Effect of dibutyryl cyclic AMP on intracellular levels of avian sarcoma virus specific RNA

Abstract

AVIAN sarcoma viruses readily induce neoplastic transformation of fibroblasts in culture. Genetic and biochemical studies suggest that a single gene, generally referred to as src, is responsible for transformation^1–3. Nucleic acid hybridisation data, with purified src nucleotide sequences, have revealed that the majority of avian and mammalian RNA tumour viruses that are capable of transforming fibroblasts contain a species-specific src gene in viral as well as their host genomes^4–7. The nature and function of the src gene product and the mechanism by which it transforms fibroblasts remain to be elucidated. Indirect evidence, derived from using conditional mutants in the transforming (src) gene, suggests that the src gene product acts directly on the surface, modulating assembly of the cells⁸. Cyclic AMP seems to be involved in the growth control of a variety of cells⁹. From studies with ts mutants in the src gene, Pastan et al.¹⁰ have proposed that the src gene product modifies adenylate cyclase activity directly or indirectly, leading to a decreased level of intracellular cyclic AMP, which in turn enhances the growth rate and alters other morphological features. Here we present evidence that led us to conclude that cyclic AMP, in the presence of the src gene product, in fact, decreases the intracellular level of virus-specific RNA.