Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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    Leucine-rich repeat receptor-like kinase II phylogenetics reveals five main clades throughout the plant kingdom
    Hosseini, Samin ; Schmidt, Ed D.L. ; Bakker, Freek T. - \ 2020
    The Plant Journal 103 (2020)2. - ISSN 0960-7412 - p. 547 - 560.
    kinase - leucine-rich repeat receptor - LRR-RLKII - phylogeny - SERK

    Receptor-like kinases (RLKs) represent the largest group of cell surface receptors in plants. The monophyletic leucine-rich repeat (LRR)-RLK subfamily II is considered to contain the somatic embryogenesis receptor kinases (SERKs) and NSP-interacting kinases known to be involved in developmental processes and cellular immunity in plants. There are only a few published studies on the phylogenetics of LRR-RLKII; unfortunately these suffer from poor taxon/gene sampling. Hence, it is not clear how many and what main clades this family contains, let alone what structure–function relationships exist. We used 1342 protein sequences annotated as ‘SERK’ and ‘SERK-like’ plus related sequences in order to estimate phylogeny within the LRR-RLKII clade, using the nematode protein kinase Pelle as an outgroup. We reconstruct five main clades (LRR-RLKII 1–5), in each of which the main pattern of land plant relationships re-occurs, confirming previous hypotheses that duplication events happened in this gene subfamily prior to divergence among land plant lineages. We show that domain structures and intron–exon boundaries within the five clades are well conserved in evolution. Furthermore, phylogenetic patterns based on the separate LRR and kinase parts of LRR-RLKs are incongruent: whereas the LRR part supports a LRR-RLKII 2/3 sister group relationship, the kinase part supports clades 1/2. We infer that the kinase part includes few ‘radical’ amino acid changes compared with the LRR part. Finally, our results confirm that amino acids involved in each LRR-RLKII–receptor complex interaction are located at N-capping residues, and that the short amino acid motifs of this interaction domain are highly conserved throughout evolution within the five LRR-RLKII clades.

    Systemic Regulation of RAS/MAPK Signaling by the Serotonin Metabolite 5-HIAA
    Schmid, T. ; Snoek, L.B. ; Fröhli, E. ; Bent, M.L. van der; Kammenga, J.E. ; Hajnal, A. - \ 2015
    Plos Genetics 11 (2015)5. - ISSN 1553-7404 - 16 p.
    caenorhabditis-elegans - c-elegans - natural variation - vulvar induction - complex disease - receptor - protein - gene - kinase - activation
    Human cancer is caused by the interplay of mutations in oncogenes and tumor suppressor genes and inherited variations in cancer susceptibility genes. While many of the tumor initiating mutations are well characterized, the effect of genetic background variation on disease onset and progression is less understood. We have used C. elegans genetics to identify genetic modifiers of the oncogenic RAS/MAPK signaling pathway. Quantitative trait locus analysis of two highly diverged C. elegans isolates combined with allele swapping experiments identified the polymorphic monoamine oxidase A (MAOA) gene amx-2 as a negative regulator of RAS/MAPK signaling. We further show that the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA), which is a product of MAOA catalysis, systemically inhibits RAS/MAPK signaling in different organs of C. elegans. Thus, MAOA activity sets a global threshold for MAPK activation by controlling 5-HIAA levels. To our knowledge, 5-HIAA is the first endogenous small molecule that acts as a systemic inhibitor of RAS/MAPK signaling.
    Successful validation of genomic biomarkers for human immunotoxicity in Jurkat T cells in vitro
    Schmeits, P.C.J. ; Shao, J. ; Krieken, D.A. van der; Volger, O.L. ; Loveren, H. van; Peijnenburg, A.A.C.M. ; Hendriksen, P.J.M. - \ 2015
    Journal of Applied Toxicology 35 (2015)7. - ISSN 0260-437X - p. 831 - 841.
