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  • 1
    Publication Date: 2011-10-07
    Description: Maize smut caused by the fungus Ustilago maydis is a widespread disease characterized by the development of large plant tumours. U. maydis is a biotrophic pathogen that requires living plant tissue for its development and establishes an intimate interaction zone between fungal hyphae and the plant plasma membrane. U. maydis actively suppresses plant defence responses by secreted protein effectors. Its effector repertoire comprises at least 386 genes mostly encoding proteins of unknown function and expressed exclusively during the biotrophic stage. The U. maydis secretome also contains about 150 proteins with probable roles in fungal nutrition, fungal cell wall modification and host penetration as well as proteins unlikely to act in the fungal-host interface like a chorismate mutase. Chorismate mutases are key enzymes of the shikimate pathway and catalyse the conversion of chorismate to prephenate, the precursor for tyrosine and phenylalanine synthesis. Root-knot nematodes inject a secreted chorismate mutase into plant cells likely to affect development. Here we show that the chorismate mutase Cmu1 secreted by U. maydis is a virulence factor. The enzyme is taken up by plant cells, can spread to neighbouring cells and changes the metabolic status of these cells through metabolic priming. Secreted chorismate mutases are found in many plant-associated microbes and might serve as general tools for host manipulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Djamei, Armin -- Schipper, Kerstin -- Rabe, Franziska -- Ghosh, Anupama -- Vincon, Volker -- Kahnt, Jorg -- Osorio, Sonia -- Tohge, Takayuki -- Fernie, Alisdair R -- Feussner, Ivo -- Feussner, Kirstin -- Meinicke, Peter -- Stierhof, York-Dieter -- Schwarz, Heinz -- Macek, Boris -- Mann, Matthias -- Kahmann, Regine -- England -- Nature. 2011 Oct 5;478(7369):395-8. doi: 10.1038/nature10454.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Terrestrial Microbiology, Karl-von-Frisch-Strasse 10, D-35043 Marburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21976020" target="_blank"〉PubMed〈/a〉
    Keywords: Chorismate Mutase/*metabolism ; Cytoplasm/enzymology ; Gene Expression Regulation, Plant ; Genetic Complementation Test ; Host-Pathogen Interactions ; Metabolome ; Models, Biological ; Plant Proteins/metabolism ; Plastids/enzymology ; Protein Multimerization ; Saccharomyces cerevisiae/genetics ; Salicylic Acid/metabolism ; Two-Hybrid System Techniques ; Ustilago/*enzymology/*pathogenicity ; Virulence Factors/genetics/*metabolism ; Zea mays/*metabolism/*microbiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2011-12-14
    Description: Plants transport fixed carbon predominantly as sucrose, which is produced in mesophyll cells and imported into phloem cells for translocation throughout the plant. It is not known how sucrose migrates from sites of synthesis in the mesophyll to the phloem, or which cells mediate efflux into the apoplasm as a prerequisite for phloem loading by the SUT sucrose-H(+) (proton) cotransporters. Using optical sucrose sensors, we identified a subfamily of SWEET sucrose efflux transporters. AtSWEET11 and 12 localize to the plasma membrane of the phloem. Mutant plants carrying insertions in AtSWEET11 and 12 are defective in phloem loading, thus revealing a two-step mechanism of SWEET-mediated export from parenchyma cells feeding H(+)-coupled import into the sieve element-companion cell complex. We discuss how restriction of intercellular transport to the interface of adjacent phloem cells may be an effective mechanism to limit the availability of photosynthetic carbon in the leaf apoplasm in order to prevent pathogen infections.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Li-Qing -- Qu, Xiao-Qing -- Hou, Bi-Huei -- Sosso, Davide -- Osorio, Sonia -- Fernie, Alisdair R -- Frommer, Wolf B -- 1R01DK079109/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2012 Jan 13;335(6065):207-11. doi: 10.1126/science.1213351. Epub 2011 Dec 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Carnegie Institution for Science, 260 Panama Street, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22157085" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arabidopsis/genetics/growth & development/*metabolism ; Arabidopsis Proteins/genetics/*metabolism ; Biological Transport ; Cell Membrane/metabolism ; Fluorescence Resonance Energy Transfer ; HEK293 Cells ; Humans ; Membrane Transport Proteins/genetics/*metabolism ; Mutant Proteins/metabolism ; Oryza/metabolism ; Phloem/*metabolism ; Plant Leaves/metabolism ; Plant Proteins/genetics/metabolism ; Plant Roots/growth & development ; Promoter Regions, Genetic ; Sucrose/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2017-06-08
    Description: Understanding the genetic architecture of traits in breeding programs can be critical for making genetic progress. Important factors include the number of loci controlling a trait, allele frequencies at those loci, and allele effects in breeding germplasm. To this end, multiparental populations offer many advantages for quantitative trait locus (QTL) analyses compared to biparental populations. These include increased power for QTL detection, the ability to sample a larger number of segregating loci and alleles, and estimation of allele effects across diverse genetic backgrounds. Here, we investigate the genetic architecture of resistance to crown rot disease caused by Phytophthora cactorum in strawberry ( Fragaria x ananassa ), using connected full-sib families from a breeding population. Clonal replicates of 〉 1100 seedlings from 139 full-sib families arising from 61 parents were control-inoculated during two consecutive seasons. Subgenome-specific single nucleotide polymorphism (SNP) loci were mapped in allo-octoploid strawberry (2 n = 8 x = 56), and FlexQTL software was utilized to perform a Bayesian, pedigree-based QTL analysis. A major locus on linkage group (LG) 7D, which we name FaRPc2 , accounts for most of the genetic variation for resistance. Four predominant SNP haplotypes were detected in the FaRPc2 region, two of which are strongly associated with two different levels of resistance, suggesting the presence of multiple resistance alleles. The phenotypic effects of FaRPc2 alleles across trials and across numerous genetic backgrounds make this locus a highly desirable target for genetic improvement of resistance in cultivated strawberry.
