Functional characterization of a human cyclin T1 mutant reveals a different binding surface for Tat and HEXIM1

Virology. 2012 May 10;426(2):152-61. doi: 10.1016/j.virol.2012.01.033. Epub 2012 Feb 18.

Abstract

HIV transcription is regulated at the step of elongation by the viral Tat protein and the cellular positive transcription elongation factor b (P-TEFb; Cdk9/cyclin T1). Herein, a human cyclin T1 mutant, cyclin T1-U7, which contains four substitutions and one deletion in the N-terminal cyclin box, was stably expressed in HeLa cells. HIV transcription was efficiently inhibited in HeLa-HA-CycT1-U7 stable cells. Cyclin T1-U7 bound Tat but did not modulate its expression levels, which remained high. Importantly cyclin T1-U7 failed to interact with Cdk9 or HEXIM1 and did not interfere with endogenous P-TEFb activity to stimulate MEF2C or NFkB mediated transcription. In a T cell line and primary CD4+ cells, cyclin T1-U7 also inhibited HIV transcription. We conclude that cyclin T1-U7 sequesters Tat from P-TEFb and inhibits HIV transcription. Importantly, N-terminal residues in cyclin T1 are specifically involved in the binding of cyclin T1 to HEXIM1 but not to Tat.

MeSH terms

  • CD4-Positive T-Lymphocytes / metabolism
  • CD4-Positive T-Lymphocytes / virology
  • Cyclin T / chemistry
  • Cyclin T / genetics*
  • Cyclin T / metabolism*
  • Gene Expression Regulation, Viral
  • HIV Infections / genetics
  • HIV Infections / metabolism*
  • HIV Infections / virology
  • HIV-1 / genetics
  • HIV-1 / metabolism*
  • HeLa Cells
  • Humans
  • Mutation
  • Protein Binding
  • Protein Structure, Secondary
  • RNA-Binding Proteins / genetics
  • RNA-Binding Proteins / metabolism*
  • Transcription Factors
  • tat Gene Products, Human Immunodeficiency Virus / genetics
  • tat Gene Products, Human Immunodeficiency Virus / metabolism*

Substances

  • Cyclin T
  • HEXIM1 protein, human
  • RNA-Binding Proteins
  • Transcription Factors
  • tat Gene Products, Human Immunodeficiency Virus