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 Structural genes of the mouse major urinary protein are on chromosome 4.

1982 ◽  
Vol 94 (2) ◽  
pp. 414-417 ◽  
Author(s):  
K Krauter ◽  
L Leinwand ◽  
P D'Eustachio ◽  
F Ruddle ◽  
J E Darnell
Keyword(s):  
Protein Synthesis ◽  
Sequence Analysis ◽  
Chromosome 4 ◽  
Structural Genes ◽  
Urinary Proteins ◽  
Coding Region ◽  
Somatic Cell Genetics ◽  
Major Urinary Protein ◽  
Major Urinary Proteins ◽  
Trans Regulation

The major urinary proteins (MUPs) of mouse are a family of at least three major proteins which are synthesized in the liver of all strains of mice. The relative levels of synthesis of these proteins with respect to each other in the presence of testosterone is regulated by the Mup-a locus located on chromosome 4. In an effort to determine the mechanism of this regulation in molecular terms, a cDNA clone containing most of the coding region of a MUP protein has been isolated and identified by partial DNA sequence analysis. Using a combination of hybridization analysis and somatic cell genetics, the structural gene family has been unambiguously mapped to mouse chromosome 4. These data suggest that Mup-a regulation operates in a cis fashion and that models proposing trans regulation of MUP protein synthesis are unlikely.

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 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.

scholarly journals Silent and expressed sister Mup genes are located within distinct chromatin domains: analysis by pulsed-field gel electrophoresis and polymerase chain reaction-supplemented DNase I digestion.

1992 ◽  
Vol 12 (3) ◽  
pp. 1188-1193 ◽  
Author(s):  
M Rodriguez ◽  
E Derman
Keyword(s):  
Tissue Specificity ◽  
Submaxillary Gland ◽  
Inbred Strains ◽  
Dnase I ◽  
Chromosome 4 ◽  
Chain Reaction ◽  
Inbred Strains Of Mice ◽  
Novel Method ◽  
Polymerase Chain ◽  
High Level

We have recently described a subfamily of two genes, Mup-1.5a and Mup-1.5b, which exist as a nonallelic pair in most inbred strains of mice. The Mup-1.5a and Mup-1.5b genes are more than 99.9% homologous, yet they are differentially expressed. While the Mup-1.5a gene is expressed at a high level in the submaxillary gland, the Mup-1.5b gene does not appear to be expressed either in this or in any other tissue. The Mup-1.5b gene can, however, be expressed as a transgene with the tissue specificity of its sister gene, Mup-1.5a. We have shown before that both the Mup-1.5a and Mup-1.5b genes are located on chromosome 4, closely linked to the Mup-1 locus. In this report, we demonstrate the two genes are located within distinct chromosomal domains, separated by at least 150 to 200 kb of DNA. Using a novel method, detailed in this report, we show that in the submaxillary gland, the Mup-1.5a gene is five- to sixfold more susceptible to DNase I digestion than is the Mup-1.5b gene. This finding suggests that the inactivity of the Mup-1.5b gene is brought about by long range-acting mechanisms that establish a chromatin structure in the vicinity of this gene incompatible with transcription.

Silent and expressed sister Mup genes are located within distinct chromatin domains: analysis by pulsed-field gel electrophoresis and polymerase chain reaction-supplemented DNase I digestion

1992 ◽  
Vol 12 (3) ◽  
pp. 1188-1193
Author(s):  
M Rodriguez ◽  
E Derman
Keyword(s):  
Tissue Specificity ◽  
Submaxillary Gland ◽  
Inbred Strains ◽  
Dnase I ◽  
Chromosome 4 ◽  
Chain Reaction ◽  
Inbred Strains Of Mice ◽  
Novel Method ◽  
Polymerase Chain ◽  
High Level

