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Oncogene v-jun modulates DNA replication.

C Wasylyk1, J Schneikert, B Wasylyk

  • 1Unité 184 de Biologie Moléculaire et de Génie Génétique de l'INSERM, Institut de Chimie Biologique, Faculté de Médecine, Strasbourg, France.

Oncogene
|July 1, 1990
PubMed
Summary

Altered AP1 transcription factor activity, involving jun and fos gene families, impacts cell transformation. This study shows v-jun oncogene fusion proteins can activate DNA replication, suggesting jun

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Area of Science:

  • Molecular Biology
  • Oncogenesis
  • Virology

Background:

  • Cell transformation involves changes in transcription and DNA replication.
  • The transcription factor AP1, composed of jun and fos families, mediates oncogene-induced transcription.
  • Altered AP1 activity is a key event in cell transformation.

Purpose of the Study:

  • To investigate the role of jun oncogenes in DNA replication.
  • To determine if jun proteins can activate DNA replication from a viral origin.
  • To explore the relationship between jun's transcriptional and replication-activating functions.

Main Methods:

  • Constructing fusion proteins of v-jun and c-jun with the lex-A repressor DNA-binding domain.
  • Linking the Polyoma virus origin of replication to the lex-A operator.
  • Expressing fusion proteins in cells to assess DNA replication activation.

Main Results:

  • v-jun and c-jun fusion proteins activated DNA replication from the Polyoma virus origin.
  • The transcription-activation region of v-jun was essential for replication activation.
  • Excess v-jun expression led to replication inhibition ('squelching').

Conclusions:

  • Deregulated jun activity can lead to altered DNA replication.
  • Similar mechanisms may underlie jun's activation of both transcription and replication.
  • This highlights a potential link between oncogene activity and DNA replication control.

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