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Combining Lipophilic dye, in situ Hybridization, Immunohistochemistry, and Histology
13:05

Combining Lipophilic dye, in situ Hybridization, Immunohistochemistry, and Histology

Published on: March 17, 2011

Complementation of gene deletions by cell hybridization

C F Cori, S Gluecksohn-Waelsch, H P Klinger

    Proceedings of the National Academy of Sciences of the United States of America
    |January 1, 1981
    PubMed

    Insights

    Mouse chromosome 7 deletions cause liver enzyme deficiencies. Somatic cell hybridization revealed that the tyrosine aminotransferase (TAT) structural gene is not on chromosome 7, but other genes controlling liver cell differentiation are involved.

    Area of Science:

    • Genetics
    • Molecular Biology
    • Biochemistry

    Background:

    • Overlapping deletions on mouse chromosome 7 lead to reduced activity of liver-specific enzymes, such as tyrosine aminotransferase (TAT).
    • The precise function and location of the deleted genes responsible for these enzyme deficiencies remain unclear.

    Purpose of the Study:

    • To investigate the nature and function of genes affected by deletions on mouse chromosome 7.
    • To determine the chromosomal location of the structural gene for TAT and identify other potentially deleted genes impacting liver enzyme activity.

    Main Methods:

    • Somatic cell hybridization was employed, fusing enzyme-deficient mouse liver cells with 2S Faza rat hepatoma cells.
    • Analysis of hybrid cell colonies for TAT activity and glucose-6-phosphate isomerase 1 (GPI-1) as a marker for chromosome 7.

    Main Results:

    • Inducible mouse TAT activity was detected in hybrid cells derived from mutant mouse liver cells, ruling out the TAT structural gene being within the deleted chromosome 7 regions.
    • GPI-1 analysis confirmed that chromosome 7 does not carry the TAT structural gene, suggesting it resides on a different chromosome.
    • The deletions appear to encompass regulatory genes essential for maintaining the differentiated state of liver cells, rather than the structural genes for the affected enzymes.

    Conclusions:

    • The structural gene for TAT is not located on mouse chromosome 7.
    • The observed liver enzyme deficiencies are likely due to deletions of regulatory genes on chromosome 7 that control liver cell differentiation.
    • Further research is needed to identify the specific regulatory genes and their mechanisms of action.

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