Human T-cell leukemia virus type 1 Tax oncoprotein induces and interacts with a multi-PDZ domain protein, MAGI-3

Virology. 2004 Mar 1;320(1):52-62. doi: 10.1016/j.virol.2003.11.014.

Abstract

Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia (ATL), whereas the closely related virus HTLV-2 has not been associated with such malignant conditions. HTLV-1 Tax1 oncoprotein transforms a rat fibroblast cell line (Rat-1) much more efficiently than does HTLV-2 Tax2. By using a differential display analysis, we isolated MAGI-3 as a Tax1-inducible gene in Rat-1 cells. Reverse transcription-polymerase chain reaction (RT-PCR) analysis confirmed that Tax1 induced MAGI-3 in Rat-1 cells. MAGI-3 has multiple PDZ domains and interacted with Tax1 but not Tax2 in 293T cells. The interaction of Tax1 with MAGI-3 was dependent on a PDZ domain-binding motif, which is missing in Tax2. The interaction of Tax1 with MAGI-3 altered their respective subcellular localization, and moreover, the interaction correlated well with the high transforming activities of Tax1 in Rat-1 cells relative to Tax2. MAGI-3 mRNA and the allied MAGI-1, but not MAGI-2, were expressed in HTLV-1-infected T-cell lines. Our results suggest that the interaction of Tax1 and MAGI-3 alters their respective biological activities, which may play a role in transformation by Tax1 as well as in the pathogenesis of HTLV-1-associated diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Motifs
  • Animals
  • Cell Line / drug effects
  • Cell Line, Tumor / drug effects
  • Cell Transformation, Viral
  • Gene Expression
  • Gene Products, tax / analysis
  • Gene Products, tax / metabolism*
  • Gene Products, tax / pharmacology
  • Guanylate Kinases
  • HTLV-I Infections / etiology
  • Human T-lymphotropic virus 1 / chemistry
  • Human T-lymphotropic virus 1 / pathogenicity*
  • Humans
  • Intracellular Space / metabolism
  • Nucleoside-Phosphate Kinase / analysis
  • Nucleoside-Phosphate Kinase / biosynthesis
  • Nucleoside-Phosphate Kinase / genetics
  • Nucleoside-Phosphate Kinase / metabolism*
  • Protein Structure, Tertiary
  • RNA, Messenger / analysis
  • Rats

Substances

  • Gene Products, tax
  • RNA, Messenger
  • Nucleoside-Phosphate Kinase
  • Guanylate Kinases