The role of 9- and 13-lipoxygenase-derived oxylipins for race-cultivar-specific resistance in potato was analyzed by expressing RNA interference constructs against oxylipin biosynthetic genes in transgenic potato plants carrying the resistance gene R1 against Phytophthora infestans. Down-regulation of 9-lipoxygenase expression resulted in highly reduced levels of 9-hydroxyoctadecatrienoic acid after treatment with the pathogen-associated molecular pattern Pep-13. However, neither 9-lipoxygenase nor 9-divinyl ether synthase RNAi plants exhibited alterations in their resistance to P. infestans. Similarly, successful down-regulation of transcript accumulation of the 13-lipoxygenase pathway genes encoding allene oxide cyclase, 12-oxophytodienoic acid reductase 3 and the jasmonic acid receptor coronatine-insensitive 1 resulted in highly reduced levels of jasmonic acid after Pep-13 treatment. Race-cultivar-specific resistance, however, was not lost in these plants. Our results suggest that neither 9-lipoxygenase-derived oxylipins nor jasmonic acid are required for R-gene-mediated resistance in potato. Importantly, in tobacco, the silencing of 9-lipoxygenase expression was previously demonstrated to suppress race-cultivar-specific resistance. Thus, we conclude a differential requirement of oxylipins for R-gene-mediated resistance in different solanaceous plants.

Inducing systemic resistance responses in crop plants is a promising alternative way of disease management. To understand the underlying signaling events leading to induced resistance, functional analyses of plants defective in defined signaling pathway steps are required. We used potato, one of the economically most-important crop plants worldwide, to examine systemic resistance against the devastating late blight pathogen Phytophthora infestans, induced by treatment with dl-β-aminobutyric acid (BABA). Transgenic plants impaired in either the 9-lipoxygenase pathway, which produces defense-related compounds, or the 13-lipoxygenase pathway, which generates jasmonic acid–derived signals, expressed wild-type levels of BABA-induced resistance. Plants incapable of accumulating salicylic acid (SA), on the other hand, failed to mount this type of induced resistance. Consistently, treatment of these plants with the SA analog 2,6-dichloroisonicotinic acid restored BABA-induced resistance. Together, these results demonstrate the indispensability of a functional SA pathway for systemic resistance in potato induced by BABA.

Control over crystal growth by acidic matrix macromolecules is an important process in the formation of many mineralized tissues. Highly acidic macromolecules are postulated intermediates in tissue mineralization, because they sequester many calcium ions and occur in high concentrations at mineralizing foci in distantly related organisms. A prerequisite for biomineralization is the ability of cations like calcium to bind to proteins and to result in concert with appropriate anions like phosphates or carbonates in composite materials with bone‐like properties. For this mineralization process the proteins have to be modified with respect to acidification. In this study we modified the protein collagen by carboxymethylation using glucuronic acid. Our experiments showed unambigously, that Nε‐carboxymethyllysine is the major product of the in vitro nonenzymatic glycation reaction between glucuronic acid and collagen. We hypothesized that the function of biomimetically carboxymethylated collagen is to increase the local concentration of corresponding ions so that a critical nucleus of ions can be formed, leading to the formation of the mineral. Thus, the self‐organization of HAP nanocrystals on and within collagen fibrils was intensified by carboxymethylation.

Many tumor cells exhibit a disturbed intracellular redox state resulting in higher levels of reactive oxygen species (ROS). As these contribute to tumor initiation and sustenance, catalytic redox agents combining significant activity with substrate specificity promise high activity and selectivity against oxidatively stressed malignant cells. We describe here the design and synthesis of novel organochalcogen based redox sensor/effector catalysts. Their selective anticancer activity at submicromolar and low micromolar concentrations was established here in a range of tumor entities in various biological systems including cell lines, primary tumor cell cultures, and animal models. In the B-cell derived chronic lymphocytic leukemia (CLL), for instance, such compounds preferentially induce apoptosis in the cancer cells while peripheral blood mononuclear cells (PBMC) from healthy donors and the subset of normal B-cells remain largely unaffected. In support of the concept of sensor/effector based ROS amplification, we are able to demonstrate that underlying this selective activity against CLL cells are pre-existing elevated ROS levels in the leukemic cells compared to their nonmalignant counterparts. Furthermore, the catalysts act in concert with certain chemotherapeutic drugs in several carcinoma cell lines to decrease cell proliferation while showing no such interactions in normal cells. Overall, the high efficacy and selectivity of (redox) catalytic sensor/effector compounds warrant further, extensive testing toward transfer into the clinical arena.

