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. 2022 Oct 1;36(19-20):1062–1078. doi: 10.1101/gad.350004.122

Figure 1.

Figure 1.

Xrn2 localization at start sites does not require initiation or elongation. (A) Pol II and Xrn2 ChIP-seq on RPL23. Note Xrn2 localization at start sites in cells treated with 100 μM DRB for 1 h, 10 μM triptolide for 10 min, and 300 nM flavopiridol for 1 h (red arrows). (B) Metaplots (25-base bins) of overexpressed Avi-Xrn2 ChIP-seq in control (DMSO) and triptolide-treated cells, as in A. Note that in triptolide, the peak of Xrn2 (red arrow) is shifted upstream of the promoter-proximal pause site (see Supplemental Fig. S1C). (C–E) Heat maps (C) and genome browser screenshots (D,E) of pol II and overexpressed Avitag Xrn2 ChIP-seq in control and triptolide-treated cells, as in B. Note the 5′ peak of Xrn2 is maintained in triptolide (red arrows), while pol II is depleted from gene bodies (blue arrows). (F) Metaplots of endogenous Xrn2 ChIP-seq in control (DMSO), DRB-treated, and flavopiridol-treated cells, as in A. Note that in DRB and flavopiridol, Xrn2 colocalizes with pol II that accumulates at the promoter-proximal pause site downstream from the TSS (red arrows). Fifty-base bins; ChIP signals are relative to bin 1.