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At least 145 records · Page 8Linked to original sources
PubMed1984

Evolution and variation of renin genes in mice.

Inbred strains of mice carry Ren-1, a gene encoding the thermostable Renin-1 isozyme. Ren-1 is expressed at relatively low levels in mouse submandibular gland and kidney. Some strains also carry Ren-2, a gene encoding the thermolabile Renin-2 isozyme. Ren-2 is expressed at high levels in the mouse submandibular gland and at very low levels, if at all, in the kidney. Ren-1 and Ren-2 are closely linked on mouse chromosome 1, show extensive homology in coding and noncoding regions and provide a model for studying the regulation of gene expression. An investigation of renin genes and enzymatic activity in wild-derived mice identified several restriction site polymorphisms as well as putative variants in renin gene expression and protein structure. The number of renin genes carried by different subpopulations of wild-derived mice is consistent with the occurrence of a gene duplication event prior to the divergence of M. spretus (2.75-5.5 million yr ago). This conclusion is in agreement with a prior estimate based upon comparative sequence analysis of Ren-1 and Ren-2 from inbred laboratory mice.

Animals↗
PubMed1995

Lith1, a major gene affecting cholesterol gallstone formation among inbred strains of mice.

The prevalence of cholesterol gallstones differs among inbred strains of mice fed a diet containing 15% (wt/wt) dairy fat, 1% (wt/wt) cholesterol, and 0.5% (wt/wt) cholic acid. Strains C57L, SWR, and A were notable for a high prevalence of cholelithiasis; strains C57BL/6, C3H, and SJL had an intermediate prevalence; and strains SM, AKR, and DBA/2 exhibited no cholelithiasis after consuming the diet for 18 weeks. Genetic analysis of the difference in gallstone prevalence rates between strains AKR and C57L was carried out by using the AKXL recombinant inbred strain set and (AKR x C57L)F1 x AKR backcross mice. Susceptibility to gallstone formation was found to be a dominant trait determined by at least two genes. A major gene, named Lith1, mapped to mouse chromosome 2. When examined after 6 weeks on the lithogenic diet, the activity of hepatic 3-hydroxy-3-methylglutaryl-CoA reductase (EC 1.1.1.88) was downregulated as expected in the gallstone-resistant strains, AKR and SJL, but this enzyme failed to downregulate in C57L and SWR, the gallstone-susceptible strains. This suggests that regulation of the rate-limiting enzyme in cholesterol biosynthesis may be pivotal in determining the occurrence and severity of cholesterol hypersecretion and hence lithogenicity of gallbladder bile. These studies indicate that genetic factors are critical in determining gallstone formation and that the genetic resources of the mouse model may permit these factors to be identified.

Animals↗
PubMed1980

[Mechanical properties of the intercellular contacts of hepatocytes of inbred strains of mice and mice predisposed to spontaneous hepatomas].

The adhesiveness of hepatocytes was evaluated in 7 inbred mice and compared to the reported data on the incidence of spontaneous hepatomas. The adhesiveness was shown to be significantly less in mice predisposed to spontaneous hepatomas as compared to more resistant species. Electron microscopy revealed the presence of little and highly adhesive areas (HAA) in nonspecialized regions of hepatocytic contacts, this presence being shown by elevated (20-30 mm Hg) hydrostatic pressure in the liver blood bed. The amount and mechanical strength of HAA was less in CBA mice predisposed to spontaneous hepatomas as compared to resistant C57B1 mice, and correlated with cell adhesiveness.

Age Factors↗
PubMed1988

Prenatal development of the hippocampus in two strains of inbred mice.

In this paper we present some morphological observations on the morphogenesis of the hippocampus in two inbred strains of mice, C57BL/6J (C57) and DBA/2J (DBA), from day 16 (E16) to day 17 (E17) of prenatal life. At E16 some differences in the histoarchitecture of the hippocampal anlage begin to be detectable. At E17 the differences become more relevant, particularly those concerning the lamination pattern. The more relevant differences concern the differentiation of the pyramidal layer, which appears well defined in C57 mice, while in DBA mice there is no clearcut delimitation between the pyramidal layer and the intermediate zone, where numerous migrating neurons are present. These observations may be interpreted in terms of different migration rates for the neurons in the two strains.

Animals↗
PubMed1991

Gene trees and the origins of inbred strains of mice.

Extensive data on genetic divergence among 24 inbred strains of mice provide an opportunity to examine the concordance of gene trees and species trees, especially whether structured subsamples of loci give congruent estimates of phylogenetic relationships. Phylogenetic analyses of 144 separate loci reproduce almost exactly the known genealogical relationships among these 24 strains. Partitioning these loci into structured subsets representing loci coding for proteins, the immune system and endogenous viruses give incongruent phylogenetic results. The gene tree based on protein loci provides an accurate picture of the genealogical relationships among strains; however, gene trees based upon immune and viral data show significant deviations from known genealogical affinities.

