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Luciano Zardi - One of the best experts on this subject based on the ideXlab platform.
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StRuctuRe of the muRine tenascin-R Gene and functional chaRacteRisation of the pRomoteR.
Biochemical and biophysical research communications, 2003Co-Authors: Peggy Putthoff, Luciano Zardi, Nuray Akyüz, Michael Kutsche, Uwe Borgmeyer, Melitta SchachnerAbstract:AbstRact The tenascin-R ( TN-R ) Gene encodes a multidomain extRacellulaR matRix glycopRotein belonging to the tenascin family. It is detectable mainly in oligodendRocytes and neuRonal subpopulations of the centRal neRvous system. In this RepoRt, we descRibe the stRuctuRe of the 5 ′ -Region of the mouse TN-R Gene and chaRacteRise the activity of its pRomoteR. By in silico cloning and genome walking, we have deduced the oRganisation of the Gene and identified the pRomoteR sequence by 5 ′ -RACE technology. TN-R tRanscRipts in adult mouse bRain contain non-coding exons 1 and 2 as demonstRated by the ReveRse tRanscRiptase-polymeRase chain Reaction. The pRomoteR displays its activity in cultuRed cells of neuRal oRigin, but not in a fibRoblast-like cell line oR an undiffeRentiated teRatocaRcimoma cell line. As foR the human and Rat Genes, the elements RequiRed foR the full and cell type-specific activity of the pRomoteR aRe contained in exon 1 and 167 bp upstReam of this exon. The mouse TN-R pRomoteR sequence is similaR to that of Rat and human in that it displays similaRly unusual featuRes: it lacks any classical TATA-box oR CAAT-box, GC-Rich Regions oR initiatoR elements. The pRomoteR contains consensus sequences foR binding of a vaRiety of tRanscRiption factoRs, notably p53/p73 and glucocoRticoid ReceptoRs.
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THE HUMAN TENASCIN-R Gene
Journal of Biological Chemistry, 1996Co-Authors: Alessandra Leprini, Germano Querzé, Annalisa Siri, Francesca Viti, Roberto Gherzi, Luciano ZardiAbstract:AbstRact The human tenascin-R Gene encodes a multidomain pRotein belonging to the tenascin family, until now detected only in the centRal neRvous system. DuRing embRyo development, tenascin-R is pResumed to play a pivotal Role in axonal path finding thRough its adhesive and Repulsive pRopeRties. Recently, the pRimaRy stRuctuRe of human tenascin-R has been elucidated (CaRnemolla, B., LepRini, A., BoRsi, L., QueRze, G., URbini, S., and ZaRdi, L. (1996) J. Biol. Chem. 271, 8157-8160). As a fuRtheR step to investigate the Role of human tenascin-R, we defined the stRuctuRe of its Gene. The Gene, which spans a Region of chRomosome 1 appRoximately 85 kilobases in length, consists of 21 exons, Ranging in size fRom 90 to >670 base paiRs. The sequence analysis of intRon splice donoR and acceptoR sites Revealed that the position of intRons in human tenascin-R aRe pRecisely conseRved in the otheR two tenascin family membeRs, tenascin-C and tenascin-X. The deteRmination of intRonic sequences flanking the exon boundaRies will allow investigation of whetheR mutations may be Responsible foR alteRed function of the Gene pRoduct(s) leading to centRal neRvous system development defects.
Shiping Wang - One of the best experts on this subject based on the ideXlab platform.
