HTLV-1 bZIP factor suppresses the centromere protein B (CENP-B)-mediated trimethylation of histone H3K9 through the abrogation of DNA-binding ability of CENP-B

J Gen Virol. 2015 Jan;96(Pt 1):159-164. doi: 10.1099/vir.0.070201-0. Epub 2014 Oct 3.

Abstract

Human T-cell leukaemia virus type-1 (HTLV-1) infection causes adult T-cell leukaemia (ATL). The viral protein HTLV-1 bZIP factor (HBZ) is constitutively expressed in ATL cells, suggesting that HBZ plays a major role in the pathogenesis of HTLV-1-associated disease. Here, we identified centromere protein B (CENP-B) as a novel interacting partner of HBZ. HBZ and CENP-B associate with their central regions in cells. Furthermore, overexpression of HBZ abrogated the DNA-binding activity of CENP-B to the α-satellite DNA region containing the CENP-B box motif, which in turn inhibited the CENP-B-mediated trimethylation of histone H3K9 in T-cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • Centromere Protein B / metabolism*
  • DNA Methylation / physiology*
  • DNA-Binding Proteins / metabolism*
  • HEK293 Cells
  • HTLV-I Infections / metabolism*
  • HTLV-I Infections / virology
  • Histones / metabolism*
  • Human T-lymphotropic virus 1 / metabolism
  • Humans
  • Leukemia-Lymphoma, Adult T-Cell / metabolism*
  • Leukemia-Lymphoma, Adult T-Cell / virology
  • T-Lymphocytes / metabolism
  • T-Lymphocytes / virology
  • Viral Proteins / metabolism*

Substances

  • CENPB protein, human
  • Centromere Protein B
  • DNA-Binding Proteins
  • Histones
  • Viral Proteins