A genetic map of the mouse with 4,006 simple sequence length polymorphisms

Dietrich, William F.; Miller, Joyce C.; Steen, Robert; Merchant, Mark; Damron, Deborah; Nahf, Robert; Gross, Alec W.; Joyce, Diane C.; Wessel, Michael; Dredge, Robert; Marquis, Andre; Stein, Lincoln; Goodman, Nathan; Page, David C.; Lander, Eric S.

doi:10.1038/ng0694supp-220

Cited by 523 publications

(243 citation statements)

References 18 publications

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“…A comparison of observed versus expected revealed an excess of markers on chromosomes 3, 4, 7, and 14 and a deficiency of markers on 1, 17, 18. The greater than expected number of markers on X is opposite that observed in man and mouse (Buetow et al 1994;Dietrich et al 1994). All microsatellite markers were randomly selected from genomic libraries with the exception of 23 markers from chromosomally enriched libraries for chromosome 1 (five markers; Anderson Dear and Miller 1994), chromosome 11 (nine markers; Riquet et al 1995), and chromosome 13 (nine markers; Davies et al 1994).…”

Section: Genomic Coveragementioning

confidence: 56%

A comprehensive map of the porcine genome.

Rohrer¹,

Alexander²,

Hu³

et al. 1996

Genome Res.

448

382

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We report the highest density genetic linkage map for a livestock species produced to date. Three published maps for Sus scrofa were merged by genotyping virtually every publicly available microsatellite across a single reference population to yield 1042 linked loci, 536 of which are novel assignments, spanning 2286.2 cM (average interval 2.23 cM) in 19 linkage groups 08 autosomal and X chromosomes, n = 19). Linkage groups were constructed de novo and mapped by locus content to avoid propagation of errors in older genotypes. The physical and genetic maps were integrated with 123 informative loci assigned previously by fluorescence in situ hybridization {FISH). Fourteen linkage groups span the entire length of each chromosome. Coverage of chromosomes 11, 12, 15, and 18 will be evaluated as more markers are physically assigned. Marker-deficient regions were identified only on Ilql.7-qter and 14 cen-ql.2. Recombination rates [cM/Mbp) varied between and within chromosomes. Short chromosomal arms recombined at higher rates than long arms, and recombination was more frequent in telomeric regions than in pericentric regions. The high-resolution comprehensive map has the marker density needed to identify quantitative trait loci [QTL), implement marker-assisted selection or introgression and YAC contig construction or chromosomal microdissection.

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Section: Genomic Coveragementioning

confidence: 56%

A comprehensive map of the porcine genome.

Rohrer¹,

Alexander²,

Hu³

et al. 1996

Genome Res.

448

382

View full text Add to dashboard Cite

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“…Seventeen (CA) n microsatellite repeats (Copeland et al, 1993;Dietrich et al, 1994; Whitehead Institute/MIT Center for Genome Research, 1994) ampli®ed by PCR were used to screen eight short term cultured SCCs and 10 microdissected SCCs for LOH at 6 A1-C3 (six of these cases were common with the STC SCCs). In each case, both STCs and microdissected para n sections gave the same results.…”

Section: Resultsmentioning

confidence: 99%

“…(CA) n microsatellite repeat ampli®cation analysis Seventeen (CA) n microsatellite repeats on mchr 6 (Copeland et al, 1993;Dietrich et al, 1994; Whitehead Institute/ MIT Center for Genome Research, 1994) were ampli®ed in a Thermocycler 9600 (Perkin-Elmer Cetus, Norwalk, CT). The 25 ml reaction mixtures contained 2.5 ml of 106 standard polymerase chain reaction (PCR) bu er (PerkinElmer Cetus), 100 ng of DNA, 1 unit of Taq polymerase, 400 pM each primer and 200 mM each dNTP.…”

