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  • The 16th International Mouse Genome Conference (2002)
    LABORATORY DB Lane The Jackson Laboratory Rockwood SF Mobraaten LE Davisson MT The Jackson Laboratory Genomic and biological similarities between mice and humans and the accumulated knowledge about mouse genetics establish the mouse as the foremost research tool for studying human disease Models for studying human disease that are generated by mouse genome manipulation offer an opportunity to dissect complex etiology and an in vivo system for testing detection methods and pharmacological treatments Increasing development and use of mouse models requires cooperative resources to preserve and distribute them The Induced Mutant Resource IMR at The Jackson Laboratory allows the scientific community to access biomedically significant mouse models by collecting and distributing induced mutant mouse strains As a centralized repository and resource the IMR also ensures genetic integrity and protects each strain by cryopreservation The IMR offers support to researchers in the form of curated strain information through an online database Mutant strain records in the IMR database include information on phenotype description strain development husbandry and related references and are linked to other relevant online resources The IMR will expand the existing collection of 871 accepted strains by approximately 60 strains each year Nearly 120 000 mice are distributed each

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file129.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    Centre for Functional Genome Research Department of Medical Genetics IMBG The Panum Institute University of Copenhagen Denmark 2 Experimental Molecular Genetics Laboratory IMBG The Panum Institute University of Copenhagen Denmark ZNF genes comprise one of the largest famillies of genes several of which are associated with malignant disorder ZNF151 and the murine homologue Zfp100 contain a POZ BTB domain which obstruct the binding of nearby zinc finger domains to DNA ZNF151 was isolated and mapped to 1p36 1 p36 2 by our group and has been shown to have a potent growth reducing effect on HeLa cells In a two hybrid system ZNF151 interacts with MYC disordered expression of which alters differentiation cell proliferation and growth Furthermore ZNF151 binds and transactivates adenovirus major late and cyclin D1 promotors ZNF151 is therefore likely to be involved in important growth regulating pathways and is a candidate tumour suppressor gene To investigate the function of ZNF151 we are currently generating a mouse model where Zfp100 is knocked out Zfp100 was cloned and we have localised it to D4mit284 For this purpose we are creating a targeting vector by which we will delete the largest part of the POZ BTB domain thereby destroying the

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file130.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    ANALYSIS OF CREB BINDING PROTEIN CBP IN MICE USING AN ENU BASED MUTAGENESIS APPROACH IN EMBRYONIC STEM CELLS M K Bunger University of North Carolina Magnuson TR University of North Carolina The CREB binding protein CBP is a transcriptional coactivator with histone acetyltransferase HAT activity Through this activity CBP integrates multiple biological signals that are critical for developmental and physiological processes Several gene knockout studies indicate that functional CBP protein is necessary for embryonic development in mice Moreover heterozygotes of these null alleles also exhibit phenotypes resembling the human disease Rubenstein Taybi syndrome characterized by specific limb defects lymphoid tumors and learning deficits We are using a novel gene based mutagenesis strategy in embryonic stem cells to generate an allelic series of mutations at Cbp in mice in order to address specific roles of subdomains of CBP protein in vivo Several point mutations identified alter important amino acids and splicing in domains of CBP protein responsible for HAT activity and protein protein interactions Once mice are made a battery of in vitro tumor vascular behavioral and skeletal endpoints will be assessed to provide insight into specific contributions of individual CBP domains and interactions in mouse development and disease processes associated

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file131.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    and the CMHD 1 Centre for Modeling Human Disease 2 Canadian Mouse Mutant Repository Objectives The goal of the Centre for Modeling Human Disease CMHD is to use genome wide N Ethyl N nitros urea ENU mutagenesis in mice to functionally annotate the mouse genome The objectives of the Pathology Core within the CMHD are two fold 1 to identify mutant phenotypes that have not been detected during in life screening and 2 to better characterize mutant phenotypes that have been discovered in the CMHD s in life screening cores The Canadian Mouse Mutant Repository CMMR works in partnership with the CMHD to recover and archive the expansive germ cell and tissue resources generated by the CMHD Methods The Pathology Core PC of the CMHD provides detailed gross and histopathological immunohistochemical morphometric and slide based screens as essential components of the CMHD s dominant screen genome wide mutagenesis program We have developed a high throughput facility for morphology and tissue slide based assays of mutagenized mice Important considerations in high throughput screening of our ENU mutants include sample identification and tracking expert interpretation of bona fide phenotype in mouse tissue and reproducibility and consistency of specimen collection The pathology and

