The low tumorigenic potential of PRCII, among viruses of the Fujinami sarcoma virus subgroup, corresponds to an internal (fps) deletion of the transforming gene.

The avian sarcoma viruses FSV, PRCII, PRCIIp, and PRCIV share a related class of hybrid onc genes (delta gag-fps) defined by a specific nucleotide sequence fps and by delta gag-fps proteins of different sizes. Among these viruses, PRCII appears to have a lower tumorigenic potential than the others. Here we have compared fibroblast-transforming function and onc gene structure of these viruses. The fibroblast transforming ability of PRCII was lower than those of FSV, PRCIIp, and PRCIV. By gel electrophoresis the genomic RNA of PRCII measured 3.5 kb and those of FSV, PRCIIp, and PRCIV 4.5 kb; the delta gag-fps protein of PRCII measured 105 kilodaltons (kd), that of FSV 140 kd, and those of PRCIIp and PRCIV about 150 kd. By fingerprinting viral RNAs hybridized with molecularly cloned viral DNA the delta gag regions of PRCII and PRCIIp were defined to be 1.45 kb and that of FSV to be 1.3 kb. Fingerprint analysis of viral RNA-proto fps DNA hybrids showed the fps regions (approximately 2.8 kb) of FSV and PRCIIp to be isogenic. Compared to FSV and PRCIIp, the fps sequence of PRCII lacked a 1-kb region which maps between 0.3 and 1.3 kb from the 5' end of fps in FSV and PRCIIp. Based on oligonucleotide analysis, the shared fps complements of PRCII and PRCIIp were indistinguishable while that of FSV differed from those of the PRC viruses in scattered point mutations amounting to 1-2% of the RNA. Since all other regions of PRCII are isogenic with those of the highly tumorigenic variants PRCIIp, PRCIV, and FSV, it is concluded that the low fibroblast-transforming and oncogenic potential of PRCII reflects the internal fps deletion. Since the fps deletion reduces but does not eliminate transforming function, we suggest that the complete onc genes of viruses in the FSV subgroup include either several functional, or a regulatory and a functional fibroblast transforming domain. It has been reported that the 3' domains of the onc genes of viruses in the Fujinami subgroup and the onc genes of certain feline sarcoma viruses are distantly related. Since full transforming potential of the avian viruses depends on the 5' fps region not shared with the feline sarcoma viruses, we suggest that despite their structural homology, the avian and feline onc genes must have functionally different domains.