of antioxidant defence will help to define novel targets for breeding stress-tolerant plants. (c) 2006 Elsevier B.V. All rights reserved
The redox imbalanced mutants of arabidopsis differentiate signaling pathways for redox regulation of chloroplast antioxidant enzymes
Heiber I, Stroeher E, Raatz B, et al. The redox imbalanced mutants of arabidopsis differentiate signaling pathways for redox regulation of chloroplast antioxidant enzymes. PLANT PHYSIOLOGY. 2007;143(4):1774-1788.A network of enzymatic and nonenzymatic antioxidants protects chloroplasts from photooxidative damage. With all enzymatic components being nuclear encoded, the control of the antioxidant capacity depends on chloroplast-to-nucleus redox signaling. Using an Arabidopsis (Arabidopsis thaliana) reporter gene line expressing luciferase under control of the redox-sensitive 2-cysteine peroxiredoxin A (2CPA) promoter, six mutants with low 2CPA promoter activity were isolated, of which five mutants show limitations in redox-box regulation of the 2CPA promoter. In addition to 2CPA, the transcript levels for other chloroplast antioxidant enzymes were decreased, although a higher oxidation status of the ascorbate pool, a higher reduction state of the plastoquinone pool, and an increased oxidation status of the 2-Cys peroxiredoxin pool demonstrated photooxidative stress conditions. Greening of the mutants, chloroplast ultrastructure, steady-state photosynthesis, and the responses to the stress hormone abscisic acid were wild type like. In the rosette state, the mutants were more sensitive to low CO2 and to hydrogen peroxide. Comparison of gene expression patterns and stress sensitivity characterizes the mutants as redox imbalanced in the regulation of nuclear-encoded chloroplast antioxidant enzymes and differentiates redox signaling cascades
Linking Chloroplast Antioxidant Defense to Carbohydrate Availability: The Transcript Abundance of Stromal Ascorbate Peroxidase Is Sugar-Controlled via Ascorbate Biosynthesis
Eggshell appearance does not signal maternal corticosterone exposure in Japanese quail: an experimental study with brown-spotted eggs
Reproduction is a critical period for birds as they have to cope with many stressful events. One consequence of an acute exposure to stress is the release of corticosterone, the avian stress hormone. Prolonged stress can have negative impacts on the immune system, resulting in, for example, increased oxidative stress. Through maternal effects, females are known to modulate their investment in eggs content according to their own physiological condition. Less is known about maternal investment in eggshells, especially in pigments. The two main eggshell pigments may possess opposite antioxidant properties: protoporphyrin (brown) is a pro-oxidant, whereas biliverdin (blue-green) is an antioxidant. In Japanese quail, we know that the deposition of both pigments is related to female body condition. Thus, a chronic stress response may be reflected in eggshell coloration. Using female Japanese quails that lay brown-spotted eggs, we explored whether physiological exposure to corticosterone induces a change in female basal stress and antioxidant factors, and eggshell pigment concentration, spectrophotometric reflectance, and maculation coverage. We supplemented adult females over a 2 week period with either peanut oil (control) or corticosterone (treatment). We collected pre- and post-supplementation eggs and analysed the effect of corticosterone treatment on female physiology and eggshell appearance parameters. Except for corticosterone-fed birds which laid eggs with brighter spots, supplementation had no significant effect on female physiology or eggshell pigment concentration, reflectance and maculation. The change in eggshell spot brightness was not detected by a photoreceptor noise-limited color opponent model of avian visual perception. Our data confirms that eggshell reflectance in spotted eggs varies over the laying sequence, and spot reflectance may be a key factor that is affected by females CORT exposure, even if the changes are not detected by an avian visual model.Camille Duval, Phillip Cassey, Paul G. Lovell, Ivan Mikšík, S. James Reynolds, Karen A. Spence
Shifts in Eastern German Production Structure Under Market Forces
The paper is organized into three major sections. The first section considers agricultural production prior to German reunification in 1990. It looks at the agricultural production structure in the region prior to the division of Germany in 1945 as well as the patterns which arose under the communist government. The second section starts with the 1989 situation and then discusses the initial adjustments seen as market forces are introduced -- 1990 and 1991. The third section builds upon this base to speculate on how the production structure will unfold in the future.International Relations/Trade,
The radical induced cell death protein 1 (RCD1) supports transcriptional activation of genes for chloroplast antioxidant enzymes
