scholarly journals GENETIC REGULATION OF MUP PRODUCTION IN RECOMBINANT INBRED MICE

Genetics ◽  
1979 ◽  
Vol 93 (1) ◽  
pp. 173-181
Author(s):  
P R Szoka ◽  
K Paigen
Keyword(s):  
Recombinant Inbred ◽  
Inbred Mice ◽  
Genetic Regulation ◽  
Inbred Strains ◽  
Urinary Proteins ◽  
Major Urinary Proteins ◽  
Recombinant Inbred Mice ◽  
Inbred Strains Of Mice ◽  
Before And After ◽  
Kinetics Of

ABSTRACT 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 pheno-types before and after testosterone treatment of seven recombinant inbred strains derived from progenitor strains exhibiting different mup phenotypes. The results codirm 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 testoster- one. 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.

Genetic Regulation ofMycobacterium paratuberculosisInfection in Recombinant Inbred Mice

1990 ◽  
Vol 27 (5) ◽  
pp. 362-364 ◽  
Author(s):  
P. F. Frelier ◽  
J. W. Templeton ◽  
M. Estes ◽  
H. W. Whitford ◽  
R. D. Kienle
Keyword(s):  
Recombinant Inbred ◽  
Inbred Mice ◽  
Genetic Regulation ◽  
Recombinant Inbred Mice

Identification of a common ecotropic viral integration site, Evi-1, in the DNA of AKXD murine myeloid tumors

1988 ◽  
Vol 8 (1) ◽  
pp. 301-308
Author(s):  
M L Mucenski ◽  
B A Taylor ◽  
J N Ihle ◽  
J W Hartley ◽  
H C Morse ◽  
...  
Keyword(s):  
B Cell ◽  
Recombinant Inbred ◽  
High Frequency ◽  
Integration Site ◽  
Inbred Mice ◽  
Myeloid Cell ◽  
Inbred Strains ◽  
Viral Integration ◽  
Recombinant Inbred Mice ◽  
T Cell Lymphomas

AKXD-23 recombinant inbred mice develop myeloid tumors at a high frequency, unlike other AKXD recombinant inbred strains which develop B-cell lymphomas, T-cell lymphomas, or both. AKXD-23 myeloid tumors are monoclonal, and their DNA contains somatically acquired proviruses, suggesting that they are retrovirally induced. We identified a common site of ecotropic proviral integration that is present in the DNA of all AKXD-23 myeloid tumors that were analyzed and in the DNA of all myeloid tumors that occur in AKXD strains other than AKXD-23. We designated this locus Evi-1 (ecotropic viral integration site 1). Rearrangements in the Evi-1 locus were also detected in the DNA of a number of myeloid tumors and myeloid cell lines isolated from strains other than AKXD. In contrast, few Evi-1 rearrangements were detected in the DNA of T- or B-cell tumors. Evi-1 may thus identify a new proto-oncogene locus that is involved in myeloid disease.

scholarly journals REGULATION OF MOUSE MAJOR URINARY PROTEIN PRODUCTION BY THE MUP-A GENE

Genetics ◽  
1978 ◽  
Vol 90 (3) ◽  
pp. 597-612
Author(s):  
P R Szoka ◽  
K Paigen
Keyword(s):  
Protein Production ◽  
Inbred Strains ◽  
Electrophoretic Separation ◽  
Urinary Proteins ◽  
Major Urinary Protein ◽  
Testosterone Treatment ◽  
Major Urinary Proteins ◽  
Before And After ◽  
Daily Excretion ◽  
Induced Proteins

ABSTRACT A method was developed to quantitate the daily excretion of the three major urinary proteins (mups) to test which parameters of the mup phenotype are controlled by the the Mup-a gene. Electrophoretic separation of the mup proteins, followed by staining and spectrophotometric scanning was used to characterize the phenotypes of various inbred strains. The mup phenotype of a strain proved to have two components: the absolute levels and the relative proportions of the mups present in the urine. Testosterone treatment alters both components of the mup phenotype, increasing mup excretion and altering their relative proportions. The induced proteins are the same as the basal proteins as judged by electrophoretic mobility, molecular weight, and reactivity with antibody. All strains excrete all three mups when induced. The Mup-a gene appears to be a single, codominantly expressed regulatory locus that controls the induced proportions of the three proteins. However, other genes in addition to Mup-a participate in controlling the basal mup proportions, as well as individual and total mup levels before and after testosterone treatment.

scholarly journals Linkage between sperm abnormality level and major urinary protein phenotype in mice

