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  • 18th International Mouse Genome Conference (2004)
    Medicine Houston United States 2 Agilent Technologies Palo Alto United States Early steps for cardiac lineage specification are problematic to study in mammalian embryos which has favored the use of pluripotent cells that recapitulate the onset of cardiac myogenesis In mouse P19 cells or their derivatives it has been shown that bone morphogenetic proteins drive Nkx2 5 induction both via receptor activated Smad transcription factors and by TGF beta activated kinase 1 MAP3K7 and that Wnts a reported inhibitor of heart formation in avian or amphibian explants can activate cardiogenesis both via a non canonical pathway for Wnt11 and via the canonical beta catenin pathway acting prior to and upstream of the endogenous BMPs induction Here we have undertaken a dissection of the BMP and Wnt dependent pathways in P19Cl6 cells by DNA microarray expression profiling in the absence or presence of extracellular inhibitors Blocking Wnt signaling with soluble Frizzled protein sFz 8 Fc and BMP signaling with noggin inhibited the induction of sarcomeric myosin heavy chains suggesting that sFz 8 Fc and noggin inhibited cardiac differentiation in these cells Blocking Wnt signaling with sFz 8 Fc revealed that many reported cardiogenic or mesoderm inducing genes were Wnt dependent in

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file133.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    STRAIN INNATE IMMUNE RESPONSES Wells CA 1 Aung H 1 Himes R 1 Forrest A 1 Ravasi T 1 Grimmond S 1 Kasukawa T 2 Carninci P 2 Hayashizaki Y 3 Hume D 1 1 IMB University of QLD Brisbane Australia 2 RIKEN Genome Sciences Wako Japan 3 RIKEN Genome Sciences Yokohama Japan Pathogenic challenges are one of the primary evolutionary drivers on mammalian genomes An effective innate immune system must recognise pathogens and respond appropriately too little and the pathogen will colonise the host too much may generate local tissue damage or septic shock Inbred mice provide a spectrum of innate immune responses to a variety of pathogens and we have demonstrated by microarray expression profiling that each strain exhibits a unique transcriptional response to a single pathogenic challenge LPS This study demonstrates that macrophages derived from a single individual also demonstrate heterogeneity of responses to the same pathogenic challenge We surveyed the genomic databases using RIKEN full length cDNA clones and demonstrate that most participants in the Tlr4 signalling cascade are alternatively spliced yielding functionally distinct products We propose that most receptors and signalling molecules recruited to innate immune pathways are regulated at an allelic level Monoallelic expression

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file134.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    TECHNOLOGY Collins PJ Sun H Gao J Nguyen K Lin E Doan TB Giles S Tang S Fulmer Smentek SB Shannon KW Webb PG Agilent Technologies Inc Palo Alto United States The explosion in mouse genomic sequence availability in recent years has enabled the development of whole genome microarrays with the potential to revolutionize fundamental research Agilent s whole mouse genome microarray was developed using a powerful validation process in which optimal probes were empirically selected to represent each gene in the mouse genome The first step was to define the set of gene elements by grouping transcript sequences from well established public sources such as RefSeq Riken NIA and Ensembl based on their similarities to one another and their overlap on the mouse genome Next consensus sequences covering all the high quality transcripts in each of these gene bins were defined and a set of ten candidate 60 mer probe sequences were computationally determined to represent each consensus region These candidate probes were hybridized with ten differentially expressing sample pairs From the resulting data one optimal probe was selected from each candidate set to specifically represent each consensus region Probes were selected to represent additional transcripts to ensure whole

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file135.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    J 1 White P 1 Gorski R 1 Brestelli J 1 Arsenlis A 1 Manduchi E 1 Katokhin A 2 Belova O 2 Bogdanova V 2 Elisafenko E 2 Gubina M 2 Nizolenko L 2 Perelman P 2 Puzakov M 2 Shilov A 2 Trifonoff V 2 Vorobjeva N 2 Voronin D 2 Zykov I 2 Kolchanov N 2 Kaestner K 1 Stoeckert C 1 1 University of Pennsylvania Philadelphia United States 2 Institute of Cytology and Genetics SB RAS Novosibirsk Russia The mouse pancreas enriched microarray or mouse PancChip provides a powerful tool for studying pancreatic development and diabetes research allowing the investigation of gene expression for over 13 000 transcripts expressed in the pancreas In designing the PancChip one clone from mouse pancreas libraries was picked to represent each unique mouse transcript as identified by computational analysis using the Database of Transcribed Sequences DoTS Computational and manual annotation of the transcripts has identified known and novel transcripts and their functions Using the PancChip we show that these transcripts are expressed in purified islets and the pancreas The novel transcripts define new mouse genes when BLAT aligned to the mouse genome Genomic alignment of the transcripts also identifies alternative

