Abstract

Homotypic and heterotypic permeable junction formation between a metabolic cooperationdefective embryonal carcinoma variant R5 3 and its parent PC13TG8 have been studied by uridine prelabelling. The results indicate that the lesion results not in a modified specificity of cell recognition but in a deficiency in forming permeable junctions irrespective of contiguous cell type. New techniques have been developed for the study of intercellular transfer of sodium ions and of amino acids of the urea cycle. These have been used to demonstrate that the R5 3 lesion reduces the capacity of the cells to participate in intercellular transfer of three unrelated categories of small molecule.

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