We have recently described a subfamily of two genes, Mup-1.5a and Mup-1.5b, which exist as a nonallelic pair in most inbred strains of mice. The Mup-1.5a and Mup-1.5b genes are more than 99.9% homologous, yet they are differentially expressed. While the Mup-1.5a gene is expressed at a high level in the submaxillary gland, the Mup-1.5b gene does not appear to be expressed either in this or in any other tissue. The Mup-1.5b gene can, however, be expressed as a transgene with the tissue specificity of its sister gene, Mup-1.5a. We have shown before that both the Mup-1.5a and Mup-1.5b genes are located on chromosome 4, closely linked to the Mup-1 locus. In this report, we demonstrate the two genes are located within distinct chromosomal domains, separated by at least 150 to 200 kb of DNA. Using a novel method, detailed in this report, we show that in the submaxillary gland, the Mup-1.5a gene is five- to sixfold more susceptible to DNase I digestion than is the Mup-1.5b gene. This finding suggests that the inactivity of the Mup-1.5b gene is brought about by long range-acting mechanisms that establish a chromatin structure in the vicinity of this gene incompatible with transcription.

scholarly journals Genetic control of endotoxic responses in mice.

1978 ◽  
Vol 147 (1) ◽  
pp. 39-49 ◽  
Author(s):  
J Watson ◽  
M Largen ◽  
K P McAdam
Keyword(s):  
Genetic Control ◽  
Genetic Locus ◽  
Serum Levels ◽  
Cell Types ◽  
Inbred Strains ◽  
Amyloid Protein ◽  
Chromosome 4 ◽  
Inbred Strains Of Mice ◽  
Different Cell Types ◽  
Stimulating Factor

A number of altered immunologic responses to lipopolysaccharide (LPS) in C3H/HeJ mice result from the expression in B lymphocytes of a defective genetic locus, termed Lps. Lps has been mapped to chromosome 4 between two loci, Mup-1 and Ps. As it is difficult to type individual mice for LPS responsiveness in more than one type of assay, we have utilized Mup-1 as a genetic marker to correlate LPS responses in mice to the expression of the Lps locus. Three nonlymphoid responses to LPS have been examined in 12 recombinant inbred strains of mice and in a backcross linkage analysis, and are all regulated by the expression of the Lps locus. These responses are hypothermal changes in body temperature, and the elevation in serum levels of a colony stimulating factor and the precursor of the secondary amyloid protein AA. Therefore, the initiation of LPS responses in different cell types in mice involve the expression of a common locus. These linkage studies provide a means for analyzing the genetic control of many of the diverse reactions of the endotoxic response to LPS.

scholarly journals Differential expression in male and female mouse liver of very similar mRNAs specified by two group 1 major urinary protein genes.

1989 ◽  
Vol 9 (5) ◽  
pp. 2202-2207 ◽  
Author(s):  
I McIntosh ◽  
J O Bishop
Keyword(s):  
Mouse Liver ◽  
Hormonal Status ◽  
Oligonucleotide Probes ◽  
Urinary Proteins ◽  
Pairwise Similarity ◽  
Major Urinary Protein ◽  
Male And Female ◽  
Major Urinary Proteins ◽  
Different Levels ◽  
Group 1

The major urinary proteins of the mouse are encoded by a large multigene family composed of several distinct groups of genes distinguished by differences in sequence and expression characteristics. The genes in the largest group (group 1) show greater than 99% pairwise similarity in their exons. By hybridization between RNA and a specifically designed oligonucleotide, we confirmed that genes of this group are expressed mainly in the liver. By using additional gene-specific oligonucleotide probes, we have been able to distinguish between the species of mRNA corresponding to two of these genes and to measure their abundance in male and female liver. Both mRNAs are present in male liver at high but different levels. Both are also present in female liver, one at a much lower level than in the male and the second at a very low level indeed. Both are present at male levels in the livers of females induced with testosterone. These results show unequivocally that the expression of different group 1 Mup genes is differentially influenced by the hormonal status of the mouse.

Differential expression in male and female mouse liver of very similar mRNAs specified by two group 1 major urinary protein genes

1989 ◽  
Vol 9 (5) ◽  
pp. 2202-2207
Author(s):  
I McIntosh ◽  
J O Bishop
Keyword(s):  
Mouse Liver ◽  
Hormonal Status ◽  
Oligonucleotide Probes ◽  
Urinary Proteins ◽  
Pairwise Similarity ◽  
Major Urinary Protein ◽  
Male And Female ◽  
Major Urinary Proteins ◽  
Different Levels ◽  
Group 1

