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  • The 16th International Mouse Genome Conference (2002)
    Richter T 1 Favor J 1 Atkinson MJ 1 GSF Natl Research Center for Environment and Health Neuherberg 2 Technical University Munich Individual cancer risk can vary considerably depending on inherited genetic conditions We used a mouse model of Thorium227 induced osteosarcoma to map susceptibility loci and analyse candidate modifier genes Backcross studies from strains Balb c CBA CA C3H and 102 revealed genetic linkage to loci on distinct chromosomes A locus on chromosome 14 about 5cM including the Rb1 gene exhibited the most significant linkage and was thus considered the major susceptibility locus Comparative sequencing of the Rb1 gene revealed a hexanucleotide duplication in the promoter of the Balb c strain which is associated with osteosarcoma resistance with and shows enhanced transcriptional activity CAT reporter assays mRNA quantification The most significant effects upon osteosarcoma predisposition were found if multilocus inheritance was taken into account In C3H 102 testcrossed mice tumor incidence was 22 for RR genotype compared to 75 for SS genotype with indications for epistatic locus interaction About 20 of the variance can be explained by these two factors The phenotypic effect was even more striking in Balb c and CBA CA mice where 4 additional modifier loci

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file24.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    Mölndal A wide variety of pathophysiological phenotypes is common to mouse and Man The mouse has therefore become the model organism of choice for trying to identify genes involved in these phenotypes An in silico technique for QTL prediction based on multi strain comparison of SNPs has been described Here the original approach was extended by including microsatellites into the analysis and modifications introducing a higher flexibility to the approach

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file26.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    2 Case Western Reserve University School of Medicine 3 Case Western Reserve University School of Medicine and University Hospitals of Cleveland 4 HHMI and University of Pennsylvania School of Medicine X inactivation in mice requires elements within the X inactivation center Xic on the X chromosome including the X controlling element Xce Xce is believed to affect choice of which X chromosome is inactivated in the mouse While all factors necessary for X inactivation map within the Xic it is posited that unidentified autosomal factors are essential to the process To identify such novel factors we have developed a phenotype driven N ethyl N nitrosourea ENU mutagenesis screen for dominant mutations that disrupt X inactivation patterns in female mice A total of 346 G1 females were assayed and dominant mutations that perturb X inactivation patterns were identified in two independent pedigrees Science 296 1136 Carrier Xce heterozygous females exhibit a shift of their X inactivation pattern from 30 70 to 50 50 suggesting an interaction between these mutations and the Xce locus We have demonstrated the dominant transmission of the mutant phenotypes for at least six generations in both pedigrees Furthermore the mutant phenotypes are present in all tissues examined

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file28.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    Research Institute 2 Hogenesh J 1 2 Kay S 2 Wiltshire T 1 The Scripps Research Institute 2 Genomics Institute of the Novartis Research Foundation Use of recombinant inbred RI mice allows for the mapping of genes affecting multiple and widely varying phenotypes without requiring new genotyping data for each mapping exercise Therefore a detailed map of strain distribution patterns for RIs linked to physical chromosomal positions provides a resource that rapidly define candidate regions for quantitative trait loci QTL of any phenotype characterized in the mice We have typed all 13 publicly available CxB RI strains with 505 single nucleotide polymorphism SNP based markers and combined the new data with the existing genotype data from another 845 genetic markers Sequence for the 1350 markers roughly one marker every 2MB were compared against both the Ensemble and Celera genomic sequence assemblies and ordered accordingly The combined genetic physical map contained an additional 57 strain distribution patterns compared to the older data set As a test of the integrated map previously described phenotype data for differences in the ratio of light dark activity rates in CxB RI strains was applied and a 4 35 MB region on chromosome 19 was indicated