Section: Dna Extraction From Para N Sectionsmentioning

confidence: 99%

Loss of heterozygosity on murine chromosome 6 in two-stage carcinogenesis: evidence for a conserved tumor suppressor gene

1997

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We have recently demonstrated that loss of heterozygosity (LOH) at 7q31 is frequent in many kinds of human primary tumors and that introducing a single human chromosome (hchr) 7 into a murine squamous cell carcinoma (SCC)-derived cell line suppresses the malignant phenotype. To investigate whether the putative tumor suppressor gene on hchr 7 is conserved in mice, we studied LOH on mouse chromosome (mchr) 6 in chemically induced SCCs in (C57BL6DBA2) F1 (B6D2F1) females. LOH analysis was performed by polymerase chain reaction ampli®cation of 17 (CA) n microsatellite repeats in mchr 6 A1-C3. As expected, all the B6D2F1-derived tumors were informative for all the locus assayed. The highest percentage of LOH in the hchr 7q-homologous segment was found at D6Mit50 (60.0%) and the other markers in this segment had LOH incidences normally distributed around the peak. The high incidence of LOH in the tumors studied suggests that a tumor suppressor gene relevant to the development of epithelial cancers is present on mchr 6 A2. As this segment is homologous with hchr 7q31, these data suggest that the putative tumor suppressor gene is conserved in the two species and explains the suppression of tumorigenicity when a single hchr 7 is introduced to a murine SCC cell line.

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“…The source and derivation of congenic A 2A R knockout (KO) mice was described previously (13,16). To generate Adora2a null (A 2A RKO) mice congenic to BALB/c (17)(18)(19), a mapping panel of 55 microsatellite loci informative for a (C57BL/6J ϫ BALB/cByJ) cross was identified with coverage for every chromosome, except X and Y, at a density of Ͻ30 cM. The mapping panel is available on request (mjm7e@virginia.edu).…”

Section: Animalsmentioning

confidence: 99%

Activation of Adenosine 2A Receptors Attenuates Allograft Rejection and Alloantigen Recognition

Sevigny¹,

Li²,

Awad³

et al. 2007

The Journal of Immunology

129

101

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The current studies investigated the in vitro and in vivo effect of adenosine 2A receptor (A2AR) agonists to attenuate allogenic immune activation. We performed MLRs with spleen T lymphocytes and APCs isolated from wild-type and A2AR knockout mice of both C57BL/6 and BALB/c background strains. Two-way MLR-stimulated T cell proliferation was reduced by ATL313, a selective A2AR agonist in a dose-responsive manner (∼70%; 10 nM), an effect reversed by the A2AR antagonist ZM241385 (100 nM). By one-way MLRs, we observed that ATL313’s inhibitory effect was due to effects on both T cells and APCs. ATL313 suppressed the activation markers CD25 and CD40L and the release of inflammatory cytokines IFN-γ, RANTES, IL-12P70, and IL-2. ATL313 also increased negative costimulatory molecules programmed death-1 and CTLA-4 expressed on T cells. In lymphocytes activated with anti-CD3e mAb, ATL313 inhibited the phosphorylation of Zap70, an effect that was reversed by the protein kinase A inhibitor H-89. In skin transplants, allograft survival was enhanced with ATL313, an effect blocked by ZM241385. These results indicate that A2AR agonists attenuate allogenic recognition by action on both T lymphocytes and APCs in vitro and delayed acute rejection in vivo. We conclude that A2AR agonists may represent a new class of compounds for induction therapy in organ transplantation.

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A genetic map of the mouse with 4,006 simple sequence length polymorphisms

Cited by 523 publications

References 18 publications

A comprehensive map of the porcine genome.

A comprehensive map of the porcine genome.

Loss of heterozygosity on murine chromosome 6 in two-stage carcinogenesis: evidence for a conserved tumor suppressor gene

Activation of Adenosine 2A Receptors Attenuates Allograft Rejection and Alloantigen Recognition

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