Envelope gene sequences which encode the gp52 protein of spleen focus-forming virus are required for the induction of erythroid cell proliferation.

AUTOR(ES)

Linemeyer, D L

RESUMO

A series of insertion-deletion mutants was constructed in a molecularly cloned DNA copy of the Friend strain of spleen focus-forming virus (SFFV). The mutants were produced by inserting a synthetic oligonucleotide linker containing the recognition sequence of SalI endonuclease into several different locations of the SFFV DNA. Three classes of mutants were isolated: insertion-deletion mutants in the 5' half of the SFFV genome, in the long terminal repeat of the SFFV genome, and in the env gene of the SFFV genome. The env gene mutant has a deletion of sequences shared in common between the env gene of SFFV and the env genes of mink cell focus-inducing murine leukemia viruses. From analyses of the biological activity of the various mutants and a biologically active subgenomic SFFV DNA fragment described herein, we can deduce that the coding sequence encompassing the env gene of SFFV is required for the biological activity. This region, required for the pathogenic phenotype, cannot be larger than 1.5 kilobase pairs, a size only slightly more than that sufficient to encode the nonglycosylated precursor of the gp52 env gene product.

Documentos Relacionados

• The hydrophobic membrane-spanning sequences of the gp52 glycoprotein are required for the pathogenicity of Friend spleen focus-forming virus.
• Env-derived gp55 gene of Friend spleen focus-forming virus specifically induces neoplastic proliferation of erythroid progenitor cells.
• Analysis of spleen focus-forming virus-specific RNA sequences coding for spleen focus-forming virus-specific glycoprotein with a molecular weight of 55,000 (gp55).
• Monoclonal antibody to spleen focus-forming virus-encoded gp52 provides a probe for the amino-terminal region of retroviral envelope proteins that confers dual tropism and xenotropism.
• Conversion of Friend mink cell focus-forming virus to Friend spleen focus-forming virus by modification of the 3' half of the env gene.