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  • transgenic  (1)
  • transgenic mice  (1)
  • 1
    ISSN: 1573-9368
    Keywords: transgenic mice ; insertional mutagenesis ; microphthalmia ; depigmentation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Transgenic mice were produced by microinjection of a humanAγ-globin gene construct containing site 2 of the locus control region and theAγ-globin gene with its 3′ enhancer sequence. One transgenic mouse line 95′HS2γen91) displayed an altered phenotype when the insertion event of this transgenic line was homozygous. These animals lack the normal pigmentation seen in their hemizygous and non-transgenic littermates, thus appearing white with unpigmented eyes. In addition, their eyes are underdeveloped, consistent with the phenotype associated with mutations at themicrophthalmia (mi) locus. Backcrosses of transgenic mice withmi mutant mice result in phenotypes showing a lack of complementation, demonstrating that the site of transgene insertion is allelic withmi. Electron microscopic analysis of hair follicles and culturing of melanocytes from the skin of transgenic animals reveals an absence of cutaneous melanocytes in homozygotes and aberrant growth and morphology of the melanocytes isolated from hemizygous animals. The results presented here summarize the effects of this new allele of themi locus.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-9368
    Keywords: human β globin ; 3′ enhancer ; transgenic ; promoter
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Our interest in thecis-acting elements that promote the up-regulation of the β globin gene has led to a systematic deletion analysis of portions of the β globin gene in the context of the HS2 and γ globin gene using transgenic mice. In constructs that delete the 5′ region to only 265 bp, high-level erythroid-specific expression was observed. Further deletion to 122 bp, however, results in significantly reduced expression levels A substitution of a minilocus control region for the single HS2 site was also produced, resulting in increased β globin expression over that seen with the HS2 alone. These results are consistent with the presence of an enhancer-like element between −122 and −265. In addition, a construct in which the entire β globin gene promoter was replaced by a thymidine kinase promoter was tested. Interestingly, no expression was detected in these transgenic mice. This may indicate the requirement for an erythroid-specific promoter to drive this gene. Finally, the 3′ region of the β globin gene was deleted in order to examine the effect of a previously defined 3′ enhancer region. With deletion of this region, the expression of the human β globin gene in transgenic mice is unchanged relative to the parental constructs.
    Type of Medium: Electronic Resource
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