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Phosphorylation of v-mos Ser 47 by the mitotic form of p34cdc2

W L Bai1, B Singh, W L Karshin

  • 1Department of Molecular Pathology, University of Texas M.D. Anderson Cancer Center, Houston 77030.

Oncogene
|October 1, 1991
PubMed

Insights

Mitotic cdc2 kinase (M-phase kinase) phosphorylates the viral mos protein at Serine 47. This phosphorylation occurs in Moloney murine sarcoma virus-transformed cells during mitosis, identifying a key regulatory event.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Virology

Background:

  • P85gag-mos protein undergoes hyperphosphorylation during mitosis in virus-transformed cells.
  • The role of specific kinases in mos protein regulation during cell division is under investigation.

Purpose of the Study:

  • To investigate the specific kinase responsible for P85gag-mos hyperphosphorylation during mitosis.
  • To identify the precise phosphorylation site on the viral mos protein.

Main Methods:

  • In vitro kinase assays using purified M-phase kinase (p34cdc2) from transformed cells.
  • Tryptic peptide mapping to identify phosphorylation sites.
  • Site-directed mutagenesis and synthetic peptide analysis to confirm phosphorylation site specificity.
  • Protein sequencing to determine the exact residue phosphorylated.

Main Results:

  • The mitotic form of cdc2 kinase (M-phase kinase) was identified as the enzyme phosphorylating P85gag-mos in vitro.
  • The major phosphorylation site was mapped to the amino-terminal region (residues 45-53) of the viral mos protein.
  • Serine 47 (Ser 47) was confirmed as the specific phosphorylation site.
  • In vivo phosphorylation patterns in mitotic cells corroborated the in vitro findings.

Conclusions:

  • M-phase kinase directly phosphorylates the viral mos protein at Ser 47 during mitosis.
  • This phosphorylation event is crucial for understanding mos protein regulation in the context of viral transformation and cell cycle progression.
  • The findings offer new insights into kinase-substrate interactions, potentially diverging from known roles in oocyte maturation.

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