HMGA1 recruits CTIP2-repressed P-TEFb to the HIV-1 and cellular target promoters.

Eilebrecht S, Le Douce V, Riclet R, Targat B, Hallay H, Van Driessche B, Schwartz C, Robette G, Van Lint C, Rohr O, Benecke AG

Active positive transcription elongation factor b (P-TEFb) is essential for cellular and human immunodeficiency virus type 1 (HIV-1) transcription elongation. CTIP2 represses P-TEFb activity in a complex containing 7SK RNA and HEXIM1. Recently, the inactive 7SK/P-TEFb small nuclear RNP (snRNP) has been detected at the HIV-1 core promoter as well as at the promoters of cellular genes, but a recruiting mechanism still remains unknown to date. Here we show global synergy between CTIP2 and the 7SK-binding chromatin master-regulator HMGA1 in terms of P-TEFb-dependent endogenous and HIV-1 gene expression regulation. While CTIP2 and HMGA1 concordingly repress the expression of cellular 7SK-dependent P-TEFb targets, the simultaneous knock-down of CTIP2 and HMGA1 also results in a boost in Tat-dependent and independent HIV-1 promoter activity. Chromatin immunoprecipitation experiments reveal a significant loss of CTIP2/7SK/P-TEFb snRNP recruitment to cellular gene promoters and the HIV-1 promoter on HMGA1 knock-down. Our findings not only provide insights into a recruiting mechanism for the inactive 7SK/P-TEFb snRNP, but may also contribute to a better understanding of viral latency.

Chromatin Shearing

Share this article

April, 2014



  • "Molecular Biosystems" Conference on Eukaryotic Gene Regulation and Functional Genomics
    Puerto Varas, Región de Los Lagos, Chile
    Sep 23-Sep 26, 2017
  • The 76th Annual Meeting of the Japanese Cancer Association
    Tokyo, Japan
    Sep 28-Sep 30, 2017
 See all events

Twitter feed


 See all news