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PubMed2003

The comprehensive mouse radiation hybrid map densely cross-referenced to the recombination map: a tool to support the sequence assemblies.

We have developed a unique comprehensive mouse radiation hybrid (RH) map of nearly 23,000 markers integrating data from three international genome centers and over 400 independent laboratories. We have cross-referenced this map to the 0.5-cM resolution recombination-based Jackson Laboratory (TJL) backcross panel map, building a complete set of RH framework chromosome maps based on a high density of known-ordered anchor markers. We have systematically typed markers to improve coverage and resolve discrepancies, and have reanalyzed data sets as needed. The cross-linking of the RH and recombination maps has resulted in a highly accurate genome-wide map with consistent marker order. We have compared these linked framework maps to the Ensemble mouse genome sequence assembly, and show that they are a useful medium resolution tool for both validating sequence assembly and elucidating chromosome biology.

Animals↗

PubMed1988

Reproductive performance in C57BL and I strain mice.

Mice of the I strain are regarded as difficult to breed. To characterize and elucidate the cause of poor reproductive performance in I strain mice, records of reproductive performance were analyzed from Cancer Research Laboratory, Kirschbaum Memorial Laboratory and Strong Research Laboratories which had bred the I strain mice and a control strain, C57BL, and compared with data from Jackson Laboratory and from three dietary studies conducted in this laboratory. Reproductive performance in the I strain mice is characterized by fewer productive matings, fewer litters and smaller litters than C57BL mice. Also, fewer mice of the I strain survive to weaning. These factors result in the production of only half as many mice per dam in the I strain as the C57BL mice. The fewer number of litters is not due to a greater proportion of resorptions in the I mice, nor are there differences in the survival of either sex. Diets which contain slightly higher (8-12 mg per kg of diet) amounts of pyridoxine (PN) than recommended (1-6 mg per kg of diet) improve performance in the I strain. However, 410 or 1230 mg PN does not increase productivity further. That survival rate of the C57BL mice improves with higher amounts of PN (410 and 1230 mg diets), suggests another dietary factor may be limiting for I strain mice. The reproductive performance in I strain mice is better with diets which result in a higher body weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1980

Coincidental development of forestomach papilloma and prepyloric ulcer in nontreated mutant mice of W/Wv and SI/SId genotypes.

A double gene dose of mutant alleles at either the W or Sl locus produces the pleiotropic effects of anemia, sterility, lack of hair pigmentation, and lack of tissue mast cells. Coincidental development of forestomach papilloma and prepyloric ulcer was observed in about 40% of nontreated (WB X C57BL/6) F1-W/Wv mice raised in our laboratory. The stomach lesions of the W/Wv mice could be detected at the 15th day after birth, and such lesions never appeared in the W/+, Wv/+, and +/+ littermates maintained under the same laboratory conditions. Since the stomach lesions were also observed in (WC X C57BL/6) F1-Sl/Sld mice purchased from The Jackson Laboratory, phenotypes common to both W/Wv and Sl/Sld mice seem to play an essential role in the spontaneous development of the forestomach papilloma and prepyloric ulcer.

Anemia↗

PubMed2003

Survey of 21 inbred mouse strains in two laboratories reveals that BTBR T/+ tf/tf has severely reduced hippocampal commissure and absent corpus callosum.

A morphometric survey of brain size and forebrain commissures of 21 inbred mouse strains from the Jackson Laboratory was done with animals tested in two laboratories as part of the Mouse Phenome Project. Strain BTBR T/+ tf/tf was found to have 100% total absence of the corpus callosum as well as severe reduction of the hippocampal commissure in almost every animal, the most severe commissure defect observed to date in any commercially available mouse strain. The strain 129S1/SvImJ had a milder defect with incomplete penetrance. Crosses of BTBR mice with inbred strains BALB/cWah1, 129P1/ReJ, and the recombinant strain 9XCA/Wah having a severe commissure defect supported a two-locus model of the genetic defect in these strains. Brain size varied greatly among strains but for any one strain was almost identical in mice housed for 5 weeks in the two laboratories. Sex differences in brain weight and forebrain commissure sizes were not statistically significant.

Agenesis of Corpus Callosum↗

PubMed1999

An encyclopedia of mouse genes.