    polycyclic aromatic-hydrocarbons - brominated flame retardants - tetrabromobisphenol-a - balb/c mice - vitamin-c - chlorpyrifos - activation - exposure - rats - kinase
    Previously, we identified 25 classifier genes that were able to assess immunotoxicity using human Jurkat T cells. The present study aimed to validate these classifiers. For that purpose, Jurkat cells were exposed for 6¿h to subcytotoxic doses of nine immunotoxicants, five non-immunotoxicants and four compounds for which human immunotoxicity has not yet been fully established. RNA was isolated and subjected to Fluidigm quantitative real time (qRT)–PCR analysis. The sensitivity, specificity and accuracy of the screening assay as based on the nine immunotoxicants and five non-immunotoxicants used in this study were 100%, 80% and 93%, respectively, which is better than the performance in our previous study. Only one compound was classified as false positive (benzo-e-pyrene). Of the four potential (non-)immunotoxicants, chlorantraniliprole and Hidrasec were classified immunotoxic and Sunset yellow and imidacloprid as non-immunotoxic. ToxPi analysis of the PCR data provided insight in the molecular pathways that were affected by the compounds. The immunotoxicants 2,3-dichloro-propanol and cypermethrin, although structurally different, affected protein metabolism and cholesterol biosynthesis and transport. In addition, four compounds, i.e.¿chlorpyrifos, aldicarb, benzo-e-pyrene and anti-CD3, affected genes in cholesterol metabolism and transport, protein metabolism and transcription regulation. qRT–PCR on eight additional genes coding for similar processes as defined in ToxPi analyzes, supported these results. In conclusion, the 25 immunotoxic classifiers performed very well in a screening with new non-immunotoxic and immunotoxic compounds. Therefore, the Jurkat screening assay has great promise to be applied within a tiered approach for animal free testing of human immunotoxicity.
    Natural loss-of-function mutation of EDR1 conferring resistance to tomato powdery mildew in Arabidopsis thaliana accession C24
    Gao, D. ; Appiano, M. ; Huibers, R.P. ; Loonen, A.E.H.M. ; Visser, R.G.F. ; Wolters, A.M.A. ; Bai, Y. - \ 2015
    Molecular Plant Pathology 16 (2015)1. - ISSN 1464-6722 - p. 71 - 82.
    salicylic-acid - downy mildew - gene - defense - plants - microsatellites - mechanism - evolution - cloning - kinase
    To screen for potentially novel types of resistance to tomato powdery mildew Oidium neolycopersici, a disease assay was performed on 123 Arabidopsis thaliana accessions. Forty accessions were fully resistant, and one, C24, was analysed in detail. By quantitative trait locus (QTL) analysis of an F2 population derived from C24 × Sha (susceptible accession), two QTLs associated with resistance were identified in C24. Fine mapping of QTL-1 on chromosome 1 delimited the region to an interval of 58¿kb encompassing 15 candidate genes. One of these was Enhanced Disease Resistance 1 (EDR1). Evaluation of the previously obtained edr1 mutant of Arabidopsis accession Col-0, which was identified because of its resistance to powdery mildew Golovinomyces cichoracearum, showed that it also displayed resistance to O.¿neolycopersici. Sequencing of EDR1 in our C24 germplasm (referred to as C24-W) revealed two missing nucleotides in the second exon of EDR1 resulting in a premature stop codon. Remarkably, C24 obtained from other laboratories does not contain the EDR1 mutation. To verify the identity of C24-W, a DNA region containing a single nucleotide polymorphism (SNP) unique to C24 was sequenced showing that C24-W contains the C24-specific nucleotide. C24-W showed enhanced resistance to O.¿neolycopersici compared with C24 not containing the edr1 mutation. Furthermore, C24-W displayed a dwarf phenotype, which was not associated with the mutation in EDR1 and was not caused by the differential accumulation of pathogenesis-related genes. In conclusion, we identified a natural edr1 mutant in the background of C24.
    MAP3K8 (TPL2/COT) Affects Obesity-Induced Adipose Tissue Inflammation without Systemic Effects in Humans and in Mice
    Ballak, D.B. ; Essen, P. van; Diepen, J.A. van; Jansen, H. ; Hijmans, A. ; Matsuguchi, T. ; Sparrer, H. ; Tack, C.J. ; Netea, M.G. ; Joosten, L.A. ; Stienstra, R. - \ 2014
    PLoS ONE 9 (2014)2. - ISSN 1932-6203 - 8 p.
