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. Author manuscript; available in PMC: 2018 Jul 15.
Published in final edited form as: Cancer Res. 2018 Jan 8;78(2):313–319. doi: 10.1158/0008-5472.CAN-17-2175

Figure 2. PD2/PAF1 as the regulator of RNA Pol II promoter-proximal pausing.

Figure 2

Although PD2/PAF1 is found to regulate promoter-proximal Pol II pause release, two opposing models have been proposed. In one model, positive transcription elongation factor b (P-TEFb) as a part of the super elongation complex (SEC) is responsible for serine 5 (S5) phosphorylation of the CTD (C-terminal domain) of the largest subunit of Pol II, DSIF and negative elongation factor (NELF), leading to subsequent dissociation of NELF. Further, P-TEFb recruits PAF1C to promoter proximal regions, which in turn recruits the CDK12/Cyclin K complex for serine 2 (S2) phosphorylation of the Pol II CTD, resulting in productive Pol II elongation (left panel) (17). In another model, the loss of PAF1C is essential for recruitment of SEC, which mediates Pol II CTD S2 phosphorylation (right panel) (19). Phosphorylation of DSIF and NELF (and subsequent dissociation) is also required for effective Pol II pause release along with S2 phosphorylation of the Pol II CTD.