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Publications - Stress and Develop Biology

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Publications

Clemens, S.; Toxic metal accumulation, responses to exposure and mechanisms of tolerance in plants Biochimie 88, 1707-1719, (2006) DOI: 10.1016/j.biochi.2006.07.003

Over the past 200 years emissions of toxic heavy metals have risen tremendously and significantly exceed those from natural sources for practically all metals. Uptake and accumulation by crop plants represents the main entry pathway for potentially health-threatening toxic metals into human and animal food. Of major concern are the metalloids arsenic (As) and selenium (Se), and the metals cadmium (Cd), mercury (Hg), and lead (Pb). This review discusses the molecular mechanisms of toxic metal accumulation in plants and algae, the responses to metal exposure, as well as our understanding of metal tolerance and its evolution. The main emphasis will be on cadmium, which is by far the most widely studied of the non-essential toxic metals/metalloids. Entry via Zn2+, Fe2+, and Ca2+ transporters is the molecular basis of Cd2+ uptake into plant cells. Much less is known about the partitioning of non-essential metals and about the genes underlying the enormous diversity among plants with respect to Cd accumulation in different tissues. Numerous studies have described symptoms and responses of plants upon toxic metal exposure. Mysterious are primary targets of toxicity, the degree of specificity of responses, the sensing and the signaling events that lead to transcriptional activation. All plants apparently possess a basal tolerance of toxic non-essential metals. For Cd and As, this is largely dependent on the phytochelatin pathway. Not understood is the molecular biology of Cd hypertolerance in certain plant species such as the metallophytes Arabidopsis halleri or Thlaspi caerulescens.
Books and chapters

Clemens, S.; Simm, C.; Maier, T.; Heavy Metal‐binding Proteins and Peptides (2005) DOI: 10.1002/3527600035.bpol8010

IntroductionHistorical OutlineChemical StructuresNomenclature and Structure of MetallothioneinsPhytochelatins and Phytochelatin–Metal ComplexesStructural Properties of MetallochaperonesChemical Analysis and DetectionMetallothioneinsPhytochelatinsOccurrenceMetallothioneinsPhytochelatinsMetallochaperonesFunctionsMetal Homeostasis and the Role of MetallochaperonesBuffering and DetoxificationPhytochelatin FunctionsMetallothionein FunctionsPhysiologyMetallothionein Localization and IsoformsLocalization and Compartmentation of Phytochelatin SynthesisBiochemistryMetal‐binding Characteristics of MetallothioneinsBiochemistry of Phytochelatin SynthesisMolecular GeneticsMetallothionein Genes and Their RegulationPhytochelatin Synthase GenesBiotechnological ApplicationsPatentsOutlook and Perspectives
Books and chapters

Scheel, D.; Nuernberger, T.; Signal Transduction in Plant Defense Responses to Fungal Infection 1-30, (2004)

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Books and chapters

Rosahl, S.; Feussner, I.; Oxylipins 329-354, (2004)

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Books and chapters

Lee, J.; Nürnberger, T.; Is Pore Formation Activity of HrpZ Required for Defence Activation in Plant Cells? 165-173, (2003) DOI: 10.1007/978-94-017-0133-4_18

The HrpZ gene product, harpin, is an export substrate of the type III secretion system of phytopathogenic Pseudomonas syringae. The role of this protein in pathogenesis is largely unknown. We previously determined that HrpZ binds to lipids and can form cation pores in synthetic lipid bilayers. Such pore-forming activity may allow nutrient release during bacterial colonisation of host plants. In addition. HrpZ is known to trigger plant defence responses in a variety of plants, such as tobacco. We have previously also characterised a binding site in tobacco plasma membranes that likely mediates HrpZ-induced defence responses. In order to reconcile these findings, we pose the question as to whether the activation of plant defence responses by HrpZ is mediated through a “classical” receptor perception mode or if plant membrane perturbation through the inherent pore-forming activity of HrpZ may induce defence responses. As defence in parsley cells can be induced both in a receptor-mediated manner or through ionophores these cells served as an ideal system for our analysis. We first performed ligand binding studies to characterise the presence of a binding site/receptor. We further digested HrpZ with endopeptidases and used subfragments of HrpZ to assess the elicitor-active domain of HrpZ. A C-terminal region of HrpZ appears to be sufficient to elicit plant defence responses. A novel assay involving dye-loaded liposomes was developed to validate previous electrophysiological findings on HrpZ-mediated cation pore formation. More importantly, this assay was used to establish if the elicitor-active C-terminal fragment of HrpZ could form pores. Our findings suggest that the structural requirements for ion pore formation and activation of plant defence responses by HrpZ are different. Thus, ion pore formation alone may not explain the activation of plant defence by HrpZ.
Books and chapters

Scheel, D.; Oxidative burst and the role of reactive oxygen species in plant-pathogen interactions (Inzé, D. & van Montagu, M., eds.). 137-153, (2002)

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Books and chapters

Clemens, S.; Thomine, S.; Schroeder, J. I.; Molecular mechanisms that control plant tolerance to heavy metals and possible roles towards manipulating metal accumulation 665-691, (2002)

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Books and chapters

Scheel, D.; Blume, B.; Brunner, F.; Fellbrich, G.; Dalbøge, H.; Hirt, H.; Kauppinen, S.; Kroj, T.; Ligterink, W.; Nürnberger, T.; Tschöpe, M.; Zinecker, H.; zur Nieden, U.; Receptor-mediated signal transduction in plant defense 131-135, (2000)

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Books and chapters

Bruns, I.; Sutter, K.; Neumann, D.; Krauss, G.-J.; Glutathione accumulation - a specific response of mosses to heavy metal stress 389-391, (2000)

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