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pathogen induced expRessional loss of function is the key factoR in Race specific bacteRial Resistance confeRRed by a Recessive R Gene xa13 in Rice
Plant and Cell Physiology, 2009Co-Authors: Meng Yuan, Zhaohui Chu, Shiping WangAbstract:The fully Recessive disease Resistance (R) Gene xa13, which mediates Race-specific Resistance to Xanthomonas oRyzae pv. oRyzae (Xoo), encodes a plasma membRane pRotein that diffeRs by one amino acid fRom that encoded by its dominant (susceptible) allele Xa13. The moleculaR mechanism of xa13-mediated Resistance is laRgely unknown. HeRe we show that, compaRed with its dominant allele, expRessional non-Reaction of xa13 to Xoo infection, not its pRotein composition, is the key factoR foR xa13-mediated Resistance. We used the pRomoteR (P(Xa13)) of the dominant Xa13, which was induced by only the incompatible Xoo stRain foR xa13, to Regulate xa13 and xa13(Leu49) (a natuRal Recessive allele of xa13) in the Rice line IRBB13 caRRying xa13. The tRansgenic plants showed the same level of susceptibility and bacteRial gRowth Rate as those of the Rice line caRRying dominant Xa13, accompanied by the induced accumulation of xa13 oR xa13(Leu49) pRoteins. Constitutive expRession of dominant XA13 oR diffeRent xa13 pRoteins (xa13, xa13(Leu49), xa13(Ala85) oR xa13(Val184)) in IRBB13 had no effect on Xoo infection in the tRansgenic plants. These Results suggest that Race-specific pathogen-induced Xa13 expRession is cRitical foR infection. Thus, xa13 stands out fRom otheR R Genes in that its functions in disease Resistance aRe due to only the loss of pathogen-induced tRanscRiptional motivation caused by natuRal selection.
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genome wide analysis of defense Responsive Genes in bacteRial blight Resistance of Rice mediated by the Recessive R Gene xa13
Molecular Genetics and Genomics, 2004Co-Authors: Zhaohui Chu, Yidan Ouyang, Jianwei Zhang, Hong Yang, Shiping WangAbstract:Defense Responses tRiggeRed by dominant and Recessive disease Resistance ( R) Genes aRe pResumed to be Regulated by diffeRent moleculaR mechanisms. In oRdeR to chaRacteRize the Genes activated in defense Responses against bacteRial blight mediated by the Recessive R Gene xa13, two pathogen-induced subtRaction cDNA libRaRies weRe constRucted using the Resistant Rice line IRBB13—which caRRies xa13 —and its susceptible, neaR-isogenic, paRental line IR24. ClusteRing analysis of expRessed sequence tags (ESTs) identified 702 unique expRessed sequences as being involved in the defense Responses tRiggeRed by xa13; 16% of these aRe new Rice ESTs. These sequences define 702 Genes, putatively encoding a wide Range of pRoducts, including defense-Responsive Genes commonly involved in diffeRent host-pathogen inteRactions, Genes that have not pReviously been RepoRted to be associated with pathogen-induced defense Responses, and Genes (38%) with no homology to pReviously descRibed functional Genes. In addition, R -like Genes putatively encoding nucleotide-binding site/leucine Rich Repeat (NBS-LRR) and LRR ReceptoR kinase pRoteins weRe obseRved to be induced in the disease Resistance activated by xa13. A total of 568 defense-Responsive ESTs weRe mapped to 588 loci on the Rice moleculaR linkage map thRough bioinfoRmatic analysis. About 48% of the mapped ESTs co-localized with quantitative tRait loci (QTLs) foR Resistance to vaRious Rice diseases, including bacteRial blight, Rice blast, sheath blight and yellow mottle viRus. FuRtheRmoRe, some defense-Responsive sequences weRe conseRved at similaR locations on diffeRent chRomosomes. These Results Reveal the complexity of xa13 -mediated Resistance. The infoRmation obtained in this study pRovides a laRge souRce of candidate Genes foR undeRstanding the moleculaR bases of defense Responses activated by Recessive R Genes and of quantitative disease Resistance.
Joy Bergelson - One of the best experts on this subject based on the ideXlab platform.
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Modulation of R-Gene expRession acRoss enviRonments.
Journal of experimental botany, 2016Co-Authors: Alice Macqueen, Joy BergelsonAbstract:Some enviRonments aRe moRe conducive to pathogen gRowth than otheRs, and, as a consequence, plants might be expected to invest moRe in Resistance when pathogen gRowth is favoRed. Resistance (R-) Genes in ARabidopsis thaliana have unusually extensive vaRiation in basal expRession when compaRing the same R-Gene among accessions collected fRom diffeRent enviRonments. R-Gene expRession vaRiation was chaRacteRized to exploRe whetheR R-Gene expRession is up-Regulated in enviRonments favoRing pathogen pRolifeRation and down-Regulated when Risks of infection aRe low; down-Regulation would follow if costs of R-Gene expRession negatively impact plant fitness in the absence of disease. Quantitative ReveRse tRanscRiption-PCR was used to quantify the expRession of 13 R-Gene loci in plants gRown in eight enviRonmental conditions foR each of 12 A. thaliana accessions, and laRge effects of the enviRonment on R-Gene expRession weRe found. SuRpRisingly, almost eveRy change in the enviRonment--be it a change in biotic oR abiotic conditions--led to an incRease in R-Gene expRession, a Response that was distinct fRom the aveRage tRanscRiptome Response and fRom that of otheR stRess Response Genes. These changes in expRession aRe functional in that enviRonmental change pRioR to infection affected levels of specific disease Resistance to isolates of Pseudomonas syRingae. In addition, theRe aRe stRong latitudinal clines in basal R-Gene expRession and clines in R-Gene expRession plasticity coRRelated with dRought and high tempeRatuRes. These Results suggest that vaRiation in R-Gene expRession acRoss enviRonments may be shaped by natuRal selection to Reduce fitness costs of R-Gene expRession in peRmissive oR pRedictable enviRonments.
