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  • 18th International Mouse Genome Conference (2004)
    first in the germ cell lineage sharing many features with the embryonic stem cells Unlike differentiated somatic cells the PGCs possess ability to erase epigenetic modifications on the genome accumulated during development Thus PGCs can be regarded as the cells programmed to rejuvenate the genomic status Despite of this biological importance molecular nature of the PGCs remains largely unknown We have established systematic methodologies to analyze PGCs and related embryonic cells PGCs were purified from transgenic mouse embryos in which the PGCs were marked by GFP reporter expression and cDNA libraries were made with the purified PGCs transcriptome of the PGCs were explored by EST analyses and microarray ESTs were classified according to the NIA Mouse Gene Index the analyzed 18 293 ESTs were clustered into 6 159 transcripts and 4 833 genes of which 435 were unknown genes Analysis of EST frequency suggested expression level of each gene and identified signature genes for PGCs Principal component analysis of EST frequency showed that PGCs are more similar to blastocyst or Trophoblast stem TS cells rather than undifferentiated ES cells or embryonic germ EG cells which were derived from PGCs We compared gene expression profiles of ES EG PGC and PGC

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file42.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    DL Matera I Baxter LL Elliott G Rivas C Incao A Pavan WJ National Human Genome Institute NIH Bethesda MD United States We have established an enhancer screen in mouse to identify novel mutations disrupting development of the neural crest derived melanocyte lineage Our focused phenotype screen is based on the prediction that ENU induced mutations acting synergistically with the neural crest transcription factor Sox10 will cause white spotting larger than the typical spot 1 3 1 0 of total ventral body area that we observe in Sox10 LacZ heterozygous mutant control animals In screening 100 first generation pedigrees we have identified 2 heritable phenotypes that display a significant increase in white spotting on the Sox10 LacZ heterozygous background The BALB cJ and C57BL 6J mixed genetic background of our cross has facilitated subsequent mapping of these ENU induced mutations to two independent regions of the genome distinct from loci previously implicated in known coat color mutants Positional cloning is currently underway to identify the mutations responsible for these ENU induced alleles In addition to the second generation phenotype screen third generation embryos from 20 lines have been screened for both dominant and recessive embryonic phenotypes that alter expression of

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file43.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    genomic instability to processes of biological aging will be reviewed in the context of a classification of gene actions that escape the force of natural selection Murine models are increasingly utilized to address these issues Examples have implicated important contributions of mitochondrial and nuclear genomic instability and of epigenetic and genetic instability Senescent phenotypes will be shown to be associated with early gene actions that are either adaptive or non

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file11.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    MB Luo G Department of Genetics Case Western Reserve University and Ireland Cancer Center University Hospitals of Cleveland Cleveland United States Rothmund Thomson Syndrome RTS is a genetically heterogeneous autosomal recessive disorder Type II RTS patients have RECQL4 mutations abnormalities of the skin and skeleton and increased risk for developing osteosarcoma Karyotypic analyses of type II patient derived cells demonstrate unusually high frequencies of chromosomal aberrations including aneuploidy While chromosomal instability likely contributes to the patients increased susceptibility to osteosarcoma the nature of genomic instability induced by RECQL4 deficiency and the disease etiology of RTS remains elusive We generated Recql4 deficient mice to study the role of Recql4 in maintaining genomic stability Recql4 deficient mice recapitulate the hallmark features of RTS with skeletal abnormalities of the palate and limbs ultraviolet light induced hyperpigmentation associated with premature photoaging and increased susceptibility to osteosarcoma and lymphoma Cells from Recql4 deficient mice display aneuploidy and chromosomal instability with an increased incidence of anaphase lagging chromosomes and high rates of spontaneous micronuclei formation Remarkably in Recql4 deficient cells aneuploidy manifests in the absence of defects in spindle checkpoints or aberrant centrosomes hyperamplification Further analysis revealed that premature centromere separation induced unequal chromosome partitioning is

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file44.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    States Pinkie is a recessive ENU induced mutation homozygotes develop premature graying and subsequently progressive alopecia Histologically the skin is characterized by the destruction of hair follicle architecture formation of dermal cysts and appearance of black papules throughout the ventral skin late in life The Pinkie mutation was mapped to the retinoid X receptor alpha Rxr a locus chromosome 2 on 700 meioses and positionally cloned As a component of the nuclear receptors for retinoic acid and other bioactive molecular ligands RXR a plays an irreplaceable role during embryogenesis and a null allele of RXR a inevitably causes embryonic lethality Pinkie which results from the amino acid substitution N273I in the ligand binding domain is the first viable germline hypomorphic mutation of RXR a Transfection studies suggest that the abnormal protein retains only 10 to 20 of the activity of the wild type receptor Pinkie homozygotes develop a progressive phenotype part of which entails a severe age dependent imbalance of Th1 Th2 differentiation upon antigenic challenge When immunized with ovalbumin OVA pinkie homozygotes displayed markedly decreased IgG1 levels in serum as compared with normal C57BL 6 mice in vitro OVA re stimulation of pinkie splenocytes causes greatly enhanced IFN g

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file45.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    DL 1 1 Medical College of Ohio Toledo United States 2 Spanish National Cancer Center Madrid Spain 3 Cancer Research UK London Research Institute Hertfordshire United Kingdom Homologous recombination HR is a double strand break repair pathway required for resistance to DNA damage and maintaining genomic integrity In mitotically dividing cells the primary proteins involved in HR repair are RAD51 and the five RAD51 paralogs RAD51B RAD51C RAD51D XRCC2 and XRCC3 By investigating Rad51d knockout mice and mammalian cell lines we demonstrate that RAD51D is critical for maintaining chromosome stability and telomere protection Homozygous mice defective for Rad51d die prior to birth and cells derived from mutant embryos fail to proliferate in culture likely as a result of genomic instability and p53 activation A p53 deletion is sufficient to extend the lifespan of Rad51d deficient embryos by up to 6 days and rescue the cell lethal phenotype Rad51d Trp53 mouse embryo derived fibroblasts were sensitive to DNA damaging agents particularly interstrand crosslinks and exhibited extensive chromosome instability including aneuploidy chromosome fragments deletions and complex rearrangements Additionally loss of Rad51d resulted in increased centrosome fragmentation and reduced levels of radiation induced RAD51 focus formation Spontaneous frequencies of sister chromatid exchange SCE

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file46.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    disruption of Eg5 function leads to mitotic arrest monopolar spindles and aneuploidy In cultured post mitotic axons inhibition can disturb axonal outgrowth Additionally Eg5 has been shown to be regulated by the centrosomal kinase Aurora A STK15 which is often over expressed in numerous cancers We showed that Eg5 is up regulated in B cell leukemias from AKXD recombinant inbred mice with proviral insertions at lymphoid viral insertion site Lvis1

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file47.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    Attendees Awards PLENARY PRESENTATION THURSDAY OCTOBER 21 8 30am 9 00am Genetics of host resistance to cytomegalovirus infection Role of h2 and nk receptors Vidal S McGill University Montreal Canada Human cytomegalovirus CMV infection can cause life threatening disease in immunodeficient hosts Experimental infection in mice has revealed that natural resistance to mouse CMV is genetically determined and mediated by binding of the natural killer NK cell activating receptor Ly49H

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file12.shtml (2016-02-17)
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