Algorithms↗
PubMed1995

Identification and minisatellite linkage analysis of SMXA recombinant inbred strains of mice by DNA fingerprinting.

SMXA recombinant inbred (RI) strains of mice were produced by systematic inbreeding from the F2 generation of a cross between two progenitor inbred strains, A/J and SM/J, which differ considerably with respect to many characteristics, and consists of 28 inbred strains. In this study, we investigated the applicability of DNA fingerprinting with M13 phage DNA to the identification of these closely related strains. DNA fingerprints of the SMXA RI strains and their progenitors, SM/J and A/J, showed strain-specific patterns, with the same banding patterns within each strain. Linkage analysis by using strain distribution patterns of minisatellite loci with 108 genetic markers containing microsatellites, biochemical and immunological marker genes allowed 23 minisatellite loci to be assigned to 11 chromosomes. The results suggested that DNA fingerprinting with M13 phage DNA is applicable not only for strain identification but also for genetic monitoring of RI strains on almost all chromosomes.

Animals↗
PubMed1979

Genetic regulation of mup production in recombinant inbred mice.

Inbred strains of mice excrete all three major urinary proteins (mups) when induced by testosterone, but differ as to the relative proportions and total levels of each mup present. We have now determined the urinary mup phenotypes before and after testosterone treatment of seven recombinant inbred strains derived from progenitor strains exhibiting different mup phenotypes. The results confirm previous observations indicating that total control of mup protein production is a multigenic process. One locus, Mup-a on chromosome 4, determines the relative mup protein proportions after induction by testosterone. Mup-a, together with other genetic sites, determines the basal mup proportions. Genes other than Mup-a determine the kinetics of mup induction and total mup excretion.

Alleles↗
PubMed1991

Lung adenoma structure among inbred strains of mice: the pulmonary adenoma histologic type (Pah) genes.

Urethane-induced, lung adenoma multiplicity and histologic type vary among mouse strains. We asked whether the Pas genes which control multiplicity also determine adenoma structure. Lung adenomas from inbred mice, F1 hybrids, and recombinant inbred mice were classified by growth pattern as either solid or papillary. Since no correlation was observed between adenoma multiplicity and histologic type, no linkage apparently exists between the Pas genes and adenoma morphology. We propose the name Pah (Pulmonary Adenoma Histologic type) for the genes controlling lung adenoma growth patterns. Genetic analysis indicated dominance of the papillary phenotype, and that two or more Pah genes determine adenoma structure.

Adenoma↗
PubMed2001

Strain-related differences in bioactivation of vinyl carbamate and formation of DNA adducts in lungs of A/J, CD-1, and C57BL/6 mice.

Inbred strains of mice exhibit differing susceptibilities to formation of lung tumors induced by procarcinogens including ethyl carbamate (EC) and vinyl carbamate (VC). Strain A/J mice are susceptible, whereas C57BL/6 mice are resistant to lung tumor development. In this study, we tested the hypothesis that differential susceptibilities of A/J, CD-1, and C57BL/6 mice to lung tumor development are associated, in part, with their capacities for VC bioactivation and with the extents of DNA adduct formation. Previous studies have shown that the P450 isozyme CYP2E1 and microsomal carboxylesterases are involved in activation and detoxication of VC, respectively. Bioactivation capacity, as estimated by ratios of p-nitrophenol hydroxylase, a CYP2E1 catalytic marker, to carboxylesterase activities, was greater in control A/J (1.32 +/- 0.18 x 10(-6)) and CD-1 (1.25 +/- 0.29 x 10(-6)) mice than in control C57BL/6 (0.69 +/- 0.12 x 10(-6)) mice. The ratios were reduced in all three strains of mice treated with VC. Covalent binding of [(14)C-carbonyl]-VC to lung proteins was time- and dose-dependent, and was significantly higher in A/J and CD-1 mice than in C57BL/6 mice. Experiments using (32)P-postlabeling/thin-layer chromatography showed formation of the DNA adducts 1,N:(6)-ethenodeoxyadenosine and 3,N:(4)-ethenodeoxycytidine in lungs of mice treated with VC. The DNA adducts were detected at 30 min after treatment, peaked at 60 min, and declined thereafter. Levels of 1,N:(6)-ethenodeoxyadenosine and 3,N:(4)-ethenodeoxycytidine were about 70% higher in A/J and CD-1 mice than in C57BL/6 mice. These results indicated that formation of VC metabolites in these murine strains is linked to their bioactivation capacities, and suggested that this attribute may confer differing susceptibilities to lung tumor development.

Animals↗