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  • 17th International Mouse Genome Conference (2003)
    Genomics of Infectious Disease Verne Chapman Memorial Lecture Table of Contents Sponsor Exhibitor List Awards Photographs POSTER 12 CHARACTERIZATION OF EXPRESSION DIFFERENCES IN WAVED 3 MICE THAT LEAD TO ABNORMAL HEART AND SKIN DEVELOPMENT Herron B 1 Wadsworth Center NYS DOH 2 SUNY Albany Co Authors 2 Oliveri E 1 Parker A 1 Kinne J 4 Lien E 4 Olsen E 3 Beier D Institutions 1 Wadsworth Center NYS DOH 2 SUNY Albany 3 Harvard Medical School 4 UT South western Medical school We are characterizing a novel mouse phenotype that is due to a mutation in Nfkb Nkx interacting protein 1 Nkip1 Waved 3 wa3 mice are phenotypically similar to wa1 and wa2 mice but also have a progressive and ultimately lethal form of dilated cardiomyopathy Nkip1 has been shown to interact with several transcription factors including the RelA subunit of NFkB and Nkx2 5 Nkip1 is thought to repress the activity of these proteins however this function has only been investigated through in vitro studies To identify what transcriptional networks are abnormal in wa3 wa3 mice and ultimately find genes that are direct targets of Nkip1 we are surveying expression of genes previously shown to be targets of

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file60.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    Katayama K Graduate School of Natural Science and Technology University of Okayama Co Authors Miyamoto S Furuno A Tsuji T Kunieda T Institutions Graduate School of Natural Science and Technology University of Okayama Eh and Koa mutant mice have chromosomal inversions on chromosome 15 and most of their inverted regions are common to the both mutants Eh heterozygotes have hairy short pinna and slightly roundy shaped face and Koa heterozygotes exhibit hairy pinna and swell of whisker pad It is likely that the phenotypes of these mutants are caused by disruption and or altered expression of gene s which localized on or near the breakpoints of the inversions In this study we defined the breakpoints of the both inversions by creating the mice with chromosomal deletions which result from the recombination within the common inverted region of the both mutations The deleted regions must be flanked by the breakpoints of Eh and Koa mutants Consequently the Eh inversion was revealed to occur in a 47Mbp region of distal half of chromosome 15 and the proximal and distal breakpoints are located at 39 kb proximal to LOC223591 gene and at 8kb distal to Hoxc 4 gene respectively The Koa inversion was

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file61.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    Genomics of Infectious Disease Verne Chapman Memorial Lecture Table of Contents Sponsor Exhibitor List Awards Photographs POSTER 14 BCL11B A TUMOR SUPPRESSOR GENE IN T CELL DEVELOPMENT Kominami R Niigata University Co Authors Yu ichi Wakabayashi Institutions Niigata University Lymphocyte development is a complex process that involves the coordinated action of many transcription factors We show here that a Kruppled like factor Bcl11b is required in T cell development which was isolated as a tumor suppressor gene by analyzing a region of loss of heterozygosity in thymic lymphomas Its paralog Bcl11a is involved in B cell development and the two genes are associated with immune system malignancies We have generated Bcl11b deficient miceto elucidate roles of Bcl11b in T cell and lymphoma development Bcl11b mice showed a developmental arrest at the CD4 CD8 double negative stage of thymocyte development without any impairment in cells of B or γδ T cell lineages Their thymocytes showed unsuccessful Vβ to Dβ recombination and lacked the pre TCR complex on the cell surface due to the lack of T cell receptor β mRNA expression In addition profound apoptosis was seen in the thymus of neonatal Bcl11b mice The thymic arrest and apoptosis are the

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file62.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    Co Authors 1 Smiraldo P 1 Gruver A 1 Osborn J 2 Miller K 2 Albala J 3 Tarsounas M 3 Claas A 3 West S Institutions 1 Medical College of Ohio 2 Lawrence Livermore National Laboratory 3 Cancer Research UK London Research Institute A large part of biology is defined by the reshuffling of genomes Chromosome rearrangements are origins for genetic variation speciation and immunological diversity Yet genome instability is a cancer initiating event and errors during meiosis cause syndromes and infertility Homologous recombination is a pathway for maintaining genomic stability and is directed primarily by the Rad51 gene family We currently focus our attention on Rad51d Embryos deficient for Rad51d died midway through gestation and lethality was partially bypassed by introducing an additional disruption in the Trp53 tumor suppressor gene At the cellular level Rad51d deficient mouse embryo fibroblast MEF cells were hypersensitive to DNA damaging agents failed to recruit the Rad51 protein to sites of DNA damage and exhibited gross chromosomal instability Moreover the Rad51d protein localizes to telomeres of meiotic and mitotic cells Elevated anaphase bridges and end to end mitotic chromosome fusions in MEF cells indicated direct involvement of Rad51d in telomere maintenance Additionally inhibition

