The Tax oncogene enhances ELL incorporation into p300 and P-TEFb containing protein complexes to activate transcription

• We investigated the role of ELL during HTLV-1 Tax oncogene induced transactivation.
• Tax enhances ELL incorporation into p300 and P-TEFb transcriptional complexes.
• Depletion of endogenous ELL abrogates Tax induced transactivation.
• ELL is an essential cellular cofactor of the Tax oncogene.

The eleven-nineteen lysine-rich leukemia protein (ELL) is a key regulator of RNA polymerase II mediated transcription. ELL facilitates RNA polymerase II transcription pause site entry and release by dynamically interacting with p300 and the positive transcription elongation factor b (P-TEFb). In this study, we investigated the role of ELL during the HTLV-1 Tax oncogene induced transactivation. We show that ectopic expression of Tax enhances ELL incorporation into p300 and P-TEFb containing transcriptional complexes and the subsequent recruitment of these complexes to target genes in vivo. Depletion of ELL abrogates Tax induced transactivation of the immediate early genes Fos, Egr2 and NF-kB, suggesting that ELL is an essential cellular cofactor of the Tax oncogene. Thus, our study identifies a novel mechanism of ELL-dependent transactivation of immediate early genes by Tax and provides the rational for further defining the genome-wide targets of Tax and ELL.