Mapping by in vitro constructs of the P100gag-mil region, accounting for induction of chicken neuroretina cell proliferation

J Virol. 1988 Aug;62(8):2808-16. doi: 10.1128/JVI.62.8.2808-2816.1988.

Abstract

The v-mil oncogene of the avian retrovirus MH2 is expressed as a fusion protein with viral gag determinants in infected cells. This P100gag-mil protein accounts for the proliferation of chicken embryo neuroretina cells (CNR) induced by MH2 in vitro. We constructed a series of mutants by in-frame deletions in different parts of the gag and mil domains and tested their ability to induce CNR growth. We show that gag sequences, as well as 200-base-pair 5' mil sequences, were not required to induce such a proliferation. However, gag sequences seem to contribute to a full proliferation of growing CNR. In contrast, deletions in the kinase domain abolish this induction. In particular, by deleting only 9 nucleotides localized around the unique SphI site of v-mil, we produced a totally inactive mutant (BalSp). This mutant directs the synthesis of a v-mil protein lacking the dipeptide Tyr-Leu, which is conserved in almost all the members of the large protein kinase family, and a histidine residue highly conserved in Ser-Thr protein kinase members.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Cycle*
  • Cells, Cultured
  • Chromosome Deletion
  • Chromosome Mapping
  • Coturnix
  • DNA Mutational Analysis
  • Gene Expression Regulation
  • Gene Products, gag
  • Oncogene Proteins, Viral / genetics*
  • Oncogenes*
  • Retina / cytology*
  • Retina / microbiology
  • Retroviridae Proteins / genetics*
  • Structure-Activity Relationship
  • Transfection
  • Virus Replication

Substances

  • Gene Products, gag
  • Oncogene Proteins, Viral
  • Retroviridae Proteins