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Cellular adhesiveness reduced in ricin-resistant hamster fibroblasts

Abstract

THE means by which tissue cells adhere to one another and to non-cellular surfaces is not known, although complex carbohydrate of their surface membrane may be involved1,2. To test this, one can ask whether mutations which affect the structure of surface carbohydrate also alter cellular adhesiveness. Meager et al.3 have isolated a series of stable variants of baby hamster kidney fibroblasts (BHK 21, clone 13) which are resistant to the toxic lectin ricin. The first step in killing of cells by ricin is binding of the lectin to galactosyl- or N-acetylgalactosaminyl residues at the cell surface4,5, and many ricin-resistant clones yield cell lines with reduced glycosylation of their cell surfaces3. We now report that, judged by their ability to form aggregates in suspension, the intercellular adhesiveness of a number of ricin-resistant lines is less than unselected lines. We have also found that cells of most lines attach less readily than controls to glass coverslips bearing adsorbed films of serum or gelatin.

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EDWARDS, J., DYSART, J. & HUGHES, R. Cellular adhesiveness reduced in ricin-resistant hamster fibroblasts. Nature 264, 66–68 (1976). https://doi.org/10.1038/264066a0

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