Substitution mutations affecting a small region of the Moloney murine leukemia virus MA gag protein block assembly and release of virion particles.
A series of substitution mutations affecting the Moloney murine leukemia virus MA protein were introduced into a cloned proviral DNA, and the mutant DNAs were tested for their biological activity in NIH/3T3 cells and COS cells. Many of the mutant viruses were viable and replicated with kinetics indistinguishable from the wild type. Seven mutants with alterations in a small region (residues 7-14 from the amino terminus) were replication-defective. These mutants were blocked in assembly and release of the virion particles in NIH/3T3 cells and were defective in both gag and gag-pol gene function. The results suggest that this very small region near the amino terminus of both proteins is required for their membrane targeting or self-association. Three of the defective mutant DNAs were able to induce virion particle formation when present at high copy number in COS cells.
Department of Biochemistry and Molecular Biophysics, College of Physicians and Surgeons, Columbia University, New York, New York 10032.
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D016475:3T3 Cells; D000595:Amino Acid Sequence; D000818:Animals; D002460:Cell Line; D004279:DNA, Viral; D015683:Gene Products, gag / Q000235:genetics*; D015684:Gene Products, pol / Q000235:genetics; D015750:Genes, gag; D051379:Mice; D008969:Molecular Sequence Data; D008979:Moloney murine leukemia virus / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D009154:Mutation; D014779:Virus Replication
D004279:DNA, Viral; D015683:Gene Products, gag; D015684:Gene Products, pol