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file63.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    Genetics and Genomics of Infectious Disease Verne Chapman Memorial Lecture Table of Contents Sponsor Exhibitor List Awards Photographs POSTER 16 DELTA NOTCH SIGNALLING IS REQUIRED FOR PROPER NODE FORMATION Przemeck GKH GSF Institute of Experimental Genetics Co Authors 1 Vogel C 2 Heinzmann U 1 Beckers J Hrabe de Angelis M Institutions 1 GSF Institute of Experimental Genetics 2 GSF Institute of Pathology Abstract Left right L R axis formation in vertebrates is a fundamental and evolutionary conserved process of early embryonic development and is crucial also for the proper morphogenesis of internal organs Several genes required for the establishment and or maintenance of L R asymmetry include genes also expressed before node and midline development Recently we reported that Delta Notch signalling is required for normal L R determination in mice and that the loss of function of the Delta1 Dll1 gene results in randomization of the direction of heart looping and embryonic turning Along with altered expression patterns of the TGF beta family genes Nodal Leftb and Ebaf and the Notch pathway genes Notch1 Notch2 and Lfng Delta1 mutant embryos display alterations in the morphology and fine structure of the node To investigate the latter defects in more

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file64.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    Pathology and Developmental Biology Howard Hughes Medical Institute Stanford University Medical School Co Authors Wu J I Artzt K Institutions Departments of Pathology and Developmental Biology Howard Hughes Medical Institute Stanford University Medical School The Notch1 Delta1 signaling pathway is notably one of the most crucial during early embryonic development and is highly conserved Regulation of Notch1 has been extensively studied There are several Ubiquitin E3 ligases that play important roles in either activating Notch1 or for the turn over of different proteins in this pathway Mind bomb mib is a Ubiquitin E3 ligase that when mutated in zebrafish has been observed to over produce neurons Delta was shown to be a target for this E3 ligase Itoh et al 2003 Interestingly a biochemical approach revealed a second target of mib1 Death Associated Protein Kinase DAPK Jin etal 2002 To study the role of Mind bomb in mammals a knockout of mib1 was generated in mouse Our analyses with mib1 embryos indicate three major phenotypes at E9 5 abnormal somitogenesis premature differentiation of the neuroepithelium and improper vasculature Mib1 mutants are embryonic lethal between E9 5 E10 Our studies indicate that Delta Dll1 transcript is misexpressed and the levels are

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file65.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    Johns Hopkins University School of Medicine Co Authors South S T Reeves R H Institutions Johns Hopkins University School of Medicine Abstract Down syndrome DS trisomy 21 is the most frequent human aneuploidy compatible with survival Neural crest cells NCC contribute prominently to many of the structures affected in DS including craniofacial heart and peripheral nervous system and it has been hypothesized that trisomy 21 causes a defect in NCC Although widely accepted due to circumstantial evidence no direct experiments have proven or disproven an effect on NCC in DS Conceivably any parameter of NCC generation migration signaling or differentiation could be affected by trisomy The Ts65Dn mouse is at dosage imbalance for orthologs of about half of the genes on human Chr 21 and provides a genetic model with direct parallels in phenotypes and etiology of DS By generating Ts65Dn mice with a reporter gene specifically labeling cranial NCC during early development we can visualize and quantify the number of NCC and volume occupied by structures containing NCC Ts65Dn mice were bred to mice homozygous for the Wnt1 lacZ transgene and the offspring were dissected from Ts65Dn mothers at embryonic day 9 5 Trisomic and euploid embryos were identified

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file66.shtml (2016-02-17)
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  • 17th International Mouse Genome Conference (2003)
    BY CONDITIONAL GENE KNOCKOUT IN MICE Sasaki H 1 National Institute of Genetics 2 Graduated University for Advanced Studies Co Authors 1 2 Kaneda M 1 2 Sado T 3 Okano M 1 Hata K 4 Li E Institutions 1 National Institute of Genetics 2 Graduated University for Advanced Studies 3 RIKEN 4 Massachusetts General Hospital DNA methylation marks the imprinted genes differently during male and female gametogenesis and the epigenetic differences imprints between the two gametes lead to parental origin specific gene expression in the offspring However since disruptions of DNA methyltransferases Dnmt1 3a and 3b in mice resulted in embryonic or early postnatal lethality their effect on the establishment of imprints in the germline has not been studied To circumvent this problem we took advantage of the Cre loxP system and inactivated the two de novo DNA methyltransferases preferentially in the germline The resulting conditional knockout mice Dnmt3a 2lox TNAP Cre and Dnmt3b 2lox TNAP Cre were viable and reached the reproductive age Successful inactivation of the 2lox alleles in the germline and the resulting homozygous state of the germ cells were confirmed by PCR Interestingly offsprings from the conditional Dnmt3a females crossed with wildtype males lacked the

    Original URL path: http://www.imgs.org/Archive/abstracts/2003abstracts/file67.shtml (2016-02-17)
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