archive-org.com » ORG » I » IMGS.ORG

Total: 854

Choose link from "Titles, links and description words view":

Or switch to "Titles and links view".
  • The 16th International Mouse Genome Conference (2002)
    Eppig JT and the Mouse Genome Informatics Staff The Jackson Laboratory The Mouse Genomic Nomenclature Committee MGNC under the auspices of the International Committee on Standardized Nomenclature for Mice provides official nomenclature for mouse genes Likewise the HUGO Gene Nomenclature Committee HGNC provides official nomenclature for human genes MGNC and HGNC work collaboratively in establishing and revising standardized nomenclature for genes and gene groupings for the scientific community This joint effort has significantly increased in the last few years as a result of the co identification of human and mouse genes by both the research community and large scale sequencing centers Yearly meetings between MGNC and HGNC address nomenclature needs such as streamlining the correspondence between the two nomenclature groups achieving consistency in gene names defining working terms e g gene family vs gene grouping splice variant handling large scale annotation projects e g FANTON 2 HAWK1 and exchanging nomenclature data files between the Mouse Genome Database MGD http www informatics jax org Genew http www gene ucl ac uk cgi bin nomenclature searchgenes pl and LocusLink http www ncbi nlm nih gov genome guide human MGNC is now also actively involved in a collaboration with the Rat Genome and

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file103.shtml (2016-02-17)
    Open archived version from archive


  • The 16th International Mouse Genome Conference (2002)
    and Comparative Analysis of Genomes Attendees Sponsors Table of Contents Photographs Awards POSTER 104 Frap IS A CANDIDATE GENE FOR THE PLASMACYTOMA SUSCEPTIBILITY RESISTANCE LOCUS Pctr2 V Bliskovski NCI NIH 1 Ramsay E 1 Shi W 1 Scott J 1 Zhang S 2 Qian X 2 Lowy D 1 Mock B 1 Laboratory of Genetics CCR NCI NIH 2 Laboratory of Cellular Oncology CCR NCI NIH Mouse plasmacytomas provide a model for the dissection of complex genetic traits associated with cancer The Pctr2 locus resides in the telomeric region of mouse Chr 4 and the resistant DBA 2 allele delays the onset of plasmacytomagenesis in inbred strains of mice In the current study we report the identification of Frap as a candidate gene residing in the appropriate interval for the Pctr2 locus The Frap FKBP12 rapamycin associated protein gene encodes a kinase capable of phosphorylating many substrates and interacting with a large number of proteins involved in the PI 3 kinase signal transduction pathway which can be activated by IL6 We found that Frap may act as a tumor suppressor locus for pristane induced plasmacytomas by biochemical and biological assays Although studies with other systems have suggested that Frap may

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file104.shtml (2016-02-17)
    Open archived version from archive

  • The 16th International Mouse Genome Conference (2002)
    NULL BACKGROUND A R Mohn Duke University Medical Center 1 Hooker PE 1 Gainetdinov RR 2 Caron MG 1 Duke University Medical Center 2 Howard Hughes Medical Institute Duke University Medical Center Psychostimulants such as cocaine amphetamine and methamphetamine elicit their psychoactive and addictive effects in large part by the disruption of dopamine transporter function Dopamine transporter null mice dat exhibit physiological and behavioral states similar to chronic psychostimulant exposure including elevated extracellular dopamine postsynaptic receptor downregulation and hyperactivity Mice with this genetic alteration can be used in a screen to identify new genes that modify the dat phenotype Such genes will be expected to interact with the dopamine system directly or indirectly Because dopaminergic pathways are strongly implicated in reward mechanisms a subset of these genes may in fact play a role in the process of addiction Towards this goal we have begun a dominant modifier screen breeding ENU induced mutations onto a dat null background We have generated dat and dat G2 mice which have been screened initially by assessing intrinsic locomotor activity Dat mice with a significantly attenuated or exacerbated phenotype have been identified as putative mutants carrying dominant modifying mutations Further breeding and secondary phenotypic screens

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file105.shtml (2016-02-17)
    Open archived version from archive

  • The 16th International Mouse Genome Conference (2002)
    A TASTE RECEPTOR GENE TAS1R3 WITH SACCHARIN PREFERENCE X Li Monell Chemical Senses Center 1 Bachmanov AA 2 Li S 1 Tordoff MG 3 West DB 3 Ohmen JD 1 Beauchamp GK 1 Reed DR 1 Monell Chemical Senses Center 2 University Pennsylvania 3 Pfizer Global Research and Development Recent work suggests that the Tas1r3 is identical to the mouse saccharin preference Sac locus The goal of this study was to identify the sequence variant or variants most likely to account for the phenotype We sequenced 6 7 kb of the Tas1r3 gene and flanking region of six inbred mouse strains selected for high and low saccharin preference including the strains in which the Sac alleles were originally described C57BL 6J Sacb DBA 2J Sacd Sixty sequence variants were detected Of these sixty variants there were eight sites in which all three high preferring strains had one variant and all three low preferring strains had the other Each of these variant sites were genotyped in twenty four additional inbred mouse strains In most strains these eight variant sites were found in only two configurations the High and Low Preference haplotype In three inbred strains the haplotypes were recombinant Analysis of