The laboratory mouse is the premier model system for studies of mammalian development due to the powerful classical genetic analysis possible (see also the Jackson Laboratory web site, http://www.jax.org/) and the ever-expanding collection of molecular tools. To enhance the utility of the mouse system, we initiated a program to generate a large database of expressed sequence tags (ESTs) that can provide rapid access to genes. Of particular significance was the possibility that cDNA libraries could be prepared from very early stages of development, a situation unrealized in human EST projects. We report here the development of a comprehensive database of ESTs for the mouse. The project, initiated in March 1996, has focused on 5' end sequences from directionally cloned, oligo-dT primed cDNA libraries. As of 23 October 1998, 352,040 sequences had been generated, annotated and deposited in dbEST, where they comprised 93% of the total ESTs available for mouse. EST data are versatile and have been applied to gene identification, comparative sequence analysis, comparative gene mapping and candidate disease gene identification, genome sequence annotation, microarray development and the development of gene-based map resources.

Animals↗

PubMed2001

Genetic analysis of cholesterol accumulation in inbred mice.

Genetic linkage analysis in the laboratory mouse identified chromosomal regions containing genes that contribute to cholesterol accumulation in the liver and plasma. Comparisons between five inbred strains of mice obtained from the Jackson Laboratory (DBA/2, AKR, C57BL/6, SJL, and 129P3) revealed a direct correlation between intestinal cholesterol absorption and susceptibility to diet-induced hypercholesterolemia. This correlation was lost in the F1 generation arising from crosses between high- and low-absorbing strains. Linkage analyses in AKxD recombinant inbred strains and 129xSJL129F1 N2 backcross mice identified four quantitative trait loci (QTL) that influenced Liver cholesterol accumulation (Lcho1-4) and one locus that affected Plasma cholesterol accumulation (Pcho1). These loci map to five chromosomes and, with one exception, are different from the seven QTL identified previously that influence intestinal cholesterol absorption. We conclude that a large number of genes affects the amount of cholesterol absorbed in the small intestine and its accumulation in the liver and plasma of inbred mice.

Animals↗

PubMed1995

Structure of the mouse tyrosinase-related protein-2/dopachrome tautomerase (Tyrp2/Dct) gene and sequence of two novel slaty alleles.

We have isolated the eight exons and 5' and 3' flanking regions of the mouse tyrosinase-related protein-2 (dopachrome tautomerase) gene (Tyrp2/Dct), which is mutated in slaty mice. The gene has a structure that is considerably different from those of other tyrosinase family members in both the number and the position of introns, consistent with the suggestion that the divergence of the family represents an ancient gene duplication. We also identify in the 5' flanking DNA an 11-bp element, the M-box, conserved in other tyrosinase family genes. We have characterized point mutations in two slaty alleles recently identified at the Jackson Laboratory: slaty-2J (slt2J) has a similar phenotype to the original slaty (slt) mutation, and slaty light (Sltlt), which has a more severe effect and is semidominant. We suggest that the slaty-light phenotype is a result of the failure of the enzyme to be correctly targeted to its normal location on the inner face of the melanosomal membrane.

Alleles↗

PubMed1990

Further studies on variable resistance of 129/J and C57BL/6 mice to infection with Schistosoma japonicum and Schistosoma mansoni.

Two mouse strains maintained in this laboratory (WEHI) are variably resistant to infection with Schistosoma japonicum and S. mansoni in that worms cannot be found in the liver and portal system in a high proportion (WEHI 129/J mice) or low proportion (C57BL/6 mice) some weeks after exposure to cercariae. Resistance can be as high as 100% in WEHI 129/J mice and is usually around 20% in C57BL/6 mice. The proportion of resistant mice closely parallels the proportion of mice that demonstrate a shunting of microbeads, injected into a mesenteric vein, from liver to lungs. This applies to F1 x WEHI 129/J backcross mice in which the data suggest oligogenic genetic effects although no evidence for a participation of MHC-linked genes in the phenomenon has emerged. 129/J mice derived from the Jackson Laboratory do not show a shunting of beads from the portal system to the lungs but their progeny bred at WEHI do. Germ-free WEHI 129/J mice resemble conventionally-maintained, SPF-derived WEHI 129/J mice in their variable resistance to schistosome infection. No satisfactory explantation for hepato-portal system peculiarities in WEHI 129/J and C57BL/6 mice can be advanced as yet and a possibility raised in this paper is a contribution from nutritional factors such as hypervitaminosis A superimposed on a genetic predisposition in these two related mouse strains.

