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. 2020 Mar 3;2(1):zcaa003. doi: 10.1093/narcan/zcaa003

Figure 2.

Figure 2.

CDK12 kinase stimulates optimal transcription elongation and prevents premature termination of predominantly long, polyadenylation-site-rich genes. Working model: (top) the active CycK/CDK12 complex is recruited to the promoters (TSS) of genes by SETD1A and PAF1C proteins. CDK12 phosphorylates (thin black arrows) the CTD (light blue oval with two, five and seven in circles) of RNAPII, which results in productive elongation (thick black arrow) in gene bodies, the accumulation of P-Ser2 (2 in yellow circle) at the end of genes and optimal termination at canonical polyadenylation sites. Full-length mRNAs are produced. (Bottom) Upon CDK12 inhibition, the CTD is differentially phosphorylated (for simplicity not shown), which results in slower elongation (dotted black arrow) in the gene bodies of predominantly long, polyadenylation-site-rich genes with a low ratio of U1 snRNA binding to polyadenylation sites (U1/pA). P-Ser2 levels accumulate (2 in yellow circle) in the bodies of these genes approximately in the positions where RNAPII prematurely terminates (often at positions of internal cryptic polyadenylation sites). Shorter mRNAs are produced. pA = polyadenylation site.