    insulin-resistance - kinase - oncoprotein - disease - tpl-2
    Chronic low-grade inflammation in adipose tissue often accompanies obesity, leading to insulin resistance and increasing the risk for metabolic diseases. MAP3K8 (TPL2/COT) is an important signal transductor and activator of pro-inflammatory pathways that has been linked to obesity-induced adipose tissue inflammation. We used human adipose tissue biopsies to study the relationship of MAP3K8 expression with markers of obesity and expression of pro-inflammatory cytokines (IL-1ß, IL-6 and IL-8). Moreover, we evaluated obesity-induced adipose tissue inflammation and insulin resistance in mice lacking MAP3K8 and WT mice on a high-fat diet (HFD) for 16 weeks. Individuals with a BMI >30 displayed a higher mRNA expression of MAP3K8 in adipose tissue compared to individuals with a normal BMI. Additionally, high mRNA expression levels of IL-1ß, IL-6 and IL-8, but not TNF -a, in human adipose tissue were associated with higher expression of MAP3K8. Moreover, high plasma SAA and CRP did not associate with increased MAP3K8 expression in adipose tissue. Similarly, no association was found for MAP3K8 expression with plasma insulin or glucose levels. Mice lacking MAP3K8 had similar bodyweight gain as WT mice, yet displayed lower mRNA expression levels of IL-1ß, IL-6 and CXCL1 in adipose tissue in response to the HFD as compared to WT animals. However, MAP3K8 deficient mice were not protected against HFD-induced adipose tissue macrophage infiltration or the development of insulin resistance. Together, the data in both human and mouse show that MAP3K8 is involved in local adipose tissue inflammation, specifically for IL-1ß and its responsive cytokines IL-6 and IL-8, but does not seem to have systemic effects on insulin resistance.
    Nod factor receptors form heteromeric complexes and are essential for intracellular infection in Medicago nodules
    Moling, S. ; Pietraszewska-Bogiel, A. ; Postma, M. ; Fedorova, E.E. ; Hink, M.A. ; Limpens, E.H.M. ; Gadella, T.W.J. ; Bisseling, T. - \ 2014
    The Plant Cell 26 (2014)10. - ISSN 1040-4651 - p. 4188 - 4199.
    rhizobium-leguminosarum - n-2-fixing symbiosomes - root-nodules - kinase - truncatula - arabidopsis - lyk3 - phosphorylation - perception - nodulation
    Rhizobial Nod factors are the key signaling molecules in the legume-rhizobium nodule symbiosis. In this study, the role of the Nod factor receptors NOD FACTOR PERCEPTION (NFP) and LYSIN MOTIF RECEPTOR-LIKE KINASE3 (LYK3) in establishing the symbiotic interface in root nodules was investigated. It was found that inside Medicago truncatula nodules, NFP and LYK3 localize at the cell periphery in a narrow zone of about two cell layers at the nodule apex. This restricted accumulation is narrower than the region of promoter activity/mRNA accumulation and might serve to prevent the induction of defense-like responses and/or to restrict the rhizobium release to precise cell layers. The distal cell layer where the receptors accumulate at the cell periphery is part of the meristem, and the proximal layer is part of the infection zone. In these layers, the receptors can most likely perceive the bacterial Nod factors to regulate the formation of symbiotic interface. Furthermore, our Förster resonance energy transfer-fluorescence lifetime imaging microscopy analysis indicates that NFP and LYK3 form heteromeric complexes at the cell periphery in M. truncatula nodules.
    Prediction uncertainty assessment of a systems biology model requires a sample of the full probability distribution of its parameters
    Mourik, S. van; Braak, C.J.F. ter; Stigter, J.D. ; Molenaar, J. - \ 2014
    PeerJ 2 (2014). - ISSN 2167-8359 - 17 p.
    identifiability analysis - regulatory networks - experimental-design - profile likelihood - sloppy models - oscillations - proteins - cyclin - kinase - cdc2
    Multi-parameter models in systems biology are typically ‘sloppy’: some parameters or combinations of parameters may be hard to estimate from data, whereas others are not. One might expect that parameter uncertainty automatically leads to uncertain predictions, but this is not the case. We illustrate this by showing that the prediction uncertainty of each of six sloppy models varies enormously among different predictions. Statistical approximations of parameter uncertainty may lead to dramatic errors in prediction uncertainty estimation. We argue that prediction uncertainty assessment must therefore be performed on a per-prediction basis using a full computational uncertainty analysis. In practice this is feasible by providing a model with a sample or ensemble representing the distribution of its parameters. Within a Bayesian framework, such a sample may be generated by a Markov Chain Monte Carlo (MCMC) algorithm that infers the parameter distribution based on experimental data. Matlab code for generating the sample (with the Differential Evolution Markov Chain sampler) and the subsequent uncertainty analysis using such a sample, is supplied as Supplemental Information.