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file30.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    1 Kitasaka Y 5 Ichikawa Y 4 Moriaki Kusakabe 1 RIKEN Tsukuba Institute 2 Natinal Cancer Center Research Institute 3 Balylor College of Medicine 4 ANB Tsukuba Institute 5 Nihon Medical University Mouse hair mutants are useful animal models to study molecular mechanism of hair development and human hair disease A spontaneous mouse hair mutation Hague Japanese word for bald on Chromosome 15 was recovered in C3H HeN mice colony The purpose of this study is to clarify pathological characteristics of the mutant hair follicle and to identify the causative gene The original mutant was recovered as wavy hair mouse In homozygote mice lost most hairs around 1 month of age This mutation was shown to be unstable since its transmission could be switched from semi dominant to recessive Histopathological analyses demonstrated that the significant abnormality was detected in the inner root sheath IRS To identify the causative gene and the nature of the mutation a YAC and BAC physical map of the critical region was constructed Meanwhile subtraction of differentially expressed genes between mutant and normal mice skin recovered keratin2 6g as a candidate gene which mapped in the critical region This keratin2 6g was reported as a novel

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file31.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    Biomedical Research Center Mahli N Pennington Biomedical Research Center A subcongenic mouse strain derived from the B10 LP H3bH13b strain has been generated on the C57BL 6J B6 genetic background This B6 LPa strain contains 5 2 6 5 cM of LP J derived DNA spanning D2Mit444 to D2Mit304 Two main phenotypes are observed between B6 LPa and B6 mice One the congenic strain is resistant to the development of obesity in response to a high fat high sucrose HF diet and two B6 LPa mice possesses significantly lower fasting insulin levels than B6 on both low fat chow and HF diets The genetic region containing this QTL overlaps with body weight adiposity hyperinsulinemia and diabetes QTL reported by others including a QTL regulating insulin levels in mice heterozygous for the null allele of the insulin receptor gene It is possible that polymorphism of a single gene may underlie some or all of these phenotypes Although the region contains many candidate genes we describe our characterization of one polymorphic gene that is overexpressed in insulin receptor deficient mice This gene Zfp106 encodes a downstream target of the insulin signaling pathway but was initially identified as the polymorphic gene encoding the

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file32.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    of Cytology Genetics Osadchuk AV Siberian Banch of the Russian Academy of Sciences Our aim was to explore variability of heritable pattern of the Leydig cell responsiveness LCR during the postnatal development For this purpose a diallel analysis of hCG cAMP and pregnenolone stimulated testosterone production by Leydig cells during the postnatal development was performed in males of four inbred mouse strains BALB c PT CBA Lac and A He and their F1 reciprocal hybrids These strains were chosen as most contrasting in the adult LCR The cAMP and substrate dependent testosterone production in vitro was analyzed on days 20 35 60 and 100 of the postnatal life which are the critical periods in the Leydig cell development Testosterone content in the incubation medium was determined by RIA Based on two way ANOVA we demonstrated highly significant interaction between genotype and age effects The genotype effect was characterized by two specific features First the coordinated genetic variability in the cAMP and substrate dependent LCR was observed in each postnatal stage examined Second the coordinated genetic variability was subjected to substantial developmental changes In particular adult heritable pattern in the LCR was mainly formed at the late pubertal early postpubertal stage

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file33.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    Davies J Alexander E Heines H Madge J Napper H Robertson L McKeone R Southwell A Denny P Arkell R Mouse Genome Centre Mammalian Genetics Unit MRC A recessive two generation screen for mouse mutants that affect postimplantation embryonic development is underway ENU induced mutations are recovered in the region of the Del 13 Svea36H Del36H deletion on chromosome 13 This cytogenetically visible deletion removes a 13 Mb region of MMu13 that includes the satin locus Foxq1 Mice that are homozygous null for Foxq1 have a glossy coat and are distinguishable from their littermates at 10 days post birth This locus is used to follow the mutagenised chromosome throughout the recessive screen In the screening protocol male mice with a satin coat are mutagenised and crossed to wild type BALB C females F1 male progeny are then crossed to female carriers of Del36H and the prevalence of progeny with a satin coat used to indicate those lines that potentially carry a new recessive lethal mutation Once the presence of a mutation is confirmed the time of lethality and the associated embryonic phenotype is investigated and recombination mapping is performed to further localise the mutation within the deleted region In parallel

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file34.shtml (2016-02-17)
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