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. 2006 Apr 15;20(8):954–965. doi: 10.1101/gad.1409106

Figure 3.

Figure 3.

Coordinate recruitment of Rat1 and the 3′-processing factor Pcf11. (A) Highly coincident patterns of Pcf11 and Rat1 recruitment at the ADH4 3′ end. (Left) Pol II, Pcf11, and Rat1-GFP ChIP on galactose-induced GAL1-ADH4 in wild-type cells (DBY786) at 25°C. (Right) ChIP signals normalized to input were normalized relative to the value at position 1 in the ORF. Means and standard deviations from three experiments are shown in the graphs. (B) Termination defects in pcf11-2 and pcf11-9 mutants. Pol II ChIP of wild type (WT), pcf11-2, and pcf11-9 (DBY548, DBY585, DBY593) at 25°C and 37°C. Note delayed termination in pcf11-2 at 25°C (lane 5) and failure to terminate at 37°C (lane 6). (C) Rat1 recruitment to the ADH4 3′ end requires functional Pcf11. (Lanes 1–6) Rat1-GFP ChIP in wild-type (WT) and pcf11-2 strains (DBY786, DBY815) and the untagged control (C, DBY548). (Lanes 7–10) Rat1-GFP ChIP in pcf11-9 (DBY794) transformed with PCF11 plasmid (DBY796) or control vector (DBY795). β-globin is a loading control.