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.
Granowitz
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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