Transformation-defective mutants of feline sarcoma virus which express a product of the viral src gene.

摘要: Mink cell cultures infected with the Snyder-Theilen strain of feline sarcoma-leukemia virus were cloned from single cells under conditions favoring virus-single interactions. The primary colonies included (i) typical sarcoma (FeSV)-transformed nonproducer clones, one which segregated revertants, and (ii) FeSV-infected, phenotypically normal three spontaneously converted to transformed phenotype. revertants spontaneous transformants compared parental sister clones expressing opposite Transformed subclones formed in agar, tumorigenic nude mice, failed bind epidermal growth factor, whereas flat indistinguishable uninfected mink each these assays. Sister derived same infectious event contained FeSV proviruses integrated at molecular site, regardless phenotype was expressed. One revertant clone, however, lacked most proviral DNA sequences but retained terminal portions genome persisted original site insertion. Two expressed viral RNA phosphorylated "gag-x" polyprotein (pp78gag-x) encoded by gag src genome. Both susceptible retransformation FeSV. Although unable induce foci, viruses rescued as much focus-forming could be retransmitted cells, again inducing gene products without signs morphological transformation. We conclude that genomes represent transformation-defective mutants.