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  • The 16th International Mouse Genome Conference (2002)
    00 HRS X INACTIVATION MEDIATES AN EFFECT ON MATERNAL RECOMBINATION AND MEIOTIC DRIVE E de la Casa Esperon Temple University School of Medicine Co Authors 1 Loredo Osti J C 2 Pardo Manuel de Villena F 4 Briscoe T L 5 Malette J M 6 Vaughan J E 1 Morgan K 8 Sapienza C Institutions 1 McGill University 2 University of North Carolina F 4 Temple University School of Medicine 5 Temple University School of Medicine 6 Temple University School of Medicine 7 McGill University 8 Temple University School of Medicine Crosses between the DDK inbred mouse strain and other inbred strains and their F1 hybrids show two interesting phenomena early embryonic lethality DDK syndrome and preferential segregation of chromosomes during female meiosis meiotic drive at the second meiotic division Components of both phenotypes have been mapped to the central region of chromosome 11 We now observe a third phenomenon overall levels of meiotic recombination differ between females of identical C57BL 6 Pgk1a x DDK F1 genotype and this variability correlates with their pattern of X inactivation Because meiotic drive is affected by recombination a correlation is also observed between the levels of transmission ratio distortion at chromosome 11 and

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file221.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    1 Wang X P 1 Shaposhnik Z 3 Funk CD 1 Lusis AJ Institutions 1 UCLA 2 University of Virginia 3 University of Penn We identified a locus on mouse chromosome 6 that dramatically reduces aortic lesion formation in an intercross between the susceptible strain C57BL6 J and the resistant strain CAST Ei We constructed a congenic strain CON6 in which the chromosome 6 interval from CAST was transferred onto a hypercholesterolemic LDLR background CON6 was almost completely resistant to diet induced atherosclerosis even under conditions of extreme hyperlipidemia Studies of genes in the region indicated that 5 lipoxygenase 5LO expression was decreased by 5 fold relative to B6 in CON6 5LO is rate limiting for synthesis of leukotrienes LT inflammatory lipids biosynthesized from arachidonic acid LTB4 levels were only 2 in CAST when compared with B6 controls There were two amino acid differences between the two strains at positions 645 CAST Val B6 Ile and 646 CAST Ile B6 Val located within a region conserved among proteins that translocate from the cytosol to the nucleus We bred 5LO onto an LDLR background These mice showed a dramatic decrease in aortic lesion development similar to the CON6 mice 5 LO

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file222.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    Mock NCI NIH Co Authors 1 Bliskovski V 1 Zhang S 1 Ramsay ES 1 Shi W 1 Scott J 2 Qian X 2 Lowy DR Institutions 1 Laboratory of Genetics CCR NCI NIH 2 Laboratory of Cellular Oncology CCR NCI NIH The susceptibility of BALB c mice to plasmacytomas is a complex genetic trait We have identified candidate genes for two of the susceptibility resistance loci Pctr1 was mapped to a region on Chr 4 including Cdkn2a which encodes p16INK4a and p19ARF C57BL 6 mice from which both genes of the Cdkn2a locus have been knocked out developed plasma cell tumors over a shorter latency period than the susceptible BALB cAn strain Biological assays of p16INK4a and p19ARF alleles from BALB c and DBA 2 indicated that the BALB c p16INK4a allele was less active than its DBA 2 counterpart in inducing growth arrest of mouse plasmacytoma cell lines while the two p19ARF alleles displayed similar potencies in both assays Recently we have identified promoter variation which affects p16 expression in BALB c versus DBA B cells and have identified a transcription factor which negatively regulates the p16 gene more effectively in BALB c mice Thus BALB c p16

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file223.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    research Lund University Co Authors Wester L Selva NK Holmdahl M Holmdahl R Institutions Medical Inflammation Research Lund University A locus on chromosome 3 that controls severity of both CIA collagen induced arthritis and EAE experimental allergic encephalomyelitis has earlier been identified denoted eae3 and cia5 In a novel congenic strain B10 RIIIEae3 we have now confirmed both linkages For both diseases RIIIS J genes on B10 RIII background made the disease less severe Many loci have been mapped in different F2 crosses but it has been difficult to identify the actual genes Several of the loci analysed with congenic strains have turned out to be a cluster of genes controlling the complex disease With this in mind we chose a new strategy to dissect eae3 and cia5 When investigating the congenic strain we did not only look at the diseases mapped in the original crosses we also investigated subphenotypes related to the diseases For example B10 RIIIEae3 cells showed a lower ability to present antigen and they were also resistant to antibody transfer induced arthritis TIA a disease that the B10 RIII mice are highly susceptible to These results suggest that different genes in the fragment are regulating different

