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  • Genetics  (2)
  • response to androgen  (2)
  • enzyme loss  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Biochemical genetics 16 (1978), S. 897-903 
    ISSN: 1573-4927
    Keywords: β-glucuronidase synthesis ; enzyme loss ; recombinant-inbred strains ; induction by testosterone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract A set of recombinant-inbred strains developed from mouse strains BALB/c and C57BL/6 includes two β-glucuronidase phenotypes that are not seen in either of the progenitor strains. These new recombinant phenotypes indicate that glucuronidase levels are regulated by genes additional to the Gur locus, which is closely linked to the glucuronidase structural gene (Gus) and is known to regulate the rate of glucuronidase synthesis. In this study, induced rates of glucuronidase synthesis were determined for these recombinant-inbred strains, and rate constants for enzyme loss were calculated. The rate of synthesis was found to segregate with the Gus gene in all of the strains, and only the determinants for rate of enzyme loss recombined to give new phenotypes. It was concluded that at least two genes affect the rate of enzyme loss, that these genes are not closely linked to each other or to the Gur-Gus region on chromosome 5, and that no major determinants of glucuronidase synthesis segregate independently of Gur.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-4927
    Keywords: β-glucuronidase ; gene regulation ; response to androgen ; response to estrogen ; regulatory locus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Both enzyme activity and mRNA concentration of β-glucuronidase were measured in kidneys of mice treated with testosterone and the synthetic estrogen, diethylstilbestrol. Six congenic strains, all having a C57BL6/J genetic background but each having a different haplotype of the β-glucuronidase gene complex, were compared. In each strain the induction caused by androgen was partially repressed by estrogen. The extent of this antagonism varied among the six haplotypes and was not coordinate with the extent of induction by androgen alone. Antagonism appears to be regulated by at least two alleles of a new locus,Gus-e, within the β-glucuronidase gene complex. Repression by estrogen, like induction by androgen, appears to take place primarily at the transcriptional level. Kinetic studies revealed that estrogen causes the androgen response curve to plateau earlier and at a lower level. This suggests that estrogen increases the rate of gene deactivation rather than decreasing the rate of gene activation, Isoelectric focusing of β-glucuronidase fromGus-e a andGus-e b mice and their F1 progeny revealed that the genes are regulated incis. Together, these findings support a model in which both sex hormones exert their effects on separate DNA response elements located in close proximity to the gene or within the gene itself.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-4927
    Keywords: β-glucuronidase ; gene regulation ; response to androgen ; response to estrogen ; regulatory locus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Both enzyme activity and mRNA concentration of β-glucuronidase were measured in kidneys of mice treated with testosterone and the synthetic estrogen, diethylstilbestrol. Six congenic strains, all having a C57BL6/J genetic background but each having a different haplotype of the β-glucuronidase gene complex, were compared. In each strain the induction caused by androgen was partially repressed by estrogen. The extent of this antagonism varied among the six haplotypes and was not coordinate with the extent of induction by androgen alone. Antagonism appears to be regulated by at least two alleles of a new locus,Gus-e, within the β-glucuronidase gene complex. Repression by estrogen, like induction by androgen, appears to take place primarily at the transcriptional level. Kinetic studies revealed that estrogen causes the androgen response curve to plateau earlier and at a lower level. This suggests that estrogen increases the rate of gene deactivation rather than decreasing the rate of gene activation, Isoelectric focusing of β-glucuronidase fromGus-e a andGus-e b mice and their F1 progeny revealed that the genes are regulated incis. Together, these findings support a model in which both sex hormones exert their effects on separate DNA response elements located in close proximity to the gene or within the gene itself.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Chichester [u.a.] : Wiley-Blackwell
    Developmental Genetics 5 (1984), S. 83-91 
    ISSN: 0192-253X
    Keywords: temporal genes ; acid hydrolases ; liver ; mice ; hepatocytes ; nonhepatocytes ; Life and Medical Sciences ; Genetics
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: The cell specificity of expression of three distinct trans acting temporal gene systems determining the developmental control of α-galactosidase, β-galactosidase and β-glucuronidase was tested in mouse liver. For α-galactosidase and β-galactosidase, expression was limited to hepatocytes; no effect was seen in nonhepatocytes. For β-glucuronidase the data suggest that expression of the Gus-t temporal locus is also limited to hepatocytes, and that the smaller enzyme reduction seen in nonhepatocytes of some strains is due to a separate systemic regulatory locus that is also present in the [Gus] gene complex. We conclude that the temporal gene-determined timing mechanisms initiating switches in rates of enzyme synthesis are intrinsic to the cells themselves and are not communicated to adjacent cells. This conclusion applies to the temporal locus for β-glucuronidase that is proximate to its structural gene as well as those for α-galactosidase and β-galactosidase that are distant from the structural genes that they regulate.
    Additional Material: 5 Tab.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Chichester [u.a.] : Wiley-Blackwell
    Developmental Genetics 2 (1981), S. 269-277 
    ISSN: 0192-253X
    Keywords: β-glucuronidase ; androgen ; receptor ; development ; mouse ; kidney ; Life and Medical Sciences ; Genetics
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: During postnatal development of mouse kidney the androgen responsiveness of epithelial cells for β-glucuronidase induction, cellular hypertrophy, and other enzyme inductions appears coincidentally with a rise in androgen receptor protein. Initially, a low level of receptor is present but no response is seen. Beginning at about 12 days of age responsiveness begins to increase, reaches a half-maximal level at 18-20 days, and full responsiveness by 28-30 days. The limiting factor appears to be levels of androgen receptor protein.Our experiments shed no light on the question of why each androgen responsive cell type in the organism differentiates the capacity to induce a different array of proteins. However, they do suggest that responsiveness of the β-glucuronidase gene does not appear until a minimum threshold level of receptor is exceeded, and that the response of the gene may not be saturated even at the highest levels of receptor reached.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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