scholarly journals Strain variation in spermatozoal glycosidases in inbred mice

1978 ◽  
Vol 32 (2) ◽  
pp. 183-193 ◽  
Author(s):  
Steven J. Self ◽  
Bryan G. Winchester ◽  
James R. Archer

SUMMARYTen glycosidases were measured in suspensions of spermatozoa from the vasa deferentia of two inbred mouse strains and their intercrosses. Eight of these glycosidases were associated with the sperm cells and all of these showed genetical variation between the strains except α-l-fucosidase with optimal activity at pH 5·4. In contrast liver enzyme activities showed no significant variation except α-l-fucosidase. Genetic studies indicated that the variation of spermatozoal β-d-hexosaminidase, α-d-mannosidase, α-l-fucosidase and β-d-galactosidase are inherited at autosomal loci and α-d-galactosidase variation shows X-linked inheritance. We propose a new provisional gene symbol (Afuc-2) for a spermatozoal variant of α-l-fucosidase.

1992 ◽  
Vol 262 (6) ◽  
pp. R1025-R1032 ◽  
Author(s):  
D. B. West ◽  
C. N. Boozer ◽  
D. L. Moody ◽  
R. L. Atkinson

The effect of 7 wk consumption of a diet containing 32.6% of kilocalories as fat [condensed milk (CM) diet] on body composition and energy intake was evaluated in nine strains of inbred mice (AKR/J, C57L/J, A/J, C3H/HeJ, DBA/2J, C57BL/6J, SJL/J, I/STN, and SWR/J). Control animals were fed a high-carbohydrate diet containing 11.6% of energy as fat (Purina Rodent Chow diet). Relative to Chow diet controls, the CM diet significantly increased carcass lipid content in six strains (AKR/J, C57L/J, A/J, C3H/HeJ, DBA/2J, and C57BL/6J), but had no or a marginal effect on adiposity in three strains of mice (SJL/J, I/STN, and SWR/J). The obesity produced by the CM diet in six strains was not due to hyperphagia. Only one of six (AKR/J) of the strains that increased adiposity on the CM diet consumed more energy than controls during the 7 wk of the experiment. The identification of inbred mouse strains that are sensitive to dietary obesity, vs. others that are resistant, provides a useful tool to pursue the metabolic and genetic basis of this trait in the mouse.


2019 ◽  
Author(s):  
Corey T. Watson ◽  
Justin T. Kos ◽  
William S. Gibson ◽  
Leah Newman ◽  
Gintaras Deikus ◽  
...  

ABSTRACTThe genomes of classical inbred mouse strains include genes derived from all three major subspecies of the house mouse, Mus musculus. We recently posited that genetic diversity in the immunoglobulin heavy chain (IGH) gene loci of C57BL/6 and BALB/c mice reflect differences in subspecies origin. To investigate this hypothesis, we conducted high-throughput sequencing of IGH gene rearrangements to document IGH variable (IGHV), joining (IGHJ), and diversity (IGHD) genes in four inbred wild-derived mouse strains (CAST/EiJ, LEWES/EiJ, MSM/MsJ, and PWD/PhJ), and a single disease model strain (NOD/ShiLtJ), collectively representing genetic backgrounds of several major mouse subspecies. A total of 341 germline IGHV sequences were inferred in the wild-derived strains, including 247 not curated in the International Immunogenetics Information System. In contrast, 83/84 inferred NOD IGHV genes had previously been observed in C57BL/6 mice. Variability among the strains examined was observed for only a single IGHJ gene, involving a description of a novel allele. In contrast, unexpected variation was found in the IGHD gene loci, with four previously unreported IGHD gene sequences being documented. Very few IGHV sequences of C57BL/6 and BALB/c mice were shared with strains representing major subspecies, suggesting that their IGH loci may be complex mosaics of genes of disparate origins. This suggests a similar level of diversity is likely present in the IGH loci of other classical inbred strains. This must now be documented if we are to properly understand inter-strain variation in models of antibody-mediated disease.


