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. Author manuscript; available in PMC: 2018 Dec 7.
Published in final edited form as: Mol Cell. 2017 Dec 7;68(5):913–925.e3. doi: 10.1016/j.molcel.2017.11.020

Figure 7. Role of CTD Tyr1 and Slt2 kinase in activating transcription of stress-inducible genes.

Figure 7

In the absence of activation by a stress-induced signaling cascade, Slt2 is inactive and Tyr1 is not phosphorylated. The Nrd1-containing NNS complex is thus recruited to a primarily Ser5P CTD and transcripts are prematurely terminated and degraded. Activation of Slt2 enables the kinase to associate with RNAP II and Mediator/SBF, promoting Cdk8/CycC degradation and RNAP II Tyr1 phosphorylation. This combination of events facilitates activation and prevents termination factor (e.g., NNS) association with the CTD until the 3′ end, when Tyr1 is dephosphorylated, the transcript 3′ processed and transcription terminated.