The rimb1 (redox imbalanced 1) mutation was mapped to the RCD1 locus (radical-induced cell death 1; At1g32230) demonstrating that a major factor involved in redox-regulation genes for chloroplast antioxidant enzymes and protection against photooxidative stress, RIMB1, is identical to the regulator of disease response reactions and cell death, RCD1.Discovering this link let to our investigation of its regulatory mechanism. We show in yeast that RCD1 can physically interact with the transcription factor Rap2.4a which provides redox-sensitivity to nuclear expression of genes for chloroplast antioxidant enzymes. In the rimb1 (rcd1-6) mutant a single nucleotide exchange results in a truncated RCD1 protein lacking the transcription factor binding site. Protein-protein interaction between full-length RCD1 and Rap2.4a is supported by H2O2, but not sensitive to the antioxidants dithiotreitol and ascorbate. In combination with transcript abundance analysis in Arabidopsis, it is concluded that RCD1 stabilizes the Rap2.4-dependent redox-regulation of the genes encoding chloroplast antioxidant enzymes in a widely redox-independent manner.Over the years, rcd1-mutant alleles have been described to develop symptoms like chlorosis, lesions along the leaf rims and in the mesophyll and (secondary) induction of extra- and intra-plastidic antioxidant defense mechanisms. All these rcd1 mutant characteristics were observed in rcd1-6 to succeed low activation of the chloroplast antioxidant system and glutathione biosynthesis. We conclude that RCD1 protects plant cells from running into ROS (reactive oxygen species)-triggered programs, such as cell death and activation of pathogen-responsive genes (PR genes) and extra-plastidic antioxidant enzymes, by supporting the induction of the chloroplast antioxidant system
The Plant Immunity Regulating F-Box Protein CPR1 Supports Plastid Function in Absence of Pathogens
The redox imbalanced 6 mutant (rimb6) of Arabidopsis thaliana was isolated in a genetic screening approach for mutants with defects in chloroplast-to-nucleus redox signaling. It has an atypically low activation status of the 2-Cys peroxiredoxin-A promoter in the seedling stage. rimb6 shows wildtype-like germination, seedling development and greening, but slower growth and reduced biomass in the rosette stage. Mapping of the casual mutation revealed that rimb6 carries a single nucleotide polymorphism in the gene encoding CONSTITUTIVE EXPRESSER OF PATHOGENESIS RELATED (PR) GENES 1, CPR1 (At4g12560), leading to a premature stop codon. CPR1 is known as a repressor of pathogen signaling and regulator of microtubule organization. Allelism of rimb6 and cpr1 revealed a function of CPR1 in chloroplast stress protection. Expression studies in pathogen signaling mutants demonstrated that CPR1-mediated activation of genes for photosynthesis and chloroplast antioxidant protection is, in contrast to activation of pathogen responses, regulated independently from PAD4-controlled salicylic acid (SA) accumulation. We conclude that the support of plastid function is a basic, SA-independent function of CPR1
Hetrocyclic methacrylate systems as vehicles for the release of active species.
PhDThe room temperature polymerising heterocyclic polymer system, poly(ethyl
methacrylate)/tetrahydrofurfuryl methacrylate (PEM/THFM) has been shown
previously to be biocompatible and supported tissue repair, specifically for bone
and cartilage, and biologically inert when in contact with the dental pulp. It
proved more effective, than other glassy methacrylates in the release of active
species.
The PEM/THFM system is a rigid material. The aim of this study was to develop
and characterise the use of this system as a flexible patch, for application and
retention to the buccal mucosa, thus facilitating sustained regulated release.
Model species, dextrans, were used to represent macromolecular drugs whereby
the effect of molecular weight could be studied. N-methyl pyrrolidone was added
to the polymer system as a biocompatible plasticiser to enhance molecular
mobility, and hence the transport of species. The effect of the addition of chitosan
was also studied, due to its bioadhesiveness and permeation enhancing ability.
A range of systems was investigated both in terms of water and species release.
The release of the agent was measured by a fluorometer, the leachable
components by HPLC and Confocal microscopy demonstrated the transport of
water and active species through the system. Immunological and viability studies
established whether the leachants or released components of the polymeric
systems had an inflammatory or irritant action on `in vitro' stratified epithelium.
The addition of N-methyl pyrrolidone, dextran and chitosan substantially
increased water uptake, thus affecting the release kinetics. Analysis of the
kinetics of water uptake showed Case I, combination of Case I and Case II, and
Case II kinetics, depending on the systems studied. Dextran release was largely
diffusion controlled, from which diffusion coefficients were calculated; the
amount released varied between the systems studied
