onc sequences (v-fes) of Snyder–Theilen feline sarcoma virus are derived from noncontiguous regions of a cat cellular gene (c-fes)

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Abstract
Type C sarcoma viruses are genetic recombinants containing portions of replication-competent helper viruses linked to sarcoma virus-specific sequences (generically designated onc genes) presumably required for acute fibroblast transformation. The onc elements of different avian and mammalian sarcoma viral isolates are each homologous to subsets of cellular DNA sequences which have no well-defined role in normal cells. Because of the lack of significant homology between helper viral genes and cellular onc sequences, the recombinational mechanisms which facilitate the formation of sarcoma viral genomes remain unclear. In Moloney murine sarcoma virus, viral onc (or v-mos) and cellular onc (or c-mos) sequences exhibit complete and uninterrupted homology as determined by heteroduplex and restriction enzyme analyses of molecularly cloned DNA. The cellular counterparts of the onc elements of Rous sarcoma virus, avian erythroblastosis virus, Abelson leukemia virus, Harvey sarcoma virus, and simian sarcoma virus are now known to contain intervening sequences which do not appear in the respective viral genomes. The Southern blot technique was used to examine cat cellular DNA sequences (c-fes) homologous to the onc gene (v-fes) of Snyder-Theilen feline sarcoma virus (ST-FeSV). Cloned DNA probes containing defined portions of the ST-FeSV genome were used to show that v-fes sequences originate from at least 4 noncontiguous sequences in cat cellular DNA, separated from each other by intervening sequences.