scholarly journals LINKAGE OF GENETIC DETERMINANTS FOR MOUSE β-GALACTOSIDASE ELECTROPHORESIS AND ACTIVITY

Genetics ◽  
1977 ◽  
Vol 85 (1) ◽  
pp. 73-84
Author(s):  
Gail A M Breen ◽  
Aldons J Lusis ◽  
Kenneth Paigen
Keyword(s):  
Inbred Strains ◽  
Mammalian Genome ◽  
Chromosome 9 ◽  
Structural Genes ◽  
Genetic Determinants ◽  
Developmental Program ◽  
Inbred Strains Of Mice ◽  
Close Proximity ◽  
Mendelian Factor ◽  
Electrophoretic Polymorphism

ABSTRACT An electrophoretic polymorphism for β-galactosidase has been identified among common inbred strains of mice. It is inherited as a single Mendelian factor with two alleles showing codominant expression. This structural gene, Bge, is closely linked (0/163 recombinants) with the Bgs site on chromosome 9 which regulates systemic levels of β-galactosidase. The distribution of electrophoretic and activity phenotypes among inbred strains is not concordant, indicating that they result from separate mutations. Three aspects of β-galactosidase realization, its structure, systemic regulation and developmental program, are now known to be organized in close proximity on chromosome 9. Considered in conjunction with evidence from other mammalian systems, this suggests that the mammalian genome, like Drosophila, is organized into large functional units in which relevant regulatory and developmental information is closely associated with individual structural genes.

scholarly journals INHERITANCE OF A PAROTID SECRETORY PROTEIN IN MICE AND ITS USE IN DETERMINING SALIVARY AMYLASE QUANTITATIVE VARIANTS

Genetics ◽  
1980 ◽  
Vol 95 (1) ◽  
pp. 129-141
Author(s):  
David Owerbach ◽  
J Peter Hjorth
Keyword(s):  
Cyanogen Bromide ◽  
Inbred Strains ◽  
Secretory Protein ◽  
Major Protein ◽  
Chromosome 2 ◽  
Parotid Glands ◽  
Salivary Amylase ◽  
Inbred Strains Of Mice ◽  
Mendelian Factor ◽  
Parotid Secretory Protein

ABSTRACT Among inbred strains of mice, a major protein, PSP, produced and secreted by the parotid glands, shows variation in electrophoretic mobility and in the peptides produced by cyanogen bromide treatment. This variation is inherited as a single Mendelian factor with two alleles showing co-dominant expression. In genetic crosses, it segregates independently from the amylase complex and is closely linked to the agouti locus on chromosome 2. The protein ratios between amylase and PSP in saliva, obtained by scanning of electrophoretic gel separations, were found to reflect genetic differences in salivary amylase production in strains YBR/Cv and C3H/As.

A twenty strain survey and backcross localization of the erythrocytic GTP concentration determining locus Gtpc on mouse chromosome 9

Genome ◽  
1999 ◽  
Vol 42 (3) ◽  
pp. 447-452 ◽  
Author(s):  
G J Wiebe ◽  
E Fung ◽  
F G Biddle ◽  
F F Snyder
Keyword(s):  
Microsatellite Markers ◽  
Mouse Chromosome ◽  
Gene Order ◽  
Inbred Strains ◽  
Genetic Distances ◽  
Chromosome 9 ◽  
Atp Concentration ◽  
Inbred Strains Of Mice ◽  
Significant Difference ◽  
Kidney Liver

Erythrocyte nucleotide concentrations were surveyed among 20 inbred strains of mice in order to further assess the variability in GTP concentration. There was no significant difference in erythrocytic ATP concentration (Scheffé's test at P = 0.01), 678-1154 nmol/mL packed cells, among the strains surveyed. Two groups were distinguishable with respect to erythrocytic GTP concentration, 8 strains having high GTP, 215 ± 44 nmole/mL packed cells, and 12 strains having low GTP, 34 ± 12 nmole/mL packed cells. The erythrocytic GTP concentration determining trait Gtpc was previously shown to be linked to transferrin, Trf, on chromosome 9. Analysis of 232 [(B6 × WB) F1 × B6] backcross individuals for Gtpc and 8 microsatellite markers restricted the localization of Gtpc to a 5.6 ± 2.1 cM region. The gene order and genetic distances in cM ± SE are: (D9Mit14) 0.4 ± 0.4 (D9Mit24) 1.7 ± 0.8 (Gtpc, D9Mit51, D9Mit116, D9Mit212) 3.9 ± 1.3 (D9Mit200) 3.0 ± 1.1 (D9Mit20) 7.8 ± 1.8 (D9Mit18). The GTP concentration determining trait appears to be a property of erythrocytes as no differences were observed for GTP/ATP ratios of brain, kidney, liver, and tongue from a low GTP strain, C3H/HeHa × Pgk-1a and a high GTP strain, C57BL/6J.Key words: Gtpc, guanosine-5'-triphosphate, GTP, mouse, chromosome 9.

