Replication of a Moloney murine leukemia virus mutant lacking the ELP binding site

A mutant Moloney murine leukemia virus was created in which the binding site for the embryonal long terminal repeat binding protein had been replaced with a synthetic linker sequence. The virus was found to replicate normally in murine 3T3 fibroblasts, and the mutation was stably transmitted throughout repeated passages. The binding site is therefore dispensable with respect to viral replication. Titers of the mutant virus were comparable to those of wild-type preparations, even when supernatants were prepared from undifferentiated P19 embryonal carcinoma cells. Elimination of the repressor binding site therefore had little effect on viral replication in embryonal carcinoma cells. Elimination of the repressor binding site therefore had little effect on viral replication in embryonal cells, an unexpected result in light of the reported activity of the binding protein as a transcriptional repressor.