Stimulation of polyomavirus DNA replication by wild-type p53 through the DNA-binding site

Teru Kanda, Kaoru Segawa, Noriaki Ohuchi, Shozo Mori, Yoshiaki Ito

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

The tumor suppressor p53 possesses characteristics of a transcription factor; it binds to specific DNA sequences and activates transcription from various promoters. Here we found that murine wild-type p53 stimulated not only transcription but also polyomavirus (Py) DNA replication in a sequence- dependent manner. Oncogenic mutant p53, lacking the DNA-binding activity, showed no stimulation of Py DNA replication. Deletion of the N-terminal acidic transactivation domain of wild-type p53, which completely eliminated the ability to stimulate transcription, only impaired the function to stimulate Py DNA replication. The replication-stimulating activity of wild- type p53 was impaired by the deletion of the C-terminal oligomerization domain as well, without affecting the ability to stimulate transcription. The region responsible for the sequence-specific DNA-binding activity mapped to the central portion of the p53 molecule has a minimal activity. The results indicate that both the N-terminal and the C-terminal regions significantly contribute to the p53-mediated stimulation of Py DNA replication.

Original languageEnglish
Pages (from-to)2651-2663
Number of pages13
JournalMolecular and cellular biology
Volume14
Issue number4
DOIs
Publication statusPublished - 1994 Apr

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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