## Abstract When BHK 21 cells are exposed to high multiplicities of polyoma virus, a change in surface antigen may be detected by immunofluorescence, beginning at 18 h and affecting up to 88% of cells 24 h after infection. Time‐lapse cinematography shows that there is a concurrent change in movemen
The response of normal and polyoma virus-transformed BHK/21 cells to exogenous purines
✍ Scribed by G. D. Clarke; Carole Smith
- Publisher
- John Wiley and Sons
- Year
- 1973
- Tongue
- English
- Weight
- 552 KB
- Volume
- 81
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Adenosine (10 μM) stimulates the initial growth rate of BHK/21 cells seeded at low but not high density in monolayer culture; it does not affect final cell density or permit growth in agar. In labelling experiments With tritiated thymidine, adenosine also increases the response of quiescent cells to low concentrations of serum. Dialysis of serum to remove oxypurines only marginally reduces its effect on quiescent cell labelling or growth, indicating that BHK/21 cells are able to synthesise purines. The response of quiescent cells to 5% serum is inhibited by high MW (2 × 10^6^) dextran sulphate at 2 μg per milliliter. Low MW dextran sulphate (30,000) and heparin at 20 μg per milliliter produce the same effect. Exogenous adenosine (10 μM) prevents this inhibition. Many other purine derivatives replace adenosine for all the above activities but xanthine is completely inactive in all. It, therefore, appears that nucleotide synthesis is a necessary function of these compounds.
The growth of cells of a polyoma‐virus‐transformed BHK/21 line in monolayer is not stimulated by exogenous purine, though their colony‐forming ability in agar is increased five‐fold. The stimulating effects of exogenous purines on normal BHK/21 cells and the absolute requirement for them in the presence of polyanions is discussed in relation to possible mechanisms of growth control.
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