Hamster fibroblasts defective in thrombin-induced mitogenesis. A selection for mutants in phosphatidylinositol metabolism and other functions.
作者： H M Rath , G A Doyle , D F Silbert
DOI: 10.1016/S0021-9258(18)80006-0
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摘要: Abstract Growth of Chinese hamster lung fibroblasts (CCL39) on thrombin as sole mitogen is dependent phosphatidylinositol (PI) metabolism and activation the Na+/H+ antiporter. By modifying a H+ suicide selection developed for isolation antiporter mutants in these cells, we enriched isolated CCL39 variants deficient mitogenic response (thrombin nongrowers). These retain alternate mechanisms and, hence, grow well media containing serum. When challenged with thrombin, show decreased, increased, or unchanged levels inositol phosphates produced compared wild type cells. One (D1-6b) has decreased production not only but also serotonin (5-hydroxytryptamine) AlF4-, suggesting defect distal to receptors. Extracts this mutant reveal marked phospholipase C activity toward PI. From different phenotypes nongrowers, it clear that general various biochemical defects should lead better understanding PI cycle functions essential mitogenesis.
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