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Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)
07:02

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus (KSHV)

Published on: September 14, 2010

Transcriptional regulation of the Kaposi's sarcoma-associated herpesvirus K15 gene

Emily L Wong1, Blossom Damania

  • 1Lineberger Comprehensive Cancer Center, CB 7295, University of North Carolina, Chapel Hill, NC 27599, USA.

Journal of Virology
|January 18, 2006
PubMed

Insights

Researchers identified the Kaposi's sarcoma-associated herpesvirus (KSHV) K15 gene's transcriptional start site and promoter. This finding reveals how K15 gene expression is regulated during viral infection.

Area of Science:

  • Virology
  • Molecular Biology
  • Genetics

Background:

  • Kaposi's sarcoma-associated herpesvirus (KSHV) K15 protein is a transmembrane protein involved in B-cell signaling pathways.
  • K15 protein influences Ras/MAPK and NF-kappaB signaling, crucial for viral pathogenesis.

Purpose of the Study:

  • To identify the transcriptional start site (TSS) of the full-length K15 gene in KSHV-positive cells.
  • To characterize the promoter region regulating K15 gene expression.

Main Methods:

  • Rapid amplification of cDNA ends (RACE) and RNase protection assays were used to map the K15 TSS.
  • Reporter gene assays with 5' promoter deletion constructs were employed to analyze cis-acting elements.
  • Luciferase reporter gene assays were performed to assess promoter activity.

Main Results:

  • The K15 TSS was mapped 152 nucleotides upstream of the translation start site.
  • Chemical induction activated K15 transcription in latently infected BCBL-1 cells.
  • The viral protein Orf50/Rta mediated transactivation of the K15 promoter.

Conclusions:

  • The K15 gene has a defined transcriptional start site and a characterized promoter element.
  • K15 gene expression is regulated by chemical induction and the viral Orf50/Rta protein.
  • The K15 gene is actively transcribed during KSHV lytic replication.

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