Plant growth and proliferation control is coming into a global focus due to recent ecological and economical developments. Plants represent not only the largest food supply for mankind but also may serve as a global source of renewable energies. However, plant breeding has to accomplish a tremendous boost in yield to match the growing demand of a still rapidly increasing human population. Moreover, breeding has to adjust to changing environmental conditions, in particular increased drought. Regulation of cell-cycle control is a major determinant of plant growth and therefore an obvious target for plant breeding. Furthermore, cell-cycle control is also crucial for the DNA damage response, for instance upon irradiation. Thus, an in-depth understanding of plant cell-cycle regulation is of importance beyond a scientific point of view. The mere presence of many conserved core cell-cycle regulators, e.g. CDKs, cyclins, or CDK inhibitors, has formed the idea that the cell cycle in plants is exactly or at least very similarly controlled as in yeast or human cells. Here together with a recent publication we demonstrate that this dogma is not true and show that the control of entry into mitosis is fundamentally different in plants versus yeast or metazoans. Our findings build an important base for the understanding and ultimate modulation of plant growth not only during unperturbed but also under harsh environmental conditions.

In Arabidopsis, deactivation of cyclin-dependent kinases via phosphorylation has no function in cell proliferation, growth, and stress response. In other eukaryotes, however, this is mandatorily required for maintaining genomic integrity.

Natural variation has been observed for various traits in Arabidopsis thaliana. Here, we investigated natural variation in the context of physiological and transcriptional responses to the phytohormone auxin, a key regulator of plant development. A survey of the general extent of natural variation to auxin stimuli revealed significant physiological variation among 20 genetically diverse natural accessions. Moreover, we observed dramatic variation on the global transcriptome level after induction of auxin responses in seven accessions. Although we detect isolated cases of major-effect polymorphisms, sequencing of signaling genes revealed sequence conservation, making selective pressures that favor functionally different protein variants among accessions unlikely. However, coexpression analyses of a priori defined auxin signaling networks identified variations in the transcriptional equilibrium of signaling components. In agreement with this, cluster analyses of genome-wide expression profiles followed by analyses of a posteriori defined gene networks revealed accession-specific auxin responses. We hypothesize that quantitative distortions in the ratios of interacting signaling components contribute to the detected transcriptional variation, resulting in physiological variation of auxin responses among accessions.

Protein phosphorylation/dephosphorylation is a central post‐translational modification in plant hormone signaling, but little is known about its extent and function. Although pertinent protein kinases and phosphatases have been predicted and identified for a variety of hormone responses, classical biochemical approaches have so far revealed only a few candidate proteins and even fewer phosphorylation sites. Here we performed a global quantitative analysis of the Arabidopsis phosphoproteome in response to a time course of treatments with various plant hormones using phosphopeptide enrichment and subsequent mass accuracy precursor alignment (MAPA). The use of three time points, 1, 3 and 6 h, in combination with five phytohormone treatments, abscisic acid (ABA), indole‐3‐acetic acid (IAA), gibberellic acid (GA), jasmonic acid (JA) and kinetin, resulted in 324 000 precursor ions from 54 LC‐Orbitrap‐MS analyses quantified and aligned in a data matrix with the dimension of 6000 × 54 using the ProtMax algorithm. To dissect the phytohormone responses, multivariate principal/independent components analysis was performed. In total, 152 phosphopeptides were identified as differentially regulated; these phosphopeptides are involved in a wide variety of signaling pathways. New phosphorylation sites were identified for ABA response element binding factors that showed a specific increase in response to ABA. New phosphorylation sites were also found for RLKs and auxin transporters. We found that different hormones regulate distinct amino acid residues of members of the same protein families. In contrast, tyrosine phosphorylation of the Gα subunit appeared to be a common response for multiple hormones, demonstrating global cross‐talk among hormone signaling pathways.

The endophytic fungus Piriformospora indica colonizes the roots of the model plant Arabidopsis thaliana and promotes its growth and seed production. The fungus can be cultivated in axenic culture without a host, and therefore this is an excellent system to investigate plant–fungus symbiosis.The growth of etr1, ein2 and ein3/eil1 mutant plants was not promoted or even inhibited by the fungus; the plants produced less seeds and the roots were more colonized compared with the wild‐type. This correlates with a mild activation of defence responses. The overexpression of ETHYLENE RESPONSE FACTOR1 constitutively activated defence responses, strongly reduced root colonization and abolished the benefits for the plants.Piriformospora indica‐mediated stimulation of growth and seed yield was not affected by jasmonic acid, and jasmonic acid‐responsive promoter β‐glucuronidase gene constructs did not respond to the fungus in Arabidopsis roots.We propose that ethylene signalling components and ethylene‐targeted transcription factors are required to balance beneficial and nonbeneficial traits in the symbiosis. The results show that the restriction of fungal growth by ethylene signalling components is required for the beneficial interaction between the two symbionts.

The identity of the auxin receptor(s) and the mechanism of auxin perception has been a subject of intense interest since the discovery of auxin almost a century ago. The development of genetic approaches to the study of plant hormone signaling led to the discovery that auxin acts by promoting degradation of transcriptional repressors called Aux/IAA proteins. This process requires a ubiquitin protein ligase (E3) called SCFTIR1 and related SCF complexes. Surprisingly, auxin works by directly binding to TIR1, the F-box protein subunit of this SCF. Structural studies demonstrate that auxin acts like a “molecular glue,” to stabilize the interaction between TIR1 and the Aux/IAA substrate. These exciting results solve an old problem in plant biology and reveal new mechanisms for E3 regulation and hormone perception.