Differential control of ventilation among inbred strains of mice

1994 ◽  
Vol 267 (5) ◽  
pp. R1371-R1377 ◽  
Author(s):  
C. G. Tankersley ◽  
R. S. Fitzgerald ◽  
S. R. Kleeberger
Keyword(s):  
Minute Ventilation ◽  
Inbred Strains ◽  
Whole Body ◽  
Genetic Determinants ◽  
Ventilatory Responses ◽  
Hypoxic Conditions ◽  
Inbred Strains Of Mice ◽  
Genetic Mechanisms ◽  
The Difference ◽  
Differential Control

The role genetic factors play in ventilatory control was examined by challenging eight inbred strains of mice to acute hypercapnia under normoxic and hypoxic conditions. Age-matched mice were exposed for 3-5 min to inspired gases of the following composition (FICO2:FIO2) 0.03:0.10, 2) 0.03:0.21, 3) 0.08:0.10, and 4) 0.08:0.21, with intermittent room air exposures. Breathing frequency (f) and tidal volume (VT) of unanesthetized, unrestrained mice were assessed by whole body plethysmography. During room air breathing, significant (P < 0.01) interstrain differences were noted in the pattern, but minute ventilation (VE) did not differ among the strains. Relative to room air, mild hypercapnia with hypoxia (0.03:0.10) significantly (P < 0.01) elevated VE in each strain, and the percent increase in VE of the DBA/2J strain was significantly (P < 0.05) greater than the other strains. The ventilatory response to these conditions was achieved primarily by a significant (P < 0.01) increase in f among the strains. During severely hypercapnic normoxia (0.08:0.21) and hypoxia (0.08:0.10), the increase in VE was significantly (P < 0.01) greatest in the C57BL/6J (B6) mice and least in the C3H/HeJ (C3) mice. The difference in hypercapnic VE between B6 and C3 strains was largely due to a significantly (P < 0.01) greater increase in VT by B6 mice. On the assumption that environmental factors were identical, these data suggest that genetic determinants govern interstrain variation in the magnitude and pattern of breathing during hypoxia and hypercapnia. Moreover, hypoxic and hypercapnic ventilatory responses appear to be influenced by different genetic mechanisms.

Dental Fluorosis: Variability among Different Inbred Mouse Strains

2002 ◽  
Vol 81 (11) ◽  
pp. 794-798 ◽  
Author(s):  
E.T. Everett ◽  
M.A.K. McHenry ◽  
N. Reynolds ◽  
H. Eggertsson ◽  
J. Sullivan ◽  
...  
Keyword(s):  
Mouse Strain ◽  
Dental Fluorosis ◽  
Inbred Mouse ◽  
Inbred Strains ◽  
Rapid Onset ◽  
Mouse Strains ◽  
Genetic Determinants ◽  
Fluoride Level ◽  
Inbred Strains Of Mice ◽  
Mouse Model System

Concurrent with the decline in dental caries has been an increase in the prevalence of dental fluorosis, a side-effect of exposure to greater than optimal levels of fluoride during amelogenesis. The mechanisms that underlie the pathogenesis of dental fluorosis are not known. We hypothesize that genetic determinants influence an individual’s susceptibility or resistance to develop dental fluorosis. We tested this hypothesis using a mouse model system (continuous eruption of the incisors) where genotype, age, gender, food, housing, and drinking water fluoride level can be rigorously controlled. Examination of 12 inbred strains of mice showed differences in dental fluorosis susceptibility/resistance. The A/J mouse strain is highly susceptible, with a rapid onset and severe development of dental fluorosis compared with that in the other strains tested, whereas the 129P3/J mouse strain is least affected, with minimal dental fluorosis. These observations support the contribution of a genetic component in the pathogenesis of dental fluorosis.