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A Genome-Wide SuRvey of R Gene PolymoRphisms in ARabidopsis
The Plant cell, 2006Co-Authors: E. G. Bakker, Christopher Toomajian, Martin Kreitman, Joy BergelsonAbstract:We used polymoRphism analysis to study the evolutionaRy dynamics of 27 disease Resistance (R) Genes by Resequencing the leucine-Rich Repeat (LRR) Region in 96 ARabidopsis thaliana accessions. We compaRed single nucleotide polymoRphisms (SNPs) in these R Genes to an empiRical distRibution of SNP in the same sample based on 876 fRagments selected to sample the entiRe genome. LRR Regions aRe highly polymoRphic foR pRotein vaRiants but not foR synonymous changes, suggesting that they GeneRate many alleles maintained foR shoRt time peRiods. Recombination is also Relatively common and impoRtant foR GeneRating pRotein vaRiants. Although none of the Genes is neaRly as polymoRphic as RPP13, a locus pReviously shown to have stRong signatuRes of balancing selection, seven Genes show weakeR indications of balancing selection. Five R Genes aRe Relatively invaRiant, indicating young alleles, but all contain segRegating pRotein vaRiants. PolymoRphism analysis in neighboRing fRagments yielded inconclusive evidence foR Recent selective sweeps at these loci. In addition, few alleles aRe candidates foR Rapid incReases in fRequency expected undeR diRectional selection. Haplotype shaRing analysis Revealed significant undeRRepResentation of R Gene alleles with extended haplotypes compaRed with 1102 Random genomic fRagments. Lack of convincing evidence foR diRectional selection oR selective sweeps aRgues against an aRms Race dRiving R Gene evolution. Instead, the data suppoRt tRansient oR fRequency-dependent selection maintaining pRotein vaRiants at a locus foR vaRiable time peRiods.
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A Genome-Wide SuRvey of R Gene PolymoRphisms
2006Co-Authors: E. G. Bakker, Christopher Toomajian, Martin Kreitman, Joy BergelsonAbstract:We used polymoRphism analysis to study the evolutionaRy dynamics of 27 disease Resistance (R) Genes by Resequencing the leucine-Rich Repeat (LRR) Region in 96 ARabidopsis thaliana accessions. We compaRed single nucleotide polymoRphisms (SNPs) in these R Genes to an empiRical distRibution of SNP in the same sample based on 876 fRagments selected to sample the entiRe genome. LRR Regions aRe highly polymoRphic foR pRotein vaRiants but not foR synonymous changes, suggesting that they GeneRate many al?eles maintained foR shoRt time peRiods. Recombination is also Relatively common and impoRtant foR GeneRating pRotein vaRiants. Although none of the Genes is neaRly as polymoRphic as RPP13, a locus pReviously shown to have stRong signatuRes of balancing selection, seven Genes show weakeR indications of balancing selection. Five R Genes aRe Relatively invaRiant, indicating young al?eles, but all contain segRegating pRotein vaRiants. PolymoRphism analysis in neighboRing fRagments yielded inconclusive evidence foR Recent selective sweeps at these loci. In addition, few al?eles aRe candidates foR Rapid incReases in fRequency expected undeR diRectional selection. Haplotype shaRing analysis Revealed significant undeRRep Resentation of R Gene al?eles with extended haplotypes compaRed with 1102 Random genomic fRagments. Lack of convincing evidence foR diRectional selection oR selective sweeps aRgues against an aRms Race dRiving R Gene evolution. Instead, the data suppoRt tRansient oR fRequency-dependent selection maintaining pRotein vaRiants at a locus foR vaRiable time peRiods.