    A Versatile Toolkit to Produce Sensitive FRET Biosensors to Visualize Signaling in Time and Space
    Fritz, R.D. ; Letzelter, M. ; Reimann, A. ; Martin, K. ; Fusco, L. ; Ritsma, L. ; Ponsioen, B. ; Fluri, E. ; Schulte-Merker, S. ; Rheenen, J. ; Pertz, O. - \ 2013
    Science Signaling 6 (2013)285. - ISSN 1945-0877
    cyan fluorescent protein - rho-family gtpases - dynamic-range - living cells - in-vivo - activation - kinase - cdc42 - indicators - reporters
    Genetically encoded, ratiometric biosensors based on fluorescence resonance energy transfer (FRET) are powerful tools to study the spatiotemporal dynamics of cell signaling. However, many biosensors lack sensitivity. We present a biosensor library that contains circularly permutated mutants for both the donor and acceptor fluorophores, which alter the orientation of the dipoles and thus better accommodate structural constraints imposed by different signaling molecules while maintaining FRET efficiency. Our strategy improved the brightness and dynamic range of preexisting RhoA and extracellular signal–regulated protein kinase (ERK) biosensors. Using the improved RhoA biosensor, we found micrometer-sized zones of RhoA activity at the tip of F-actin bundles in growth cone filopodia during neurite extension, whereas RhoA was globally activated throughout collapsing growth cones. RhoA was also activated in filopodia and protruding membranes at the leading edge of motile fibroblasts. Using the improved ERK biosensor, we simultaneously measured ERK activation dynamics in multiple cells using low-magnification microscopy and performed in vivo FRET imaging in zebrafish. Thus, we provide a construction toolkit consisting of a vector set, which enables facile generation of sensitive biosensors.
    Hedgehog signaling via a calcitonin receptor-like receptor can induce arterial differentiation independently of VEGF signaling in zebrafish
    Wilkinson, R.N. ; Koudijs, M.J. ; Patient, R.K. ; Ingham, P.W. ; Schulte-Merker, S. ; Eeden, F.J.M. van - \ 2012
    Blood : journal of the American Society of Hematology 120 (2012)2. - ISSN 0006-4971 - p. 477 - 488.
    endothelial-growth-factor - embryonic vascular development - hematopoietic stem-cells - aortic endothelium - sonic-hedgehog - pathway - notch - blood - gene - kinase
    Multiple signaling pathways control the specification of endothelial cells (ECs) to become arteries or veins during vertebrate embryogenesis. Current models propose that a cascade of Hedgehog (Hh), vascular endothelial growth factor (VEGF), and Notch signaling acts instructively on ECs to control the choice between arterial or venous fate. Differences in the pheno-types induced by Hh, VEGF, or Notch inhibition suggest that not all of the effects of Hh on arteriovenous specification are mediated by VEGF. We establish that full derepression of the Hh pathway in ptc1;ptc2 mutants converts the posterior cardinal vein into a second arterial vessel that manifests intact arterial gene expression, intersegmental vessel sprouting, and HSC gene expression. Importantly, although VEGF was thought to be absolutely essential for arterial fates, we find that normal and ectopic arterial differentiation can occur without VEGF signaling in ptc1; ptc2 mutants. Furthermore, Hh is able to bypass VEGF to induce arterial differentiation in ECs via the calcitonin receptor-like receptor, thus revealing a surprising complexity in the interplay between Hh and VEGF signaling during arteriovenous specification. Finally, our experiments establish a dual function of Hh during induction of runx1(+) HSCs. (Blood. 2012;120(2):477-488)
    Apple extract induces increased epithelial resistance and claudin 4 expression in Caco-2 cells
    Vreeburg, R.A.M. ; Wezel, E.E. van; Ocana-Calahorro, F. ; Mes, J.J. - \ 2012
    Journal of the Science of Food and Agriculture 92 (2012)2. - ISSN 0022-5142 - p. 439 - 444.