1962 ◽  
Vol 48 (10) ◽  
pp. 1718-1724 ◽  
Author(s):  
J. J. Hutton ◽  
J. Bishop ◽  
R. Schweet ◽  
E. S. Russell

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11017
Author(s):  
Matthias Munz ◽  
Mohammad Khodaygani ◽  
Zouhair Aherrahrou ◽  
Hauke Busch ◽  
Inken Wohlers

Mice are the most widely used animal model to study genotype to phenotype relationships. Inbred mice are genetically identical, which eliminates genetic heterogeneity and makes them particularly useful for genetic studies. Many different strains have been bred over decades and a vast amount of phenotypic data has been generated. In addition, recently whole genome sequencing-based genome-wide genotype data for many widely used inbred strains has been released. Here, we present an approach for in silico fine-mapping that uses genotypic data of 37 inbred mouse strains together with phenotypic data provided by the user to propose candidate variants and genes for the phenotype under study. Public genome-wide genotype data covering more than 74 million variant sites is queried efficiently in real-time to provide those variants that are compatible with the observed phenotype differences between strains. Variants can be filtered by molecular consequences and by corresponding molecular impact. Candidate gene lists can be generated from variant lists on the fly. Fine-mapping together with annotation or filtering of results is provided in a Bioconductor package called MouseFM. In order to characterize candidate variant lists under various settings, MouseFM was applied to two expression data sets across 20 inbred mouse strains, one from neutrophils and one from CD4+ T cells. Fine-mapping was assessed for about 10,000 genes, respectively, and identified candidate variants and haplotypes for many expression quantitative trait loci (eQTLs) reported previously based on these data. For albinism, MouseFM reports only one variant allele of moderate or high molecular impact that only albino mice share: a missense variant in the Tyr gene, reported previously to be causal for this phenotype. Performing in silico fine-mapping for interfrontal bone formation in mice using four strains with and five strains without interfrontal bone results in 12 genes. Of these, three are related to skull shaping abnormality. Finally performing fine-mapping for dystrophic cardiac calcification by comparing 9 strains showing the phenotype with eight strains lacking it, we identify only one moderate impact variant in the known causal gene Abcc6. In summary, this illustrates the benefit of using MouseFM for candidate variant and gene identification.


2020 ◽  
Author(s):  
Matthias Munz ◽  
Mohammad Khodaygani ◽  
Zouhair Aherrahrou ◽  
Hauke Busch ◽  
Inken Wohlers

ABSTRACTMice are the most widely used animal model to study genotype to phenotype relationships. Inbred mice are genetically identical, which eliminates genetic heterogeneity and makes them particularly useful for genetic studies. Many different strains have been bred over decades and a vast amount of phenotypic data has been generated. In addition, recently whole genome sequencing-based genome-wide genotype data for many widely used inbred strains has been released. Here, we present an approach for in silico fine-mapping that uses genotypic data of 37 inbred mouse strains together with phenotypic data provided by the user to propose candidate variants and genes for the phenotype under study. Public genome-wide genotype data covering more than 74 million variant sites is queried efficiently in real-time to provide those variants that are compatible with the observed phenotype differences between strains. Variants can be filtered by molecular consequences and by corresponding molecular impact. Candidate gene lists can be generated from variant lists on the fly. Fine-mapping together with annotation or filtering of results is provided in a Bioconductor package called MouseFM. In order to characterize candidate variant lists under various settings, MouseFM was applied to two expression data sets across 20 inbred mouse strains, one from neutrophils and one from CD4+ T cells. Fine-mapping was assessed for about 10,000 genes, respectively, and identified candidate variants and haplotypes for many expression quantitative trait loci (eQTLs) reported previously based on these data. For albinism, MouseFM reports only one variant allele of moderate or high molecular impact that only albino mice share: a missense variant in the Tyr gene, reported previously to be causal for this phenotype. Performing in silico fine-mapping for interfrontal bone formation in mice using four strains with and five strains without interfrontal bone results in 12 genes. Of these, three are related to skull shaping abnormality. Finally performing fine-mapping for dystrophic cardiac calcification by comparing 9 strains showing the phenotype with 8 strains lacking it, we identify only one moderate impact variant in the known causal gene Abcc6. In summary, this illustrates the benefit of using MouseFM for candidate variant and gene identification.


1973 ◽  
Vol 33 (3) ◽  
pp. 867-877
Author(s):  
Martin Manosevitz ◽  
Stephen W. Hurt ◽  
Floyd D. Ploeger ◽  
Robert Plomin

Three studies of the reinstatement effect using inbred mice (A/J, C57BL/6J, DBA/2J) were reported. In each study there were 4 treatment groups: early shock-reinstatement shock, early shock, reinstatement shock, and no shock. In Exp. I, 1, in Exp. II, 2, and in Exp. III, 3 inbred mouse strains were studied. In Exp. III, an albino strain was also included. Significant main effects due to strain, early experience, and reinstatement were obtained. Orthogonal comparisons generally showed that the experimental groups which received some electric shocks in early experience, reinstatement experience, or both, significantly preferred the white non-shocked side of the box. There was some evidence supporting the reinstatement principle. In future studies of this kind, special attention should be given to organismic and apparatus variables.


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