    Electronic ISSN: 2160-1836
    Topics: Biology
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  • 4
    Electronic Resource
    Electronic Resource
    Chichester [u.a.] : Wiley-Blackwell
    Surface and Interface Analysis 21 (1994), S. 809-813 
    ISSN: 0142-2421
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Physics
    Notes: In this work BN films have been deposited by the plasma-enhanced chemical vapour deposition (PECVD) technique on p-type (100) silicon substrates, using borazine and nitrogen as precursors. X-ray photoelectron spectroscopy, infrared spectroscopy, x-ray diffraction, nuclear reaction analysis and Rutherford backscattering spectroscopy were used to analyse the films. The results of quantitative XPS analysis indicate the formation of a thin surface layer (∼3 nm) of boron oxynitride, BNO0.3, over a bulk of nearly stoichiometric boron nitride, BN1.1. The presence of the hexagonal phase mixed with amorphous boron nitride was identified. Infrared and Rutherford backscattering spectroscopies combined with a liquid etching technique were used to determine the composition and structure across the film thickness. From these measurements we infer that the composition across the film is nearly constant but with a gradual transition from an amorphous structure close to the Si/BN1.1 interface to an hexagonal structure towards the outer layers. Thermal treatments of the boron nitride films up to a temperature of ∼1000°C in a nitrogen atmosphere resulted in a small decrease of both the B/N atomic concentration ratio and the refractive index of the film. The insulating characteristics of the boron nitride for application as an intermetal dielectric were also treated. The electrical conduction results can be interpreted in terms of a Schottky mechanism, which allows us to calculate the high-frequency dielectric constant, εr = 3.2.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
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  • 5
    Publication Date: 2019-12-11
    Print ISSN: 2469-9950
    Electronic ISSN: 2469-9969
    Topics: Physics
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  • 6
    Publication Date: 2013-01-11
    Description: Pathogenic prions deviate PrPC signaling in neuronal cells and impair A-beta clearance Cell Death and Disease 4, e456 (January 2013). doi:10.1038/cddis.2012.195 Authors: E Pradines, J Hernandez-Rapp, A Villa-Diaz, C Dakowski, H Ardila-Osorio, S Haik, B Schneider, J-M Launay, O Kellermann, J-M Torres & S Mouillet-Richard
    Keywords: prion infectionA-betasignal transductionMMP-9
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 7
    Publication Date: 2017-07-06
    Print ISSN: 2469-9950
    Electronic ISSN: 2469-9969
    Topics: Physics
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  • 8
    Publication Date: 2019-02-28
    Print ISSN: 2469-9950
    Electronic ISSN: 2469-9969
    Topics: Physics
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  • 9
    Publication Date: 2008-11-16
    Description: Background. The identification of the somatic mutation V617F in exon 14 of the Janus kinase 2 gene (JAK2) has simplified the diagnosis of many patients affected with typical chronic myeloproliferative diseases (MPDs). In patients without the V617F the molecular basis of MPD are still unclear but, recently, mutations in exon 12 of the JAK2 gene have been identified in a minority of patients, associated with a selective increase in erythropoiesis resulting in polycythemia vera (PV) or idiopathic erythrocytosis (IE) (Scott et al, NEJM 2007). Aim. To determine the JAK2 exon 12 mutational status in a group of JAK2 V617F negative patients with PV or IE. Methods. Genomic DNA was extracted from peripheral blood leukocytes from 85 MPD patients (PV or IE) included in the present study. All the samples were tested for JAK2 V617F mutation by allele specific polymerase chain reaction (ASO-PCR) and those negative for V617F mutant allele were subjected to real time quantitative PCR (RQ-PCR) using hybridization probes. Subsequently, all JAK2 V617F negative samples by both ASO-PCR and RQ-PCR where subjected to direct sequencing to exclude JAK2 exon 12 mutations. Results. JAK2 V617F was positive in 78 (91.7%) of