    tight junction permeability - intestinal barrier function - in-vitro - disease - absorption - mechanisms - monolayer - kinase
    BACKGROUND: The small intestinal epithelium functions both to absorb nutrients, and to provide a barrier between the outside, luminal, world and the human body. One of the passageways across the intestinal epithelium is paracellular diffusion, which is controlled by the properties of tight junction complexes. We used a differentiated Caco-2 monolayer as a model for small intestinal epithelium to study the effect of crude apple extracts on paracellular permeability. RESULTS: Exposure of crude apple homogenate to the differentiated Caco-2 cells increased the paracellular resistance, determined as trans-epithelial electrical resistance (TEER). This increase was linearly related to the concentration of apple present. The TEER-enhancing effect of apple extract was due to factors mainly present in the cortex, and the induction was not inhibited by protein kinase inhibitors. Apple-induced resistance was accompanied by increased expression of several tight junction related genes, including claudin 4 (CLDN4). CONCLUSION: Crude apple extract induces a higher paracellular resistance in differentiated Caco-2 cells. Future research will determine whether these results can be extrapolated to human small intestinal epithelia
    Gene transcription analysis during interaction between potato and Ralstonia solanacearum
    Li, G.C. ; Jin, L.P. ; Wang, X.W. ; Xie, K.Y. ; Yang, Y. ; Vossen, E.A.G. van der; Huang, S.W. ; Qu, D.Y. - \ 2010
    Russian Journal of Plant Physiology 57 (2010)5. - ISSN 1021-4437 - p. 685 - 695.
    hypersensitive response - bacterial wilt - chitinase gene - resistance - arabidopsis - domain - expression - kinase - rice - phosphatase
    Bacterial wilt (BW) caused by Ralstonia solanacearum (Rs) is an important quarantine disease that spreads worldwide and infects hundreds of plant species. The BW defense response of potato is a complicated continuous process, which involves transcription of a battery of genes. The molecular mechanisms of potato-Rs interactions are poorly understood. In this study, we combined suppression subtractive hybridization and macroarray hybridization to identify genes that are differentially expressed during the incompatible interaction between Rs and potato. In total, 302 differentially expressed genes were identified and classified into 12 groups according to their putative biological functions. Of 302 genes, 81 were considered as Rs resistance-related genes based on the homology to genes of known function, and they have putative roles in pathogen recognition, signal transduction, transcription factor functioning, hypersensitive response, systemic acquired resistance, and cell rescue and protection. Additionally, 50 out of 302 genes had no match or low similarity in the NCBI databases, and they may represent novel genes. Of seven interesting genes analyzed via RNA gel blot and semi-quantitative RT-PCR, six were induced, one was suppressed, and all had different transcription patterns. The results demonstrate that the response of potato against Rs is rapid and involves the induction of numerous various genes. The genes identified in this study add to our knowledge of potato resistance to Rs.
    Protien expression profiling of mouse thymoma upon exposure to the tricothecene deoxynivalenol (DON) Implications for its mechanism of action
    Osman, A.M. ; Pennings, J.L.A. ; Blokland, M.H. ; Peijnenburg, A.A.C.M. ; Loveren, H. van - \ 2010
    Journal of Immunotoxicology 7 (2010)3. - ISSN 1547-691X - p. 147 - 156.
    ribotoxic stress-response - myb-binding-protein - gene-expression - vomitoxin deoxynivalenol - proteomic analysis - induced apoptosis - immune-response - cdna-clones - activation - kinase
    The objective of this work was to investigate whether proteomic analysis of thymoma cells treated with the trichothecene deoxynivalenol (DON) as compared to non-treated (control) cells would reveal differential protein expression, and thus would contribute to a better understanding of the mechanisms of its toxicity. For that purpose the mouse thymoma cell line EL4 was exposed to 0.5 microM DON for 6 hr. A total of 30 proteins were affected after exposure of EL4 cells to DON. Most of these proteins were up-regulated and included key metabolic enzymes (e.g., fatty acid synthase, aldose reductase, carbamoyl phosphate synthetase, glucose-6-phosphate isomerase), chaperones (e.g., HSP9AB1 and HSP70), enzymes implicated in protein folding (PDI and ERO1-l alpha), and proteins involved in protein degradation (ubiquitin-conjugating enzyme (E1) and proteasome subunit alpha type-1). In addition, an IgE-binding protein with a molecular weight of 60 kDa and My-binding protein 1a (MYBBP1A), a transcription factor, were found to be up-regulated by DON. The observed up-regulation of MYBBP1A, a known repressor of a number of transcription factors such as PGC-1 alpha, C-myb, and p65 of the NF-kappaB family, suggests that this protein might play a role in the mechanism of DON toxicity.