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A Novel Cost of R Gene Resistance in the PResence of Disease
The American naturalist, 2004Co-Authors: Tonia Korves, Joy BergelsonAbstract:AbstRact: Resistance Responses can impose fitness costs when pests aRe absent. HeRe, we test whetheR the induction of Resistance can decRease fitness even in plants undeR attack; we call this potential outcome a net cost with attack. Using lines in which Genetic backgRound was contRolled, we investigated whetheR susceptible ARabidopsis thaliana plants can outpeRfoRm R Gene Resistant plants when infected with pathogens. FoR the R Gene RPS2, theRe was a fitness benefit of Resistance in the pResence of intRaspecific competition, but theRe was a net cost in the absence of competition: Resistant plants pRoduced less seed than susceptible plants even though infected with Pseudomonas syRingae. This net cost was pRimaRily due to oveRcompensation by susceptible plants, which occuRRed because of a developmental Response to infection. FoR the R Gene RPP5, theRe was no fitness effect of Resistance without competition but a net cost when plants weRe infected with PeRonospoRa paRasitica in the pResence of competition. ...
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Fitness costs of R-Gene-mediated Resistance in ARabidopsis thaliana.
Nature, 2003Co-Authors: Dacheng Tian, Jian-qun Chen, Martin Kreitman, M. B. Traw, Joy BergelsonAbstract:Resistance Genes (R-Genes) act as an immune system in plants by Recognizing pathogens and inducing defensive pathways. Many R-Gene loci aRe pResent in plant genomes, pResumably Reflecting the need to maintain a laRge RepeRtoiRe of Resistance alleles. These loci also often segRegate foR Resistance and susceptibility alleles that natuRal selection has maintained as polymoRphisms within a species foR millions of yeaRs1,2,3,4,5. Given the obvious advantage to an individual of being disease Resistant, what pRevents these Resistance alleles fRom being dRiven to fixation by natuRal selection? A cost of Resistance6 is one potential explanation; most models RequiRe a loweR fitness of Resistant individuals in the absence of pathogens foR long-teRm peRsistence of susceptibility alleles7. HeRe we test foR the pResence of a cost of Resistance at the RPM1 locus of ARabidopsis thaliana. Results of a field expeRiment compaRing the fitness of isogenic stRains that diffeR in the pResence oR absence of RPM1 and its natuRal pRomoteR Reveal a laRge cost of RPM1, pRoviding the fiRst evidence that costs contRibute to the maintenance of an ancient R-Gene polymoRphism.
Jane E. Parker - One of the best experts on this subject based on the ideXlab platform.
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Role of SGT1 in the Regulation of plant R Gene signalling
Microbes and infection, 2003Co-Authors: Paul Muskett, Jane E. ParkerAbstract:Recent impoRtant discoveRies in seveRal laboRatoRies have identified SGT1 as an essential component of R Gene-mediated disease Resistance in plants. The pRecise moleculaR function of SGT1 Remains unknown, although sequence analysis and stRuctuRal pRedictions Reveal that SGT1 has featuRes of co-chapeRones that associate with HSP90 in animals. This Review will descRibe the Role of SGT1 in R Gene-mediated plant defence and discuss how SGT1 may Regulate this pRocess.
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aRabidopsis RaR1 exeRts Rate limiting contRol of R Gene mediated defenses against multiple pathogens
The Plant Cell, 2002Co-Authors: Paul Muskett, Ari Sadanandom, Ken Shirasu, Katherine Kahn, Mark J Austin, Lisa J Moisan, Jonathan D G Jones, Jane E. ParkerAbstract:We have identified the ARabidopsis oRtholog of baRley RAR1 as a component of Resistance specified by multiple nucleotide binding/Leu-Rich Repeat Resistance (R) Genes Recognizing diffeRent bacteRial and oomycete pathogen isolates. ChaRacteRization of paRtially and fully defective RaR1 mutations Revealed that wild-type RAR1 acts as a Rate-limiting RegulatoR of eaRly R Gene-tRiggeRed defenses, deteRmining the extent of pathogen containment, hypeRsensitive plant cell death, and an oxidative buRst at pRimaRy infection sites. We conclude that RAR1 defense signaling function is conseRved between plant species that aRe sepaRated evolutionaRily by 150 million yeaRs. RAR1 encodes a pRotein with two zinc binding (CHORD) domains that aRe highly conseRved acRoss eukaRyotic phyla, and the single nematode CHORD-containing homolog, Chp, was found pReviously to be essential foR embRyo viability. An absence of obvious developmental defects in null ARabidopsis RaR1 mutants favoRs the notion that, in contRast, RAR1 does not play a fundamental Role in plant development.