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file136.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    Life Sciences Division Oak Ridge National Laboratory Oak Ridge TN United States 2 The University of Tennessee Oak Ridge National Laboratory Graduate School of Genome Science and Technology Oak Ridge TN United States 3 SpectruMedix PA United States 4 Department of Biochemistry Cellular and Molecular Biology The University of Tennessee Knoxville TN United States The availability of the complete DNA sequence of the mouse genome coupled with the development of high throughput methods for rapid detection of single nucleotide polymorphisms SNPs have made it practical to implement genome wide gene driven approaches to mouse germline mutagenesis Such gene driven strategies enable the performance of whole genome mutagenesis and screening for alterations in any pre selected gene s To complement embryonic stem cell based gene driven mutagenesis resources such as gene trap libraries and banks of N ethyl N nitrosourea ENU mutagenized ES cells we generated a cryopreserved bank of DNA tissues for RNAs and proteins and sperm from 4 000 C57BL 6J mice that each carry a unique load of paternally induced ENU mutations This ORNL Cryopreserved Mutant Mouse Bank CMMB is a source of induced heritable SNPs in virtually every gene in the genome The ability to produce an

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file137.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    Huser N Jiang Z Hoebe K Beutler B The Scripps Research Institute La Jolla CA United States Infectious diseases are a leading cause of morbidity and mortality worldwide It is known that genetic variation foretells susceptibility to many of these diseases in both humans and animals Thus the positional identification of genes that are critical for host defense against infections looms as one of the greatest challenges in immunology The intracellular bacterium Listeria monocytogenes is one of the most studied models for such infections Resistance to this pathogen relies on both innate and adaptive immunity but many aspects of our defenses are still not completely understood To gain deeper insight into the nature of these immune responses infectious agents need to be considered in the context of their complex mammalian host For this reason an in vivo forward genetic approach has been undertaken We have implemented a screen for germline mutant mice with enhanced susceptibility to Listeria infection Mice were inoculated intravenously with Listeria and closely monitored for signs of illness A total of 4319 mice have been screened allowing us to isolate 9 transmissible mutations in genes that specifically disrupt the mouse resistance to Listeria All phenodeviants identified were

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file138.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    play a crucial role in the innate mechanisms directed against viral infections Mice represent a convenient and well established in vivo model to study the antiviral functions of NK cells as antibody depletion of these cells leads to severe susceptibility to the Mouse Cytomegalovirus MCMV a double stranded DNA Herpes family virus Recently the Ly49H receptor was shown to be of central importance in MCMV susceptibility The Ly49H gene which is absent in the MCMV sensitive BALB c strain encodes a C type lectin transmembrane receptor which associates to an accessory factor DAP12 containing an Immunoreceptor Tyrosine based Activating Motif ITAM to promote target cell lysis The ligand of the Ly49H receptor is the MCMV encoded protein m157 which supports the idea that this receptor mediates a specific innate immune response against viruses In addition dendritic cells DC have been shown to produce type I interferons IFN in response to viral infections thereby assisting the NK dependent response that eliminates the pathogen In order to provide a better understanding of the innate immune response against viral infections we designed an in vivo screen of EthylNitrosoUrea ENU mutated MCMV resistant C57BL 6 mice and searched for animals with abnormal susceptibility to

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file139.shtml (2016-02-17)
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  • 18th International Mouse Genome Conference (2004)
    Jolla United States Toll like receptors TLRs play essential roles in inflammation and innate immunity Individual TLRs respond to specific molecules of microbial origin TLR4 has been identified as the sensor for lipopolysaccharide LPS a molecular component of Gram negative bacteria TLR2 responds to molecules derived from mycobacteria yeast and Gram positive bacteria TLR5 and TLR9 recognize bacterial flagellins and unmethylated DNA bearing CpG motifs while TLR3 and TLR7 recognize viral double stranded RNA dsRNA and single stranded RNA ssRNA respectively While many of the molecules involved in TLR mediated signaling have been identified others remain obscure and numerous questions surround the sensing mechanism itself ENU mutagenesis has been used to identify novel genes in the process by screening for ENU caused germline mutants that are defective to different ligands Previous work in our lab has shown that LPS2 TRIF is required for mediating the signaling through TLR3 and TLR4 and that CD36 is involved in TLR2 6 mediated LTA sensing We now report additional mutations Insouciant Heedless and Unmindful that affect TLR sensing Insouciant macrophages show decreased responses to peptidoglycan PGN suggesting the mutated gene is involved in responses to one or more molecular components of commercial peptidoglycan preparations

    Original URL path: http://www.imgs.org/Archive/abstracts/2004abstracts/abs/file140.shtml (2016-02-17)
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