Decreased epidermal growth factor binding in cells growth arrested in G1 by nutrient deficiency

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Abstract
Previous studies have shown that the nontransformed AKR‐2B mouse embryo derived cell line may growth arrest by two separate mechanisms in the G1 phase of the cell cycle‐growth factor deficiency arrest (G0) and low molecular weight nutrient deficiency arrest. An examination of epidermal growth factor (EGF) receptors under the different resting or growth conditions has shown that rapidly growing cells or cells arrested due to growth factor deficiency have the expected amount of 125I‐EGF binding with approximately 105 receptors per cell being present in G0 arrested cells. In contrast, cells arrested due to nutrient deficiency show a reduction in 125I‐EGF binding to 10‐‐20% of that observed under the other conditions. This effect appears to be due to decreased receptor number and not to a change in the affinity of the receptor. Stimulation of DNA synthesis by nutrient replenishment causes a tenfold increase in EGF binding 20 hours later, with some increase in binding being detectable as early as six hours. The increase in binding is inhibited by cycloheximide and actinomycin D. This suggests that new mRNA synthesis as well as increased protein synthesis is required for the increase in EGF binding.

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