    Angiopoietin-Like 4 Interacts with Integrins ß1 and ß5 to Modulate Keratinocyte Migration
    Goh, Y.Y. ; Pal, M. ; Chong, H.C. ; Zhu, P. ; Tan, M.J. ; Punugu, L. ; Lam, C.R.I. ; Yau, Y.H. ; Tan, C.K. ; Huang, R.L. ; Tan, S. ; Yang Tang, M.B. ; Ling Ding, J. ; Kersten, A.H. ; Tan, N.S. - \ 2010
    American Journal of Pathology 177 (2010)6. - ISSN 0002-9440 - p. 2791 - 2803.
    induced adipose factor - cell-migration - alpha-6-beta-4 integrin - in-vivo - protein - kinase - expression - repair - metastasis - inhibition
    Adipose tissue secretes adipocytokines for energy homeostasis, but recent evidence indicates that some adipocytokines also have a profound local impact on wound healing. Upon skin injury, keratinocytes use various signaling molecules to promote reepithelialization for efficient wound closure. In this study, we identify a novel function of adipocytokine angiopoietin-like 4 (ANGPTL4) in keratinocytes during wound healing through the control of both integrin-mediated signaling and internalization. Using two different in vivo models based on topical immuno-neutralization of ANGPTL4 as well as ablation of the ANGPTL4 gene, we show that ANGPTL4-deficient mice exhibit delayed wound reepithelialization with impaired keratinocyte migration. Human keratinocytes in which endogenous ANGPTL4 expression was suppressed by either siRNA or a neutralizing antibody show impaired migration associated with diminished integrin-mediated signaling. Importantly, we identify integrins ß1 and ß5, but not ß3, as novel binding partners of ANGPTL4. ANGPTL4-bound integrin ß1 activated the FAK-Src-PAK1 signaling pathway, which is important for cell migration. The findings presented herein reveal an unpredicted role of ANGPTL4 during wound healing and demonstrate how ANGPTL4 stimulates intracellular signaling mechanisms to coordinate cellular behavior. Our findings provide insight into a novel cell migration control mechanism and underscore the physiological importance of the modulation of integrin activity in cancer metastasis
    Genetic susceptibility to respiratory syncytial virus bronchiolitis in preterm childeren is asosiated with airway remodeling genes and innate immune genes
    Siezen, C.L.E. ; Hodemaekers, H.M. ; Ermers, M.J. ; Doornbos, G. ; Slot, R. van 't; Wijmenga, I.C. ; Houwelingen, H.C. ; Kimpen, J.L.L. ; Kimman, T.G. ; Hoebee, B. ; Janssen, R. - \ 2009
    The Pediatric Infectious Disease Journal 28 (2009)4. - ISSN 0891-3668 - p. 333 - 335.
    interferon signal-transduction - lung-function - asthma - polymorphisms - adam33 - disease - kinase
    Prematurity is a risk factor for severe respiratory syncytial virus bronchiolitis. We show that genetic factors in innate immune genes (IFNA13, IFNAR2, STAT2, IL27, NFKBIA, C3, IL1RN, TLR5), in innate and adaptive immunity (IFNG), and in airway remodeling genes (ADAM33 and TGFBR1), affect disease susceptibility to a different extent in preterm children, born with underdeveloped lungs, than in term children
    Combined Genetic and Modeling Approaches Reveal That Epidermal Cell Area and Number in Leaves Are Controlled by Leaf and Plant Developmental Processes in Arabidopsis
    Tisne, S. ; Reymond, M. ; Vile, D. ; Fabre, J. ; Dauzat, M. ; Koornneef, M. ; Granier, C. - \ 2008
    Plant Physiology 148 (2008). - ISSN 0032-0889 - p. 1117 - 1127.
