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  • 18th International Mouse Genome Conference (2004)
    mitosis In addition to their role in the maintenance of expression patterns of homeotic genes these complexes also act upon other genes to maintain cellular differentiation in such processes as development hematopoiesis and tumorigenesis Mice with mutations in the Eed gene display defects in imprinted X inactivation and autosomal imprinting The major defect is a failure to maintain transcriptional repression in the silenced chromosome or alleles Data from this lab

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file91.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    Zurich Zurich Switzerland Genetic predisposition to cancers is significant to public health because a high proportion of cancers probably arise in a susceptible human subpopulation One major model for polygenic predisposition is the common variant common disease model in which common variants that have arisen only once early in the history of the population underlie disease predisposition in humans and perhaps in mice The mapping and isolation of such variants in humans are complicated by the multiplicity of unlinked loci whereas for mouse models of cancer susceptibility experimental strategies exist for fine mapping of complex traits Using a mouse model of g ray induced thymic lymphomas we performed linkage analysis and haplotype mapping that identified Mtf 1 metal responsive transcription factor 1 as a candidate lymphoma susceptibility gene The Mtf 1 allele inherited from resistant strains exhibited higher radiation inducibility of target genes than that of susceptible strains and products of the targets such as metallothionein are able to suppress cellular stresses generated by irradiation Therefore this suggests that highly inducible strains are refractory to radiation effects and hence are resistant to lymphoma development Interestingly the Mtf 1 polymorphism was common to different mouse subspecies consistent with the common variant common disease model Genetic predisposition to cancers is significant to public health because a high proportion of cancers probably arise in a susceptible human subpopulation Using a mouse model of g ray induced thymic lymphomas we performed linkage analysis and haplotype mapping that identified Mtf 1 metal responsive transcription factor 1 as a candidate lymphoma susceptibility gene The Mtf 1 allele inherited from resistant strains exhibited higher radiation inducibility of target genes than that of susceptible strains and products of the targets such as metallothionein are able to suppress cellular stresses generated by irradiation Therefore this suggests that highly inducible

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file92.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    expression of interferon gamma is regulated is limited Herein we identify two evolutionarily conserved non coding sequence elements IFNgCNS1 and IFNgCNS2 located 5kb upstream and 18kb downstream of the initiation codon of the murine Ifng gene When linked to the murine Ifng gene 3 4 to 5 6 kb and transiently transfected into EL 4 cells IFNgCNS1 enhanced IFN gamma production and this was amplified further by inclusion of IFNgCNS2

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file93.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    S 1 Sundberg J 2 Cacheiro N 1 Chao H 3 Carpenter D 1 Johnson D 1 Rinchik E 3 You Y 1 1 Oak Ridge National Laboratory Oak Ridge United States 2 The Jackson Laboratory Bar Harbor United States 3 University of Tennessee Knoxville United States The mouse Hairy Ears Eh mutation is a paracentric inversion In 15 Eh 2Rl in the distal half of Chr 15 Heterozygous Eh mice have small and hairy ears whereas Eh Eh homozygotes in C3H Rl background typically die before weaning We mapped both the proximal and distal inversion breakpoints to BAC clones using fluorescent in situ hybridization FISH on metaphase Eh cell spreads cloned the distal breakpoint and determined inversion breakpoint sequences Consequently genes surrounding the inversion breakpoints were identified No protein coding transcripts are disrupted by either inversion breakpoints The proximal breakpoint occurs between Sntb1 syntrophin 1 centromerically and Has2 hyaluronan synthase 2 telomerically while the distal breakpoint takes place between the Hoxc4 Homeobox C4 centromerically and an uncharacterized transcript GenBank accession numbers BF606930 and AK019974 telomerically Therefore the inversion spans 47 Mb Quantitative RNA analysis by TaqMan real time PCR assay for the Hoxc genes indicated that expression of many

