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. 2016 Mar 14;212(6):633–646. doi: 10.1083/jcb.201508068

Figure 3.

Figure 3.

Rpd3(L) histone deacetylase regulates INO1 gene recruitment to the nuclear periphery. (A and B) Peripheral localization of INO1. *, P ≤ 0.05 (Fisher exact test) between SDC and inducing condition. Mean and SEM from three of more biological replicates (30–50 cells per replicate). (A) Strains having the indicated cis-acting, trans-acting, and histone deacetylase mutants were scored for INO1 targeting to the nuclear periphery. A schematic of the INO1 promoter showing the 100-bp “segment 4,” GRS I, GRS II, UASINO, and URS elements is shown in C. WT, wild-type. (B) Peripheral localization of wild type, grsI, grsII, or grsI grsII mutant INO1 in the opi1Δ mutant strain grown under uninducing conditions. (C) Model for INO1 transcriptional regulation. Ino2/Ino4 binds the UASINO elements and recruits Opi1 to the promoter under uninducing conditions. Both Ume6 and Opi1 recruit Rpd3(L). (D) ChIP with anti–pan-acetyl antibody, quantified relative to ChIP with anti-histone H3 antibody from RPD3 or rpd3Δ strains. The recovery of the INO1 promoter from each IP, normalized to input, was quantified by real-time quantitative PCR (qPCR). NS, not significant. (E) ChIP of Gst-Put3 (Ahmed et al., 2010; Brickner et al., 2012) expressed in either RPD3 or rpd3Δ strains. The recovery of the INO1 promoter or the GAL1 coding sequence was quantified relative to input by qPCR. P-values determined by Student’s t test.