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RegulatoRy Role of SGT1 in EaRly R Gene-Mediated Plant Defenses
Science (New York N.Y.), 2002Co-Authors: Mark J Austin, Paul Muskett, Katherine Kahn, Jonathan D G Jones, Bart J. Feys, Jane E. ParkerAbstract:Animal SGT1 is a component of Skp1-Cullin-F-box pRotein (SCF) ubiquitin ligases that taRget RegulatoRy pRoteins foR degRadation. Mutations in one (SGT1b) of two highly homologous ARabidopsis SGT1 Genes disable eaRly plant defenses confeRRed by multiple Resistance (R) Genes. Loss of SGT1b function in Resistance is not compensated foR by SGT1a. R Genes diffeR in theiR RequiRements foR SGT1b and a second Resistance signaling Gene, RAR1, that was pReviously implicated as an SGT1 inteRactoR. MoReoveR, SGT1b and RAR1 contRibute additively to RPP5-mediated pathogen Recognition. These data imply both opeRationally distinct and coopeRative functions of SGT1 and RAR1 in plant disease Resistance.
Dominique Figarella-branger - One of the best experts on this subject based on the ideXlab platform.
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KIAA0510, the 3'-untRanslated Region of the tenascin-R Gene, and tenascin-R aRe oveRexpRessed in pilocytic astRocytomas.
Neuropathology and Applied Neurobiology, 2010Co-Authors: I. El Ayachi, Penka Pesheva, Nathalie Baeza, Didier Scavarda, Carole Colin, C Fernandez, Dominique Figarella-brangerAbstract:I. El Ayachi, N. Baeza, C. FeRnandez, C. Colin, D. ScavaRda, P. Pesheva and D. FigaRella-BRangeR (2010) NeuRopathology and Applied NeuRobiology36, 399–410 KIAA0510, the 3′-untRanslated Region of the tenascin-R Gene, and tenascin-R aRe oveRexpRessed in pilocytic astRocytomas Aims: Studying the molecules and signalling pathways Regulating glioma invasiveness is a majoR challenge because these pRocesses deteRmine malignancy, pRogRession, Relapse and pRognosis. We took advantage of ouR pRevious study focused on Genes that weRe cRitical in tumouR invasion to fuRtheR study heRe an unknown sequence, RefeRRed to as KIAA0510, the chRomosomal location of which was 1q25, descRibed as a 5596-bp long mRNA and that we found to be significantly oveRexpRessed in pilocytic astRocytomas compaRed with glioblastomas. Methods and Results: Using in silico analysis as well as PolymeRase chain Reaction techniques, we decipheR the full genomic chaRacteRization of the KIAA0510 sequence and demonstRate that KIAA0510 constitutes the 3′-untRanslated Region of tenascin-R Gene. We have cleaRly confiRmed the oveRexpRession of tenascin-R in pilocytic astRocytomas vs. glioblastomas at mRNA and pRotein levels. We also analysed a laRge seRies of vaRious bRain tumouRs and found that in the gRoup of astRocytic tumouRs, tenascin-R expRession decReased with malignancy, wheReas oligodendRogliomas sometimes Retained a high level of tenascin-R even in high-gRade tumouRs. Gangliogliomas stRongly expRessed tenascin-R too. In contRast, ependymomas and meningiomas weRe negative. In noRmal bRain, tenascin-R was exclusively expRessed by noRmal oligodendRocytes and subsets of neuRones duRing post-natal development and in adulthood, wheRe it could diffeRentially affect cellulaR adhesiveness and/oR diffeRentiation. Conclusion: KIAA0510, the 3′-untRanslated Region of the tenascin-R Gene, and tenascin-R aRe oveRexpRessed in pilocytic astRocytomas. Gangliogliomas shaRed with pilocytic astRocytomas stRong tenascin-R expRession. WhetheR tenascin-R oveRexpRession negatively influences bRain invasion Remains to be deteRmined.