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file95.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    G Bartolomei M University of Pennsylvania Philadelphia United States The 2 kb differentially methylated domain DMD 5 of H19 is exclusively methylated on the paternal allele throughout development and is required for H19 and Igf2 imprinting In mice harboring a 1 6 kb deletion of the DMD D DMD or a 3 8 kb deletion spanning the DMD D 3 8kb 5 H19 loss of H19 and Igf2 imprinting is detected in all neonatal tissues G D 12 3693 MCB 22 2450 In addition the DMD is required for full expression of H19 and Igf2 Nevertheless DMD sequence that remains in the D DMD mice acquires slightly more methylation on the paternal allele than on the maternal allele indicating that some parental specific identity is maintained that does not result in differences in parental specific expression Here we investigate allele specific DNA methylation and gene expression patterns at the H19 locus in the D DMD and the D 3 8kb 5 H19 mice in pre and post implantation embryos to determine when loss of H19 and Igf2 imprinting occurs We detect loss of imprinting at the H19 locus from the deletion alleles after embryo implantation We have also generated a

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file96.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    1 Gondo Y 5 Noda T 1 Wakana S 1 Ishino F 4 Sasaki H 2 Shiroishi T 1 1 Mouse Functional Genomics Research Group Genomics Science Center GSC RIKEN Yokohama Institute Yokohama Japan 2 Department of Integrated Genetics National Institute of Genetics Mishima Japan 3 Gene Research Center Tokyo Institute of Technology Yokohama Japan 4 Department of Epigenetics Medical Research Center Tokyo Medical and Dental University Tokyo Japan 5 Population and Quantitative Genomics Team GSC RIKEN Yokohama Japan Genomic imprinting is epigenetic regulation of gene expression depending on parental origin of the genes in mammals In order to detect and identify novel genes involved in the initiation of the genomic imprinting we have established a screening system for mutants that show impaired genomic imprinting in the RIKEN mouse ENU mutagenesis program In our screening we measure methylation levels of imprinted genes in the mature gametes using methylation sensitive enzymes or the COBRA combined bisulfite restriction analysis Both of non methylated and re methylated imprinted genes are analyzed for one individual to detect the mutants that show aberrant imprinting in the two stages erasure of parental imprints and re establishment of sex different imprints In this system we can constantly

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file97.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    EMBRYONIC LETHALITY de la Casa Esperon E 1 Gimelbrant A 3 Adey B 1 Briscoe T 1 Hao L 1 Wu G 1 Chess A 3 Pardo Manuel de Villena F 2 Sapienza C 1 1 Fels Institute Temple University School of Medicine Philadelphia PA United States 2 Department of Genetics UNC Chapel Hill Chapel Hill NC United States 3 Whitehead Institute for Biomedical Research MIT Cambridge MA United States The DDK syndrome of embryonic lethality is observed in crosses between females of the DDK inbred strain with males of other strains e g C57BL 6 in which the resulting embryos die around the time of implantation while the reciprocal cross non DDK females x DDK males is viable The lethality is the result of an interaction between a maternal gene of DDK origin which is expressed in oocytes and a non DDK paternal gene Both genes Om map in the same region of chromosome 11 Interestingly the Om candidate region in DDK chromosome 11 lacks 50 Kb present in the C57BL 6 chromosome In addition only half of the offspring of the backcross between C57BL 6xDDK F1 females and C57BL 6 males survive This observation suggests that the maternal

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file98.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    DISEASE IN SOX10 DOM MICE Owens SE 1 Broman KW 2 Smith JR 1 Southard Smith EM 1 1 Vanderbilt University Nashville United States 2 Johns Hopkins University Baltimore United States Hirschsprung disease HSCR is caused by abnormal development of the neural crest cells that comprise the enteric nervous system resulting in an absence or reduction of enteric ganglia in a variable portion of the distal gastrointestinal tract Dominant megacolon Sox10 Dom mice model the aganglionic megacolon seen in HSCR and SOX10 mutations have been identified in a subset of HSCR patients Sox10 Dom heterozygote mice on a mixed genetic background B6C3F1 mimic the variable severity of aganglionosis in HSCR patients and this variation is influenced by genetic background To establish linkage to modifier genes that modulate the severity of aganglionosis in Sox10 Dom mice we performed a genome wide scan Penetrance and extent of intestinal aganglionosis was quantified by whole mount acetylcholinesterase AChE histochemistry on gastrointestinal tracts from postnatal day 7 10 backcross n 204 and intercross n 1092 progeny Mice from the extremes of the phenotype distribution along with mice in which aganglionosis was not penetrant were genotyped by fluorescence polarization methods to distinguish 104 SNP markers at

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file99.shtml (2016-02-17)
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