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file106.shtml (2016-02-17)
    Open archived version from archive

  • The 16th International Mouse Genome Conference (2002)
    M University College London The recessive lethal teetering mutation arose spontaneously in C3H HeJ mice in 1958 Teetering mice are ataxic and have recently been shown to display bilaterally synchronous spike and wave pattern on EEG Noebels personal communication These symptoms are characteristic of other mouse models of absence epilepsy such as ducky The teetering gene tn was originally mapped to the distal end of mouse Chromosome 11 in a region showing conserved synteny with human 17q25 3 We aim to use an intersubspecific intercross to refine the location of tn and subsequently a positional candidate approach to identify the gene containing the causative mutation Over 500 F2 teetering offspring tn tn from a B6C3Fe a a tn x CAST Ei F1 intercross have been obtained and are being typed for a panel of microsatellite markers spanning the telomeric end of Chromosome 11 The results of this screen narrowed the tn critical region to 1cM between D11Mit104 79cM and D11Mit69 80cM In order to more finely map tn novel polymorphic microsatellites and SNPs within the region have been identified and utilised as markers This process has further localised tn to a region of approximately 1Mb between the genes for neuronal

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file107.shtml (2016-02-17)
    Open archived version from archive

  • The 16th International Mouse Genome Conference (2002)
    T 2 Shiroishi T 1 Gondo Y 1 Population and Quantitative Genomics Team and 2 Mouse Functional Genomics Research Group RIKEN Genomic Sciences Center Many inheritable mutants have been isolated by dominant screening in RIKEN ENU mutagenesis http www gsc riken go jp Mouse In the mutagenesis project it is crucial to identify the site of mutations in the genome for the mutants To this purpose we are currently taking three major approaches Positional cloning ENU mutagenized C57BL 6 males are mated to DBA 2 females to produce G1 for the phenotype driven approach Phenodeviant G1 are subjected to inheritance test in G2 progeny that also provide linkage for the rough mapping The sites of mutations will be identified by fine mapping and positional cloning or candidate gene approach as described below Candidate gene approach It is now plausible to list up candidate genes around the rough mapped region due to the substantial public database of mouse and or human genome We are now designing PCR primers for direct sequencing of candidate genes of some mutants We have found three possible causable point mutations in Pax 6 gene The primers that are prepared for the candidate gene approach are also

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file108.shtml (2016-02-17)
    Open archived version from archive

  • The 16th International Mouse Genome Conference (2002)
    Y 1 Taya C 2 Suzuki A 1 Yonekawa H 1 The Tokyo Metropolitan Institute of Medical Science 2 RIKEN Frontier Research System We have identified a mouse gene Gsl5 which controls the expression of a glycolipid GL Y Galbeta1 4 Fucalpha1 3 GlcNAcbeta1 6 Galbeta1 3 GalNAcbeta1 3Galalpha1 4Galbeta1 4Glcbeta1 Cer and the core2 structure of O linked glycans of glycoproteins GlcNAcbeta1 6 Galbeta1 3 GalNAcalpha Ser Thr in a kidney tubular cell specific manner The Gsl5 regulates the transcription of UDP GlcNAc beta 1 6 GlcNAc transferase c2GnT and was mapped to chromosome 19 closely linked to c2GnT gene An inbred strain DBA 2 which cannot express GL Y has a recessive allele of Gsl5 The DBA 2 phenotype is rare in the laboratory strains but found in all of mice which are derived from a M m musculus subspecies distributed from East Europe to Far East Asia A sequence comparison for the 5 flanking region of the c2GnT gene among 5 laboratory strains and 10 wild derived strains suggests that DBA 2 allele of Gsl5 was introduced into laboratory mouse strains by Asian wild derived mice BAC rescue experiment using a 150 kb clone that contains c2GnT

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file109.shtml (2016-02-17)
    Open archived version from archive

  • The 16th International Mouse Genome Conference (2002)
    T 2 Shiroishi T 1 Gondo Y 1 Population and Quantitative Genomics Team and 2 Mouse Functional Genomics Research Group RIKEN Genomic Sciences Center For gene driven mutagenesis as well as candidate gene approach it is necessary to develop an efficient system for detection of the sites of novel point mutation in the mouse genome It must be high throughput cost effective and accurate For this purpose we designed more than 200 pairs of primers to amplify target sequences of C57BL 6 genome The size of these amplicons ranges from 200 bp to 1 2 kb We have been testing the efficacy of the point mutation detection in the amplicons by using direct sequencing TGCE and DHPLC We have firstly tried the direct sequencing method to identify point mutations in target genes The sequencing data have been fairly well produced However the method is relatively expensive and slow and the analyses of numerous chromatogram data are laborious and error prone It is thus necessary to develop some primary screening method with high resolution and high throughput system to detect the site of mutations We have adopted the TGCE Temperature Gradient Capillary Electrophoresis method which can effectively detect heteroduplex DNA It

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file110.shtml (2016-02-17)
    Open archived version from archive



  •