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. 2016 Apr 22;44(15):7189–7203. doi: 10.1093/nar/gkw331

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© The Author(s) 2016. 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/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 7. — The defect to nucleosome spacing in the absence of Cac1 is restored post-replication and enhanced in the absence of replication-independent histone turnover. Alignment of nucleosomal reads on nascent DNA to the TSS in wild-type (orange) and cac1Δ strains (blue) illustrates progressive accumulation of a spacing defect in mid S-phase (A and B). This is restored in late S-phase (C). The spacing defect in asynchronous total chromatin (D) is less than that observed in mid S-phase (A and B). Nucleosomal reads from asynchronous wild-type, cac1Δ, hir1Δ and hir1Δcac1Δ strains were aligned to the TSS of all genes (n = 5015) (E). The nucleosome depleted region at promoters is partially filled in a hir1Δcac1Δ strain (green) in comparison to cac1Δ (orange), hir1Δ (blue) and wild-type (grey). The defect to nucleosome spacing is quantified in (F). The defect is increased in the hir1Δcac1Δ consistent with replication-independent histone turnover acting to restore nucleosome density on coding regions.

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