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. 2015 Apr 6;43(8):3972–3985. doi: 10.1093/nar/gkv282

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© The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 5. — Inactivation of histone chaperone Hpc2 leads to decreased histone turnover at active promoters without concomitant decrease in H3K9ac. (A) Experimental diagram. Cells from an Hpc2-anchor-away strain (Hpc2^FRB) containing the galactose-inducible H3^HA construct and from an isogenic control strain (control) lacking the Hpc2^FRB fusion were arrested in G1 by alpha factor. At T0, galactose and rapamycin were added to both cultures to, respectively, induce H3^HA expression and deplete Hpc2^FRB from the nucleus. Shown on the right is a western blot analysis of H3^HA expression in the two strains. (B) The amounts of newly incorporated H3^HA (left panels) and the levels of H3K9ac (right panels) at the promoters (PRO) and coding regions (ORF) of the indicated highly expressed genes were monitored by ChIP in the control (blue lines) and the Hpc2^FRB strains (red lines) as in Figure 4. Note the different scales used for H3K9ac at PRO and ORF. An independent biological experiment is shown in Supplementary Figure S8.