Extended Data Fig. 9 |. A model depicting how P-TEFb uses the CYCT1 HRD to target and recruit the Pol II CTD into a phase-separated compartment—which is formed by weak, multivalent homotypic interactions among the HRDs—to enable highly efficient phosphorylation of CTD by P-TEFb in the presence of ATP.
At 2.5% 1,6-hexanediol, the HRD-mediated phase separation but not the direct HRD–CTD binding is disrupted, making it impossible for P-TEFb to hyperphosphorylate the CTD.