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. Author manuscript; available in PMC: 2013 Jan 20.
Published in final edited form as: J Mol Biol. 2011 Nov 23;415(3):464–474. doi: 10.1016/j.jmb.2011.11.020

Figure 2. sin4Δ mutation facilitates PIC assembly.

Figure 2

(A) Recruitment of Yap1p to the FLR1 promoter is not altered in sin4Δ cells. Yap1p occupancy was determined with anti-Yap1p polyclonal antibody. (B) plc1Δ cells fail to recruit Swi2p to the FLR1 promoter and the defect is suppressed by sin4Δ mutation. Swi2p occupancy was determined in strains expressing Swi2p-myc18 using anti-myc antibody. (C) sin4Δ cells display increased recruitment of Ada2p to the FLR1 promoter. Ada2p occupancy was determined in strains expressing Ada2p-myc18 using anti-myc antibody. (D) sin4Δ cells display increased recruitment of TBP to the FLR1 promoter. TBP occupancy was determined in strains expressing Spt15p-3HA using anti-HA antibody. (E) sin4Δ cells display increased recruitment of RNA Pol II to the FLR1 promoter. RNA Pol II occupancy was determined by immunoprecipitation of Rpb1p (the largest subunit of RNA polymerase II) with 8WG16 mAb. (A–E) ChIP was performed using chromatin from the corresponding cells grown in YPD medium (0 h) and treated with benomyl (5 µg/ml) for 1 h. Each immunoprecipitation was performed at least three times using different chromatin samples. The occupancy was calculated with POL1 coding sequence as a negative control. The data are presented as fold occupancy over the POL1 coding sequence control and represent means ± SD.