Author/Authors :
Hidehisa Takahashi، نويسنده , , Tari J. Parmely، نويسنده , , Shigeo Sato، نويسنده , , Chieri Tomomori-Sato، نويسنده , , Charles A.S. Banks، نويسنده , , Stephanie E. Kong، نويسنده , , Henrietta Szutorisz، نويسنده , , Selene K. Swanson، نويسنده , , Skylar Martin-Brown، نويسنده , , Michael P. Washburn، نويسنده , , Laurence Florens، نويسنده , , Chris W. Seidel، نويسنده , , Chengqi Lin، نويسنده , , Edwin R. Smith، نويسنده , , Ali Shilatifard، نويسنده , , Ronald C. Conaway، نويسنده , , Joan W. Conaway، نويسنده ,
Abstract :
Promoter-proximal pausing by initiated RNA polymerase II (Pol II) and regulated release of paused polymerase into productive elongation has emerged as a major mechanism of transcription activation. Reactivation of paused Pol II correlates with recruitment of super-elongation complexes (SECs) containing ELL/EAF family members, P-TEFb, and other proteins, but the mechanism of their recruitment is an unanswered question. Here, we present evidence for a role of human Mediator subunit MED26 in this process. We identify in the conserved N-terminal domain of MED26 overlapping docking sites for SEC and a second ELL/EAF-containing complex, as well as general initiation factor TFIID. In addition, we present evidence consistent with the model that MED26 can function as a molecular switch that interacts first with TFIID in the Pol II initiation complex and then exchanges TFIID for complexes containing ELL/EAF and P-TEFb to facilitate transition of Pol II into the elongation stage of transcription.
