Aplin J D, Hughes R C
J Cell Sci. 1981 Aug;50:89-103. doi: 10.1242/jcs.50.1.89.
Trypsinized BHK cells become attached to glass that has been derivatized with a variety of lectins with well-defined specificity for cell-surface carbohydrates. Provided a threshold concentration of glass-immobilized protein is present the cells undergo a transformation to a well-spread morphology. The matrix density of lectins (ricin and concanavalin A) required to trigger this morphological transformation is higher by 10 to 40-fold thant the value determined earlier (Hughes, Pena, Clark & Dourmashkin, 1979) for fibronectin. Cells resistant to the toxic lectin, ricin, and expressing 10% or less of ricin-binding carbohydrate groups at their cell surfaces require correspondingly greater matrix densities of ricin to promote active cell spreading. All cell lines spread equally well on concanavalin A-based matrices consistent with their similar binding properties. The quantitative interaction of complementary molecules on the cell surface and matrix, promoting cell adhesion, is demonstrated by these results and a model is proposed for the events leading to a well-spread cell morphology on a protein-coated substratum.
经胰蛋白酶处理的BHK细胞会附着在已用多种对细胞表面碳水化合物具有明确特异性的凝集素衍生化的玻璃上。如果存在阈值浓度的固定在玻璃上的蛋白质，细胞会转变为形态良好伸展的形态。引发这种形态转变所需的凝集素（蓖麻毒素和伴刀豆球蛋白A）的基质密度比早期（休斯、佩纳、克拉克和杜尔马斯金，1979年）测定的纤连蛋白的值高10至40倍。对有毒凝集素蓖麻毒素具有抗性且在其细胞表面表达10%或更少蓖麻毒素结合碳水化合物基团的细胞，需要相应更高密度的蓖麻毒素基质来促进细胞的活跃铺展。所有细胞系在基于伴刀豆球蛋白A的基质上的铺展情况相同，这与它们相似的结合特性一致。这些结果证明了细胞表面和基质上互补分子促进细胞黏附的定量相互作用，并提出了一个模型，用于解释在蛋白质包被的基质上形成形态良好伸展的细胞形态的过程。
