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. 1981 Jan;78(1):479–483. doi: 10.1073/pnas.78.1.479

Complementation of gene deletions by cell hybridization.

C F Cori, S Gluecksohn-Waelsch, H P Klinger, L Pick, S L Schlagman, L S Teicher, H F Wang-Chang
PMCID: PMC319077  PMID: 6113589

Abstract

Overlapping deletions in chromosome 7 of the mouse are responsible for activity deficiencies of various liver-specific enzymes, including tyrosine aminotransferase (TAT). In an effort to elucidate the nature and type of action of the deleted genes, somatic cell hybridization experiments were carried out. Enzyme-deficient liver cells of homozygous mutant mice or normal liver cells of control newborn mice were hybridized with 2S Faza rat hepatoma cells and the hybrid cell colonies were analyzed for TAT activity, The results show the presence of inducible mouse TAT activity in mutant-2S Faza hybrid cells, thereby excluding the possibility that the structural gene for TAT is included in the gene sequences deleted in the mutants. Furthermore, determinations of mouse glucose-6-phosphate isomerase 1 as a marker eliminate chromosome 7 as the possible carrier of the TAT structural gene, which therefore appears to map on a different chromosome. The deletions interfering with normal enzyme activities apparently include genes other than the respective structural genes, namely those with essential functions in controlling the expression of the differentiated state of the liver cell.

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Selected References

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