Identification of a Gag - Related Phosphoprotein

Many RNA tumor viruses preferentially induce neoplasms of hematologic or lymphoid tissue in susceptible animals. According to their oncogenic potential, these retroviruses are divisible into two groups, the acute leukemia viruses and the slow or chronic leukemia viruses. The acute viruses, such as Abelson murine leukemia virus (AbLV), 1 cause rapid onset of neoplastic disease (2-4 wk) following infection in vivo and can transform appropriate target cells in tissue culture (1, 2). Inoculation with slow leukemia viruses, which include the avian and murine leukemia viruses (ALV and MuLV), results in neoplasia only after a prolonged latent period of 3-12 months. They have not been found to cause morphological transformation of tissue culture cells (3, 4). The mechanism(s) of oncogenesis by these viruses is not yet understood. The transforming activity of the acute viruses has been attributed to a particular genomic region termed the onc gene. Onc sequences do not encode viral structural proteins, but rather are thought to have been acquired by recombination from cellular DNA at the expense of replicativ¢ genes. As a result, these viruses are uniformly replication defective (1, 5, 6). The translation product of such an onc gene in transformed cells appears as a "fusion" protein, consisting of the putative transforming protein colinear with viral peptides. In the example of AbLV, a 120,000-dalton protein (p 120) containing portions of Mo-MuLV p 15, p 12, and p30 gag polypeptides covalently linked to a highly phosphorylated cell-derived fragment is thought responsible for transformation (7). The slow leukemia viruses, in contrast, contain no readily definable transforming genes. Neel et al. (8) and Payne et al. (9) have acquired evidence suggesting that the majority of bursal lymphomas induced in chickens by the slow ALV result from activation of a cellular oncogene by vicinal integration of viral promoter elements. How