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file132.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    Masuya H 1 Inoue M 1 Suzuki T 1 Kobayashi K 1 Wakana S 3 Gondo Y 1 Minowa O 1 Shiroishi T 1 Noda T 1 Mouse Functional Genomics Research Group RIKEN GSC 2 Department of Environmetrics and Biometrics Research Institute for Radiation Biology and Medicine Hiroshima University 3 Population and Quantitative Genomics Team RIKEN GSC To identify mouse models of human diseases we have established blood test system for screening mutagenized offspring and confirming of heritability of mutant in RIKEN ENU mutagenesis project This blood test system consists of hematological test and clinical biochemical test For hematological test about 200 micro L of blood per mouse is collected at the age of 9 weeks and 32 parameters were measured by automatic hematology analyzer ADVIA120 Bayer Using a statistical method with mixed normal models we determined normal ranges of these parameters to identify outliers For clinical biochemical test blood is collected at the age of 11 weeks About 75 micro L of serum is separated from the collected blood and applied to automatic clinical biochemical analyzer JCA BM2250 JEOL Using a similar way in hematological test normal ranges of 30 parameters were determined For each test we have screened

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file133.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    Chavez Reyes A Lang G Lozano G MD Anderson Cancer Center MDM2 is a p53 transcriptional target that binds to p53 and inhibiting it s activity Mice carrying a homozygous null allele for mdm2 exhibit an early embryonic lethality at 5 5 dpc due to increased apoptosis MDMX a homolog of MDM2 can also bind p53 and inhibit it Mdmx homozygous null mice are early embryonic lethal due to a lack of proliferation beyond 7 5 dpc Surprisingly both mdm2 and mdmx homozygous null mice are viable in a p53 null background These data further define the p53 pathway in which MDMX inhibits p53 dependent cell cycle arrest and MDM2 inhibits p53 dependent apoptosis To determine if MDM2 and MDMX were compensating for each other in p53 independent functions we attempted to generate mdm2 mdmx p53 triple null mice Surprisingly the triple null mice are viable and fertile indicating no compensatory developmental function However preliminary data suggest that the survival curve of the triple null mice is severely reduced compared to mdm2 p53 double null mdmx p53 double null or p53 null mice Thus MDMX and MDM2 may have redundant p53 independent roles Additionally we have generated mice carrying a

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file134.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    Unit 1 Edgar R 2 Holdsworth A 1 Taylor M 1 White S 2 Justice M 1 Jackson I 1 MRC Human Genetics Unit 2 Baylor College of Medicine The brown Tyrp1 locus on mouse chromosome 4 is one of the best studied regions of the mouse genome Over the last 50 years a panel of 27 independent deletions generated from a variety of mutagenic protocols have been characterised within this region We have utilised this resource and sequence from a BAC contig across this 22Mb interval to define deletion breakpoints and to identify candidate genes for several mouse phenotypes known to map to this region We have used ENU to generate mutant mice which map to this interval by crossing mutagenised animals with mice carrying brown deletions This approach has identified more than 26 recessive mutant mouse lines whose phenotypes range from lethality to defects of behaviour and development We present analysis of candidate genes for two mutants which map in the region depilated dep a spontaneous mutation affecting the coat and brown associated fitness baf a semi viable mutant which has an uncharacterised gut pathology The dep candidate Depc is part of a conserved and novel extracellular matrix

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file136.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    Medicine 1 Yang G 1 Nguyen S 2 Magnuson M 3 Bartolomei M 1 University of Pennsylvania School of Medicine 2 Vanderbilt University Medical Center 3 HHMI and University of Pennsylvania School of Medicine 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 DDMD or a 3 8 kb deletion spanning the DMD D3 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 DDMD 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 We are currently investigating allele specific DNA methylation and gene expression patterns at the H19 locus in the DDMD and the D3 8kb 5 H19 mice in early stages of development to determine when loss of H19 and Igf2 imprinting occurs We

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file137.shtml (2016-02-17)
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