Effects of Foster Nursing on Alcohol Selection in Inbred Strains of Mice

1972 ◽  
Vol 33 (2) ◽  
pp. 494-503 ◽  
Author(s):  
Setsuo Komura ◽  
Masao Ueda ◽  
Toshikiyo Kobayashi
Keyword(s):  
Inbred Strains ◽  
Inbred Strains Of Mice

Duplications and deletions of Vh genes in inbred strains of mice

1988 ◽  
Vol 28 (2) ◽  
pp. 125-135 ◽  
Author(s):  
Adele Tutte ◽  
Roy Riblet
Keyword(s):  
Inbred Strains ◽  
Inbred Strains Of Mice ◽  
Vh Genes

scholarly journals THE GENETIC DIVERGENCE OF SUBLINES AS ASSESSED BY HISTOCOMPATIBILITY TESTING

Genetics ◽  
1973 ◽  
Vol 75 (4) ◽  
pp. 671-677
Author(s):  
Willys K Silvers ◽  
David L Gasser
Keyword(s):  
Genetic Divergence ◽  
Inbred Strains ◽  
Skin Grafts ◽  
Inbred Strains Of Mice ◽  
Inbred Rats

ABSTRACT The degree of genetic divergence which has occurred between a number of inbred strains of mice and between two sublines of inbred rats was assessed by determining the fate of inter-subline skin grafts. Sublines which had been separated for 29 and 42 generations possessed no detectable incompatibility, while three combinations of sublines judged to have been maintained apart for from 123 to 129 generations showed slight degrees of histoincompatibility. One pair of sublines which had been separated for 119 generations demonstrated a marked degree of incompatibility, and an F2 test suggested that mutations had occurred at four or five histocompatibility loci.

scholarly journals A new allele of the lpr locus, lprcg, that complements the gld gene in induction of lymphadenopathy in the mouse.

1990 ◽  
Vol 171 (2) ◽  
pp. 519-531 ◽  
Author(s):  
A Matsuzawa ◽  
T Moriyama ◽  
T Kaneko ◽  
M Tanaka ◽  
M Kimura ◽  
...  
Keyword(s):  
Recessive Gene ◽  
Mutant Gene ◽  
Inbred Strains ◽  
Lymphoid Hyperplasia ◽  
Lymphoid Cells ◽  
Autoantibody Production ◽  
Genetic Studies ◽  
Inbred Strains Of Mice ◽  
Backcross Populations ◽  
Generalized Lymphadenopathy

Several mice with generalized lymphadenopathy were found in the CBA/KlJms (CBA) colony maintained at our institute. A new mutant strain of mice that develop massive lymphoid hyperplasia at 100% incidence within 5 mo after birth was established by crossing these diseased mice. Genetic studies on lymphadenopathy were conducted in F1, F2, and backcross populations from crosses between mutant CBA (CBA-m) and various inbred strains of mice. The results supported the control of lymphadenopathy by a single autosomal recessive gene. Since C3H/He-gld/gld (C3H-gld), MRL/MpJ-lpr/lpr (MRL-lpr), and C3H/HeJ-lpr/lpr (C3H-lpr) mice develop the same type of lymphoid hyperplasia, allelism of the mutant gene with gld or lpr was tested by investigating lymphadenopathy in F1 and backcross populations from crosses between CBA-m and C3H-gld, MRL-lpr, or C3H-lpr mice. The gene was confirmed to be allelic with lpr but not with gld. Interestingly, however, the mutant gene interacted with gld to induce less severe lymphadenopathy. Thus, the mutant gene was named lprcg, an lpr gene complementing gld in induction of lymphoproliferation. The genetic conclusion was supported by the same profile of surface markers of lymphoid cells with gld/gld, lpr/lpr, lprcg/lprcg, lprcg/lpr, and +/gld +/lprcg genotypes, as well as by massive lymph node hyperplasia and high titers of autoantibodies in the first four genotypes, but slight hyperplasia and insignificant autoantibody production in the last. The discovery of lprcg provided strong genetic evidence for the parallels between anomalous phenotypes of gld and lpr, and CBA/KlJms-lprcg/lprcg mice will contribute to elucidation of the mechanism of induction of the same abnormal differentiation and functions of lymphocytes by gld and lpr.

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