the 85 patients, however, in two of these patients the V617F mutation was only detected upon subjecting genomic DNA to RQ-PCR which revealed low levels of the mutant allele, 2.65 % and 3.98%. Analysis of the JAK2 exon 12 in the seven JAK2 V617F negative patients detected three previously described mutations: a duplication (V536-1546) and two deletions (H539-K540del+542K and R541-E543 delinsK)and a previously unreported splice site mutation detected in intron 12 (IVS12nt6 T-C). To our knowledge this was the first description of intronic mutations in the JAK2 gene. No mutations were detected in the remaining 3 (3.6%) patients. Conclusions. In this cohort study JAK2 mutations were observed in 82 (96,5%), of the 85 patients, of these 78 (95.12%) had the V617F allele. In two cases V617F was detected at low levels (2.65% and 3.98%) only by RQ-PCR, highlighting the need for sensitive techniques to detect somatic mutations. One of the patients, a young male with erythrocytosis and low serum Epo levels, revealed a previously unreported splicing mutation (IVS12 nt6: T-C). This study illustrates the heterogeneity at the DNA level in PV patients which may assist in better understanding the genotype and phenotype relationship in MPD patients and assist in further delineating the role of JAK2 in these disorders.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 10
    Publication Date: 2008-11-16
    Description: Aim: To evaluate the efficacy of Lenalidomide (Len) as compassionate use in relapsed or progressive Multiple Myeloma (MM) up to its approval in Spain. Patients and Methods: GEM-PETHEMA designed a transverse and retrospective, multicenter analysis of MM cases which Len compassionate use was requested until December, 2007. The decision to treat these patients was previous and independent from the decision to conduct the present analysis and depended only on the clinical criteria of the responsible doctors. At least, one response assessment was a must for efficacy analysis. Results: 111 MM patients have been included. Eligible patients for efficacy were 103. Mean age was 65.7 (38–85); 53 m, 50 f. Previous median lines of therapy were 3 (1–8): 92 (89.3%) have received bortezomib; 37 (35.9%) autologous PBSCT and 26 (25.2%) thalidomide. Extramedullary plasmocitomas were present in 25 (24.3%). Mean Len dose was 22.8 mg (± 4.9): 82 (79.6%) received the standard dose and schedule (25 mg d for 3 w every 4 w) and 21 (20.4%) received less dose and/or different schedule. 92 (89.3%) received Dexametasone (mean dose 58.33 mg/w) [± 35.8]). Response: 4 (3.9%) sCR, 11 CR (10.7%), 12 VGPR (11.7%), 41 PR (39.8%), 20 SD (19.4%), 13 PD (12.6%), 2 NE (1.9). Among groups, response equal or superior to PR was observed in all settings: 64.1% in prior exposed to bortezomib, 46.1% in prior exposed to thalidomide and 40.0% in patients with extramedullary plasmocitomas. Previous transplant, the number of previous lines received, renal failure, age, or cytogenetic did not affect significantly the overall response rate. Median duration of treatment was 7.7 m (1–21); median TTP was 8.3 m and median global survival since starting Len therapy was 11 m (6–22). Median survival since diagnostic was 49 m (40–60). At the time of analysis, 46 (45.5%) patients were still on Len therapy, and 72 (79.6%) were alive. Toxicity: ≥ grade II: neutropenia, 51 (46.4%); thrombocytopenia, 39 (35.5%); DVT, 5 (4.5%); rash, 3 (2.7%); neutropenic fever, 8 (7.3%); others, 13 (11.8%). DVT/PE prophylaxis was used in 89 (86.4%) patients: LWMH in 43.8 % and low dose aspirin in 48.3 %. No PE was reported. Conclusions: Lenalidomide is effective in this heavily pre-treated MM population-progressive or refractory to standard therapy-even in different clinical settings. The most frequent association to Len was intermediate dose of Dex. Although response rate was superior in patients exposed previously to bortezomib, no differences on duration and survival were observed. Patients with extramedullary plasmocitomas showed also response. Toxicity, mainly myelosupression was predictable and manageable with dose adjustments and cytokine support.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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