Animals↗

PubMed2003

Reducing exposure to laboratory animal allergens.

Laboratory animal allergy is a serious health problem. We examined several possible allergen-reducing strategies that might be effective in the working mouse room. Ambient allergen concentrations were measured when mice were maintained under several conditions: conventional housing versus ventilated cage racks operated under negative or positive pressure. We found that housing mice in ventilated cages operated under negative pressure and using ventilated changing tables reduced ambient mouse allergen (Mus m 1) concentrations tenfold, compared with values when mice were housed in conventional caging and using a conventional (non-ventilated) changing table. Housing mice in positively pressurized cages versus conventional cages did not reduce ambient allergen values. Cleaning mouse rooms at an accelerated frequency also did not reduce ambient Mus m 1 concentration. We also quantified ambient allergen values in several areas of The Jackson Laboratory. A facility-wide survey of Mus m 1 concentrations indicated that allergen concentrations were undetectable in control areas, but ranged from a mean (+/- SEM) 0.11 +/- 0.02 ng/m3 to 5.40 +/- 0.30 ng/m3 in mouse rooms with different cage types. The percentage of animal caretakers reporting allergy symptoms correlated significantly with ambient allergen concentrations: 12.9% reported symptoms in the rooms with the lowest allergen concentration (0.14 +/- 0.02 ng/m3), but 45.9% reported symptoms in rooms with the highest concentration (2.3 +/- 0.4 ng/m3). These data indicate that existing technology can significantly reduce exposure to laboratory animal allergens and improve the health of animal caretakers.

Air Pollution, Indoor↗

PubMed2004

Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse.

We have developed a genotyping system for detecting genetic contamination in the laboratory mouse based on assaying single-nucleotide polymorphism (SNP) markers positioned on all autosomes and the X chromosome. This system provides a fast, reliable, and cost-effective way for genetic monitoring, while maintaining a very high degree of confidence. We describe the allelic distribution of 235 SNPs in 48 mouse strains, thereby creating a database of polymorphisms useful for genotyping purposes. The SNP markers used in this study were chosen from publicly available SNP databases. Four genotyping methods were evaluated, and dynamic two-tube allele-specific PCR assays were developed for each marker and tested on a set of 48 inbred mouse strains. The minimal number of assays sufficient to distinguish groups consisting of different numbers of mouse strains was estimated, and a panel of 28 SNPs sufficient to distinguish virtually all of the inbred strains tested was selected. Amplifluor SNP detection assays were developed for these markers and tested on an extended list of 96 strains. This panel was used as a genetic quality control approach to monitor the genotypes of nearly 300 inbred, wild-derived, congenic, consomic, and recombinant inbred strains maintained at The Jackson Laboratory. We have concluded that this marker panel is sufficient for genetic contamination monitoring in colonies containing a large number of genetically diverse mouse strains and that reduced versions of the panel could be implemented in facilities housing a lower number of strains.

Alleles↗

PubMed2001

Variations in susceptibility to proteoglycan-induced arthritis and spondylitis among C3H substrains of mice: evidence of genetically acquired resistance to autoimmune disease.