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file224.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    J 4 Threadgill DW 1 Lu L Institutions 1 University of Tennessee Health Science Center 2 Roswell Park Cancer Cancer Institute 3 University of Alabama Birmingham 4 University of North Carolina Chapel Hill NC Variation in patterns of gene expression produces fundamental differences in the structure and function of cells organs and ultimately individuals Differences in transcript abundance have a sufficiently high heritability to map as complex traits This makes it practical to simultaneously discover upstream QTLs that modulate expression of thousands of transcripts using microarrays Expression levels of 12 422 transcripts were measured in triplicate using pooled forebrain samples from 24 isogenic RI lines of mice Transcript variance was mapped using computationally efficient regression methods Manly et al this meeting LOD scores above 4 5 and 6 were achieved for 3500 670 and 310 transcripts These loci influence the expression of key CNS transcripts including genes associated with neuronal excitability Kcnab Kcnj9 Gria2 memory Camk2a Grin2b neuroendocrine and reproductive behavior Chga Smstr1 Sgne1 Freq Avpr1a circadian rhythm Per3 axonal and vesicular transport Kif1a Vamp4 glial metabolism Prkab1 and psychiatric and neurodegenerative diseases Drd2 Drd4 Apba2 Transcript QTLs fall into one of three categories 1 cis acting loci that have

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file225.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    2 Gaspard R 1 Nakamura Y 1 Gibson J Institutions 1 International Livestock Research Institute ILRI 2 The Institute for Genomic Research TIGR A J mice susceptible for Trypanosoma congolense develop much higher parasitemia and die earlier than the more resistant C57BL 6 mice It is believed that identification of the genes that contribute to resistance in this mouse model will lead to new control options for this disease Intercrossing the two mouse strains and genotyping F2 mice representing the phenotypic extremes as defined by time to death allowed the identification of three major QTL regions linked with resistance Following the F2 results the QTL were fine mapped using an F6 AIL population As the genes responsible for this resistance should be linked with amplification or shut down of particular metabolic pathways a selection of differentially expressed genes may help in the identification of possible resistance genes already restricted to the QTL regions To that end spleen and liver tissues from A J and C57BL 6 mice were taken at different time points after infection with T congolense For each time point and each tissue RNA from 5 mice were pooled to minimise individual variation and subsequently used to hybridise

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file226.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    DESCENT AND CRYPTORCHIDISM A Agoulnik Baylor College of Medicine Co Authors Bogatcheva N Kamat A Gorlov I Institutions Baylor College of Medicine A distinctive manifestation of male dimorphism in many animals is a scrotal position of their gonads During development the testes descend through a complex multistage process whereby the embryonic gonads migrate from their initial abdominal position to the scrotum Recently we described a mouse transgene insertional mutation crsp causing high intra abdominal cryptorchidism in homozygous males The integration was accompanied by a 550 kb deletion in the proximal part of chromosome 5 affecting among others a new gene named Great The gene encodes a novel G protein coupled receptor and belongs to the same family of GPCRs as the glycoprotein hormone receptors We showed that genetic targeting of the Great gene in mice causes bilateral intra abdominal cryptorchidism The gubernaculae of the mutant males fail to differentiate indicating that the Great gene controls their development Using a variety of molecular and genetic methods we have established that INSL3 hormone is a cognate ligand of the GREAT receptor We have shown that the expression of GREAT is controlled by SF1 transcription factor Furthermore we have cloned the human GREAT

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file227.shtml (2016-02-17)
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  • The 16th International Mouse Genome Conference (2002)
    H 2 Babiuk RP 3 Epstein JA 2 Greer J Institutions 1 Genetics Division Brigham and Women s Hospital Harvard Medical School 2 Division of Neuroscience University of Alberta 3 Cardiovascular Division University of Pennsylvania Medical School The power of ENU mutagenesis is the ability to identify in an unbiased fashion the molecular basis of any phenotype amenable to a genetic screen This is distinct from a genotype driven analysis in which the analysis is constrained to an extent by the observers presumption of function Furthermore phenotype driven analysis allows the detection of genes whose hypomorphic function can have deleterious consequences The biological role of these genes may not be readily appreciated by examination of the null mutant We are screening ENU mutagenized mice to identify recessive mutations resulting in developmental abnormalities that are models of human congenital defects We identified a mutation that causes pulmonary hypoplasia and abnormal diaphragmatic development The mutation was mapped to a 1 cM interval and the identification of flanking markers facilitated the examination of homozygous mice at earlier developmental timepoints This revealed that most homozygotes die in mid gestation with cardiac defects identical to those reported for a targetted mutation of Friend of Gata

    Original URL path: http://www.imgs.org/Archive/abstracts/2002abstracts/file228.shtml (2016-02-17)
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