The major urinary proteins of the mouse are encoded by a large multigene family composed of several distinct groups of genes distinguished by differences in sequence and expression characteristics. The genes in the largest group (group 1) show greater than 99% pairwise similarity in their exons. By hybridization between RNA and a specifically designed oligonucleotide, we confirmed that genes of this group are expressed mainly in the liver. By using additional gene-specific oligonucleotide probes, we have been able to distinguish between the species of mRNA corresponding to two of these genes and to measure their abundance in male and female liver. Both mRNAs are present in male liver at high but different levels. Both are also present in female liver, one at a much lower level than in the male and the second at a very low level indeed. Both are present at male levels in the livers of females induced with testosterone. These results show unequivocally that the expression of different group 1 Mup genes is differentially influenced by the hormonal status of the mouse.

scholarly journals Major urinary protein levels are associated with social status and context in mouse social hierarchies

2017 ◽  
Vol 284 (1863) ◽  
pp. 20171570 ◽  
Author(s):  
Won Lee ◽  
Amber Khan ◽  
James P. Curley
Keyword(s):  
Social Status ◽  
Social Rank ◽  
Male Mice ◽  
Urinary Proteins ◽  
Major Urinary Protein ◽  
Social Hierarchies ◽  
Protein Levels ◽  
Major Urinary Proteins ◽  
Stable Linear ◽  
Lower Urinary

We have previously shown that male mice living in groups of 12 males establish and maintain stable linear social hierarchies with each individual having a defined social rank. However, it is not clear which social cues mice use to signal and recognize their relative social status within their hierarchy. In this study, we investigate how individual social status both in pairs and in groups affects the levels of major urinary proteins (MUPs) and specifically MUP20 in urine. We housed groups of adult outbred CD1 male mice in a complex social environment for three weeks and collected urine samples from all individuals repeatedly. We found that dominant males produce more MUPs than subordinates when housed in pairs and that the production of MUPs and MUP20 is significantly higher in alpha males compared with all other individuals in a social hierarchy. Furthermore, we found that hepatic mRNA expression of Mup3 and Mup20 is significantly higher in alpha males than in subordinate males. We also show that alpha males have lower urinary creatinine levels consistent with these males urinating more than others living in hierarchies. These differences emerged within one week of animals being housed together in social hierarchies. This study demonstrates that as males transition to become alpha males, they undergo physiological changes that contribute to communication of their social status that may have implications for the energetic demands of maintaining dominance.

scholarly journals Genes that modify expression of major urinary proteins in mice.

1988 ◽  
Vol 8 (7) ◽  
pp. 2705-2712 ◽  
Author(s):  
R Duncan ◽  
R Matthai ◽  
K Huppi ◽  
T Roderick ◽  
M Potter
Keyword(s):  
Restriction Fragment ◽  
Chromosomal Location ◽  
Cdna Probe ◽  
Chromosomal Marker ◽  
Chromosome 15 ◽  
Chromosome 4 ◽  
Mus Musculus Domesticus ◽  
Urinary Proteins ◽  
Major Urinary Proteins ◽  
Restriction Fragment Polymorphism

A survey of major urinary proteins (MUPs) from eight BALB/c mouse substrains by isoelectric focusing identified a common pattern with about 10 protein bands in males. One substrain, BALB/cJPt, differed in that it expressed two variant MUP patterns, designated 4.1lo and null. To find the chromosomal location of the gene which determines the 4.1lo phenotype, BALB/cJPt-MUP-4.1lo was crossed with a wild-derived Mus musculus domesticus inbred strain (CLA) that expresses the common BALB/c MUP pattern. The F1 phenotype revealed that the gene(s) controlling the MUP-4.1lo trait was recessive. A restriction fragment polymorphism between these strains found with a MUP cDNA probe allowed us to establish that a gene determining the MUP-4.1lo trait was not linked to the MUP structural genes on chromosome 4. Assays for other chromosomal marker loci revealed that a gene determining the MUP-4.1lo trait, designated Mupm-1, was closely linked to Myc-1 on chromosome 15. To determine the genetic basis of the null trait, BALB/cJPt-MUP-null mice were crossed with BALB/cJPt-MUP-4.1lo mice. A MUP restriction fragment polymorphism between these two lines was tightly linked to a gene or genes involved in determining the MUP-null phenotype. The two variant MUP phenotypes in BALB/cJ mice are determined by separate genes, one of which is located on chromosome 4 and the other on chromosome 15. The chromosomal location of Mupm-1 suggests that it produces a trans-acting factor which regulates MUP expression.

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