OBJECTIVE: To identify and screen the level of arthritis susceptibility in C3H murine strains known to be resistant to proteoglycan (aggrecan)-induced arthritis, and to measure and correlate various immunologic and inflammatory parameters with susceptibility to either arthritis or spondylitis in various C3H substrains. METHODS: Mice of 10 C3H substrains (subcolonies) were immunized with cartilage proteoglycan (aggrecan) for induction of arthritis. Animals were assessed for clinical symptoms, and the peripheral joints and spine were studied by histologic methods. Proteoglycan-specific T cell responses (T cell proliferation and production of interleukin-2 [IL-2], interferon-y, and IL-4) and the B cell response to lipopolysaccharide (LPS) were measured in spleen cell cultures. Serum levels of heteroantibodies and autoantibodies as well as various cytokines (IL-6, IL-10, IL-12, and tumor necrosis factor alpha) and soluble CD44 were determined by enzyme-linked immunosorbent assay. RESULTS: Immunization with cartilage proteoglycan induced severe arthritis in the C3H/HeJCr substrain (95-100% incidence), whereas the original parent mice of the C3H/HeJ colony were resistant to proteoglycan (aggrecan)-induced arthritis. Furthermore, the progressive polyarthritis that is characteristic in susceptible C3H/HeJCr mice was accompanied by progressive inflammation around the spine. In subsequent experiments, 10 different C3H colonies with largely identical genetic backgrounds (all originating from the National Institutes of Health or Jackson Laboratory) exhibited extreme differences in susceptibility. Although none of the laboratory findings, including LPS hyporesponsiveness, immunologic parameters, and inflammatory markers, showed a correlation with susceptibility or resistance in the C3H/HeJCr and C3H/HeJ substrains, respectively, significant differences were found when all arthritic C3H mice were compared with all nonarthritic animals, regardless of their substrain origin. CONCLUSION: Because many of the C3H substrains lost arthritis susceptibility or acquired resistance, our results suggest that a preferred site for a mutation(s) in a gene(s) in a relatively upstream position of the inflammatory cascade is present. This is the first autoimmune model that exhibits extreme differences in arthritis susceptibility in the same murine strain, and is therefore a valuable tool for identification of arthritis-susceptible (or arthritis-suppressive) genes.

Animals↗

PubMed1995

Murine model of genetic demyelinating disease: the twitcher mouse.

Twitcher mouse is an authentic murine model of human genetic demyelinating disease, globoid cell leukodystrophy (GLD), or Krabbe disease. Since its discovery at the Jackson Laboratory (Bar Harbor, ME) this model has been used extensively for the morphological, biochemical-enzymatic studies to clarify pathogenesis and also for therapeutic manipulation of genetic demyelinating disease in humans. As a result of these studies, now we know that (1) GLD is caused by a deficiency of lysosomal enzyme galactosylceramidase, and a toxic metabolite, psychosine, accumulates in the tissue, including the nervous system, damaging myelin forming cells and resulting in secondary demyelination; (2) morphological features of demyelination and associated cellular reactions in demyelination in this mutant are similar to those seen in autoimmune or toxic demyelination; and (3) with enzyme supplementation provided by bone marrow transplantation, remyelination occurs to some extent in demyelinated fibers in both central and peripheral nervous systems of twitcher mouse.

Animals↗

PubMed1980

Frequency of congenital abnormalities and of anatomical variations among JAX rabbits.

The frequency of congenital abnormalities and anatomical variations as observed among JAX rabbits is reported. Data were drawn from 32,082 inbred and partially inbred rabbits and 3,208 hybrids from the colony of the Jackson Laboratory over an eight-year period. Data reported here include stillbirths, rabbits dying from natural causes, and those killed for specific experimental regimens. Frequency data are based on the number of abnormalities observed in each category as a function of the total number of animals necropsied. This is approximately 95% of the animals born during the eight-year period and gives the frequency of abnormalities within each category rather than the number of individuals with one or more abnormalities. Anatomical variations have been found in almost all organ systems of JAX rabbits. Their presence adds to our knowledge of the characteristics of these strains, a knowledge that is critical to the understanding of the results of experimental manipulation or for determination of the presence of new mutations. There is considerable between-strain variation. Where frequencies are relatively high, the conditions are either known or suspected to be of genetic origin. Most of the anomalies are not deleterious, or their frequency is so low as to cause no problems within the colony. Hybrid populations have substantially fewer anomalies than do the parental strains. Where frequency is relatively high, it tends to be intermediate between the parental strains.

Animals↗

PubMed1998

Heme oxygenase in the experimental ALS mouse.

Heme oxygenase-1 (HO-1) is a stress protein inducible in some cells by oxidative stress. The status of heme oxygenase was investigated in a transgenic mouse model of amyotrophic lateral sclerosis (ALS) since oxidative mechanisms are postulated in neuronal injury. Three ALS mice [(SOD1-G93A)1Gur] and three controls [(SOD-1)2Gur] were obtained from The Jackson Laboratory. Behavioral differences suggestive of neurodegeneration in ALS mice developed at 4-5 months of age. All mice were killed at 7-8 months of age. Tissue vacuolation, cell loss, and the presence of GFAP+ cells were noted in the spinal cords of ALS mice. Spinal cord motor neurons in both control and ALS mice stained positive for heme oxygenase-2 (HO-2). While not precluding the presence of low levels of HO-1 neither immunohistochemical staining nor Western blot analysis provided evidence for significant HO-1 induction in degenerating spinal cord.