1991 ◽  
Vol 57 (2) ◽  
pp. 135-138 ◽  
Author(s):  
Jozefa Styrna
Keyword(s):  
Inbred Strains ◽  
Chromosome 4 ◽  
Urinary Proteins ◽  
Major Urinary Protein ◽  
Major Urinary Proteins ◽  
Abnormal Sperm ◽  
Inbred Strains Of Mice ◽  
Sperm Abnormality ◽  
High Level ◽  
Very High

SummarySegregation of sperm abnormality level and the pattern of major urinary proteins (MUPs) were investigated in F2 and B1 hybrid males obtained from crosses involving two contrasting inbred strains of mice: CBA/Kw (Mup-1a1a, 3·3% abnormal sperm) and C57BL/Kw (Mup-1b1b, 21·9% abnormal sperm). In the progeny of both crosses mean levels of abnormal spermatozoa were significantly higher for males typed as Mup-1b1b than for heterozygous Mup-1a1b males. Moreover, all F2 hybrid males showing very high percentages of abnormal sperm were Mup-1b1bhomozygotes. Similarly, among B1 males with a high level of deformed spermatozoa, a statistically significant majority were Mup-1b1b genotypes. Our results suggest that at least two genes which influence sperm abnormality level are segregating in these crosses. Both appear to be recessive for high sperm abnormality level, and one shows weak linkage to Mup-1 on chromosome 4.

scholarly journals Susceptibility to Friend helper virus leukemias in CXB recombinant inbred mice.

1983 ◽  
Vol 158 (5) ◽  
pp. 1693-1702 ◽  
Author(s):  
J E Silver ◽  
T N Fredrickson
Keyword(s):  
Recombinant Inbred ◽  
Inbred Mice ◽  
Disease Free Survival ◽  
Inbred Strains ◽  
Helper Virus ◽  
Myelogenous Leukemia ◽  
Strain Distribution Pattern ◽  
Free Survival ◽  
Recombinant Inbred Mice ◽  
Ecotropic Virus

The seven CXB recombinant inbred strains were tested for susceptibility to Friend helper virus (F-MuLV) hematopoietic neoplasms. BALB/c and CXB-H mice develop erythroblastosis after neonatal inoculation with F-MuLV, while C57BL/6 and the six other RI strains develop lymphoma and myelogenous leukemia. This strain distribution pattern is different from that for H-2, Gpd-1 (linked to Fv-1), Fv-2, Rfv-3, and Cv (linked to Rmcf) but the same as that for Bv, the endogenous ecotropic virus of C57BL/6. However, analysis of crosses segregating Bv show that resistance to F-MuLV erythroblastosis is not linked to Bv. Disease-free survival is shortest for BALB/c mice, intermediate for CXB-H and CXB-J, and longest for C57BL/6 and the other RI strains. We conclude: (a) the major C57BL/6 gene for resistance to F-MuLV erythroblastosis is different from previously identified Friend virus restriction loci; (b) latency for F-MuLV leukemias is controlled by more than one gene; and (c) latency and susceptibility to F-MuLV erythroblastosis are not inherited concordantly in the CXB-RI strains.

scholarly journals Identification of a common ecotropic viral integration site, Evi-1, in the DNA of AKXD murine myeloid tumors.

1988 ◽  
Vol 8 (1) ◽  
pp. 301-308 ◽  
Author(s):  
M L Mucenski ◽  
B A Taylor ◽  
J N Ihle ◽  
J W Hartley ◽  
H C Morse ◽  
...  
Keyword(s):  
B Cell ◽  
Recombinant Inbred ◽  
High Frequency ◽  
Integration Site ◽  
Inbred Mice ◽  
Myeloid Cell ◽  
Inbred Strains ◽  
Viral Integration ◽  
Recombinant Inbred Mice ◽  
T Cell Lymphomas

AKXD-23 recombinant inbred mice develop myeloid tumors at a high frequency, unlike other AKXD recombinant inbred strains which develop B-cell lymphomas, T-cell lymphomas, or both. AKXD-23 myeloid tumors are monoclonal, and their DNA contains somatically acquired proviruses, suggesting that they are retrovirally induced. We identified a common site of ecotropic proviral integration that is present in the DNA of all AKXD-23 myeloid tumors that were analyzed and in the DNA of all myeloid tumors that occur in AKXD strains other than AKXD-23. We designated this locus Evi-1 (ecotropic viral integration site 1). Rearrangements in the Evi-1 locus were also detected in the DNA of a number of myeloid tumors and myeloid cell lines isolated from strains other than AKXD. In contrast, few Evi-1 rearrangements were detected in the DNA of T- or B-cell tumors. Evi-1 may thus identify a new proto-oncogene locus that is involved in myeloid disease.

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