    quantitative trait loci - soil-water deficit - organ shape - thaliana - growth - expansion - erecta - kinase - division - cycle
    Both leaf production and leaf expansion are tightly linked to cell expansion and cell division, but the functional relationships between all these variables are not clearly established. To get insight into these relationships, a quantitative genetic analysis was performed in 118 recombinant inbred lines derived from a cross between the Landsberg erecta and Antwerp accessions and was combined with a structural equation modeling approach. Main effects and epistatic interactions at the quantitative trait locus (QTL) level were detected for rosette area, rosette leaf number, leaf 6 area, epidermal cell area and number. A QTL at ERECTA marker (ER) controlled cell expansion and cell division, in interaction with two other QTLs at SNP295 and SNP21 markers. Moreover, both the screening for marker association involved in the variation of the relationships between leaf growth variables and the test of alternative functional models by structural equation modeling revealed that the allelic value at ER controlled epidermal cell area and epidermal cell number in a leaf. These effects are driven both by a whole plant mechanism associated with leaf production and by a single leaf mechanism associated with leaf expansion. The complex effects of the QTL at ER were validated in selected heterogeneous inbred families. The ERECTA gene, which is mutated in the Landsberg erecta parental line, was found to be a putative candidate responsible for these mapped effects by phenotyping mutants of this gene at the cellular level. Together, these results give insight into the complex determination of leaf epidermal cell number and area
    Plasma Membrane Receptor Complexes
    Aker, J.C.M. ; Vries, S.C. de - \ 2008
    Plant Physiology 147 (2008). - ISSN 0032-0889 - p. 1560 - 1564.
    brassinosteroid signal-transduction - box protein tir1 - aaa-atpase - auxin receptor - in-vitro - arabidopsis - kinase - endocytosis - regulator - bak1
    Recent data on the plasma membrane (PM)-located LRR-RLKs (for Leu-rich repeat receptor-like kinases) BRI1 (for brassinosteroid insensitive 1) and the coreceptors BAK1 (for BRI1-associated kinase 1) and SERK1 (for somatic embryogenesis receptor-like kinase 1) that participate in the perception of brassinosteroids (BRs) suggest that they are organized into heterooligomeric protein complexes. Other components of this complex include members of the 14-3-3 family, and, in the case of SERK1, the kinase-associated protein phosphatase (KAPP) and the AAA ATPase cell division cycle 48A (CDC48A). CDC48 proteins interact with ubiquitinated target proteins in animal and plant cells. In this Update we describe the role of several of the nonreceptor partners of the PM receptor complex with an emphasis on the role of CDC48 proteins in translocation and ubiquitination as a proposed mode of regulation of plant PM receptors.
    A genome-wide functional investigation into the roles of receptor-like proteins in Arabidopsis
    Guodong Wang, G. ; Ellendorff, U. ; Kemp, B. ; Mansfield, J.W. ; Forsyth, A. ; Mitchell, K. ; Bastas, K. ; Liu, C.M. ; Woods-Tör, A. ; Zipfel, C. ; Wit, P.J.G.M. de; Jones, J.D.G. ; Tör, M. ; Thomma, B.P.H.J. - \ 2008
    Plant Physiology 147 (2008). - ISSN 0032-0889 - p. 503 - 517.
    leucine-rich repeat - disease resistance genes - cladosporium-fulvum - pseudomonas-syringae - microbial pathogens - systemic resistance - flower development - plant-pathogen - kinase - thaliana
    Receptor-like proteins (RLPs) are cell surface receptors that typically consist of an extracellular leucine-rich repeat domain, a transmembrane domain, and a short cytoplasmatic tail. In several plant species, RLPs have been found to play a role in disease resistance, such as the tomato (Solanum lycopersicum) Cf and Ve proteins and the apple (Malus domestica) HcrVf2 protein that mediate resistance against the fungal pathogens Cladosporium fulvum, Verticillium spp., and Venturia inaequalis, respectively. In addition, RLPs play a role in plant development; Arabidopsis (Arabidopsis thaliana) TOO MANY MOUTHS (TMM) regulates stomatal distribution, while Arabidopsis CLAVATA2 (CLV2) and its functional maize (Zea mays) ortholog FASCINATED EAR2 regulate meristem maintenance. In total, 57 RLP genes have been identified in the Arabidopsis genome and a genome-wide collection of T-DNA insertion lines was assembled. This collection was functionally analyzed with respect to plant growth and development and sensitivity to various stress responses, including susceptibility toward pathogens. A number of novel developmental phenotypes were revealed for our CLV2 and TMM insertion mutants. In addition, one AtRLP gene was found to mediate abscisic acid sensitivity and another AtRLP gene was found to influence nonhost resistance toward Pseudomonas syringae pv phaseolicola. This genome-wide collection of Arabidopsis RLP gene T-DNA insertion mutants provides a tool for future investigations into the biological roles of RLPs
    The human genome encodes ten alpha-crystallin-related small heat shock proteins: HspB1-10
    Kappé, G. ; Franck, E. ; Verschuure, P. ; Boelens, W.C. ; Leunissen, J.A.M. ; Jong, W.W. de - \ 2003
    Cell Stress and Chaperones 8 (2003). - ISSN 1355-8145 - p. 53 - 61.