Amyotrophic Lateral Sclerosis↗

PubMed1995

Localization of the tight junction protein gene TJP1 to human chromosome 15q13, distal to the Prader-Willi/Angelman region, and to mouse chromosome 7.

The gene encoding the tight junction (zonula occludens) protein, TJP1, was mapped to human chromosome 15q13 by fluorescence in situ hybridization (FISH) using a cDNA probe. The Jackson Laboratory backcross DNA panel derived from the cross (C57BL/6JEi x SPRET/Ei) F1 females x SPRET/Ei males was used to map the mouse Tjp1 to chromosome 7 near position 30 on the Chromosome Committee Map, a region with conserved homology to human chromosome 15q13. FISH studies on metaphases from patients with the Prader-Willi (PWS) or the Angelman syndrome (AS) showed that TJP1 maps close but distal to the PWS/AS chromosome region.

Angelman Syndrome↗

PubMed1996

The mouse glutathione peroxidase Gpx2 gene maps to chromosome 12; its pseudogene Gpx2-ps maps to chromosome 7.

The GPX2 gene codes for GSHPx-GI, a glutathione peroxidase whose mRNA is readily detectable in the gastrointestinal tract. Although GPX2 is a single gene in humans, there are two genes in the mouse genome with homology to GPX2. By analyzing a panel of mouse interspecies DNA from the Jackson Laboratory's backcross resource, we have chromosomally mapped these two genes. One was mapped to the central region of mouse chromosome 12 between D12Mit4 and D12Mit5, near fos and Tgfb3. This region is homologous to human 14q24.1, where human GPX2 has been mapped, and most likely represents the functional mouse Gpx2 gene. The other Gpx2-like gene was mapped to mouse chromosome 7 between Pcsk3 and Hbb. We have isolated the latter gene from a P1 phage library. Its pseudogene nature is revealed by the sequence analysis: (a) it is intronless; (b) it has a single nucleotide deletion in the coding region; and (c) it has a poly(A) tail at its 3'-untranslated region.

Amino Acid Sequence↗

PubMed1996

The chromosomal mapping of four genes encoding winged helix proteins expressed early in mouse development.

Members of the winged helix family of transcription factors are required for the normal embryonic development of the mouse. Using the interspecific backcross panel from The Jackson Laboratory, we have determined the chromosomal locations of four genes that encode winged helix containing proteins. Mf1 was assigned to mouse Chromosome 8, Mf2 to Chromosome 4, Mf3 to Chromosome 9, and Mf4 to Chromosome 13. Since Mf3 is located in a region of Chromosome 9 containing many well-characterized mouse mutations such as short ear (se), ashen (ash), and dilute (d), we have analyzed deletion mutants to determine the location of Mf3 more precisely.

Animals↗

PubMed1997

Identification and genetic mapping of a new polycystic kidney disease on mouse chromosome 8.

We report here a new mouse mutation, kat, that causes pleiotropic effects including facial dysmorphism, dwarfing, male sterility, anemia, and progressive polycystic kidney disease. kat (kidney anemia and testis) and a second allele, kat2J, that occurred on C57BL/ 6J were mapped to mouse chromosome (Chr) 8 using intra- and intersubspecific intercrosses. A high-resolution map for kat2J on Chr 8 was constructed using the F2 progeny from a cross between C57BL/6J-kat2J/+ and an inbred strain of Mus musculus castaneus (CAST/Ei). The kat2J mutation was localized between D8Mit129 and D8Mit128 with the gene order centromere-D8Mit100-(1.2 +/- 0.26 cM)-D8Mit231-(0.17 +/- 0.09 cM)-D8Mit129-(0.28 +/- 0.12 cM)-D8Mit128-(0.98 +/- 0.23 cM)-D8Mit25/D8Mit8. This segment is homologous to human Chr 19p. The two mutations at this locus that have occurred at The Jackson Laboratory will be invaluable for positional cloning and subsequent functional analysis of the mutated gene.

Animals↗