The avian sarcoma virus PRCII lacks 1020 nucleotides of the fps transforming gene.

Fujinami sarcoma virus (FSV) and PRCII avian sarcoma virus both encode gag-fps transforming proteins associated with tyrosine-specific protein kinase activity; however, PRCII has a lower oncogenic potential than does FSV. In this study, the genomes of PRCII and FSV have been compared. By hybridization of PRCII [32P]RNA to FSV DNA on Southern blots, a large internal deletion in the 5' half of the fps gene in PRCII has been mapped. To determine the exact size and location of the deletion in PRCII, dideoxy sequencing of PRCII RNA with FSV DNA fragments as primers was used. The FSV sequence corresponding to the deletion in PRCII was flanked by 6-base direct repeats ( AGCTGG ) at 1614-1619 and 2634-2639 nucleotides. One copy of the direct repeat was retained in the PRCII genome. The length of the deleted region was 1020 nucleotides. The deletion in fps did not alter the kinase domain or ATP-binding site of the P105 transforming protein of PRCII. It was shown that the specific kinase activity of P105 was as high as that of FSV P130 . The sequence deleted from PRCII was found to encode part of a large hydrophilic domain. In the accompanying paper [J. Woolford and K. Beemon (1984) Virology 135, 168-180], evidence that the PRCII and FSV proteins have different subcellular locations and solubility properties, possibly due to the loss of this domain, is presented. These alterations in the structure and location of the PRCII protein may prevent it from phosphorylating certain substrates involved in oncogenic transformation.