    small stress proteins - dense fiber protein - b-crystallin - gene - family - hsp27 - expression - chaperones - sequence - kinase
    To obtain an inventory of all human genes that code for alpha-crystallin-related small heat shock proteins (sHsps), the databases available from the public International Human Genome Sequencing Consortium (IHGSC) and the private Celera human genome project were exhaustively searched. Using the human Hsp27 protein sequence as a query in the protein databases, which are derived from the predicted genes in the human genome, 10 sHsp-like proteins were retrieved, including Hsp27 itself. Repeating the search procedure with all 10 proteins and with a variety of more distantly related animal sHsps, no further human sHsps were detected, as was the case when searches were performed at deoxyribonucleic acid level. The 10 retrieved proteins comprised the 9 earlier recognized human sHsps (Hsp27/HspB1, HspB2, HspB3, alphaA-crystallin/HspB4, alphaB-crystallin/HspB5, Hsp20/HspB6, cvHsp/HspB7, H11/HspB8, and HspB9) and a sperm tail protein known since 1993 as outer dense fiber protein 1 (ODF1). Although this latter protein probably serves a structural role and has a high cysteine content (14%), it clearly contains an alpha-crystallin domain that is characteristic for sHsps. ODF1 can as such be designated as HspB10. The expression of all 10 human sHsp genes was confirmed by expressed sequence tag (EST) searches. For Hsp27/HspB1, 2 retropseudogenes were detected. The HspB1-10 genes are dispersed over 9 chromosomes, reflecting their ancient origin. Two of the genes (HspB3 and HspB9) are intronless, and the others have 1 or 2 introns at various positions. The transcripts of several sHsp genes, notably HspB7, display low levels of alternative splicing, as supported by EST evidence, which may result in minor amounts of isoforms at the protein level.
    Effects of n-6 and n-3 Polyunsaturated Fatty Acids on Gap Junctional Intercellular Communication During Spontaneous Differentiation of the Human Colon Adenocarcinoma Cell Line Caco-2
    Dommels, Y.E.M. ; Alink, G.M. ; Linssen, J.P.H. ; Ommen, B. van - \ 2002
    Nutrition and Cancer 42 (2002)1. - ISSN 0163-5581 - p. 125 - 130.
    dietary-fat - tumor promotion - cancer-cells - carcinogenesis - proliferation - expression - inhibition - lipids - kinase - gene
    Gap junctional intercellular communication (GJIC), which modulates cell growth and differentiation, may play an important role in tumor growth. Cancer cells have dysfunctional GJIC, but it is not known whether GJIC is mechanistically involved in the carcinogenic and anti-carcinogenic effects of n-6 and n-3 polyunsaturated fatty acids (PUFAs) on colon tumor cells. Caco-2 cells were used as an in vitro model to study the effects of PUFAs on differentiated as well as undifferentiated human colon cells. The GJIC capacity of this cell line increased during spontaneous differentiation. However, no differential effects between n-6 and n-3 PUFAs on GJIC were observed. Short-term incubation with linoleic acid (18:2n-6), alpha-linolenic acid (18:3n-3), arachidonic acid (AA, 20:4n-6), and eicosapentaenoic acid (EPA, 20:5n-3) did not influence GJIC, while long-term incubation (>10 days) with linoleic acid and a-linolenic acid inhibited GJIC of these colon cells. Long-chain metabolites such as AA and EPA were not formed after incubation with linoleic acid and a-linolenic acid, thus excluding the involvement of prostaglandins in the observed effects. Although the exact mechanism of GJIC inhibition is unclear, cytotoxicity probably mediated by lipid peroxidation products seems to be related, because incubation with more PUFAs (AA and EPA) completely abolished GJIC.
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