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Comment
. 2022 Jun 29;13(1):3726.
doi: 10.1038/s41467-022-30350-3.

Pitfalls in using phenanthroline to study the causal relationship between promoter nucleosome acetylation and transcription

Sevil Zencir  1 , Daniel Dilg  1 , David Shore  2 , Benjamin Albert  3
Affiliations
Comment

Pitfalls in using phenanthroline to study the causal relationship between promoter nucleosome acetylation and transcription

Sevil Zencir et al. Nat Commun. .
No abstract available

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1. 1,10-pt induces a stress response affecting RNAPII and Epl1 promoter binding.
A–D Genome browser tracks showing RNAPII (Rpb3) or H3K23 acetylation ChIP-seq read counts at the indicated genes before (t = 0) or 15 min after 1,10-pt treatment. Dashed boxes indicate promoter regions where Rpb3 binding either decreases or increases (possibly in an elongation-block state) following 1,10-pt treatment. Raw data are from Martin et al.. E Scatter plot comparing H3K23ac (top) and H4K8ac (bottom) at promoters 15 min following 1,10-pt treatment (y-axis) to Rpb1 ChIP-seq (all fold-change, log2) at 5 min following heat shock (x-axis) for the 400 most highly expressed genes. Pearson coefficient is indicated. Raw data are from Martin et al. for H3K23ac and H4K8ac ChIP-seq and for Rpb1 ChIP-seq. F Scatter plot comparing two replicates (Rep1 and Rep2) measuring log2 fold change of Epl1 ChIP-seq signal before and after 1,10-pt treatment at all RNAPII promoters (gray dots) or at 562 promoters displaying high Epl1 binding in the absence of 1,10-pt (red dots), selected by Martin et al.. Raw data are from ref. .
Fig. 2
Fig. 2. 1,10-pt treatment mostly leads to a significant decrease in Epl1 promoter binding except for a small group of genes displaying a dramatic Epl1 binding increase.
A Scatter plots comparing Epl1 ChIP-seq signal before and after 1,10-pt treatment at promoters of all 562 genes (gray dots) selected by Martin et al. to study Epl1 promoter binding. Indicated gene categories (RP genes, n = 98; Hsf1 target genes, n = 34) are color-coded on the scatter plots; raw data are from replicate 1 from ref. . B Average Epl1 or Epl1(1-485) (dotted line) binding profiles on genes selected by Martin et al.) before (blue curves) or after 15 min of 1,10-pt treatment (red curves). The first four panels show data for all 562 genes divided into four separate categories, as marked: Hsf1 target genes (Hsf1, n = 34), ribosomal protein genes (RP, n = 98), genes where Epl1 ChIP-seq signal increases > 1,2 fold (Increase, n = 123), and all other genes in this group (Other, n = 307). The right-most panel shows the average for all 562 genes. Data are taken from Martin et al. and all plots are centered on the Epl1 signal peak. C Boxplots of log10 EpL1 ChIP-seq signal at promoters of the four gene categories defined in B before (−) or after (+) 15 min of 1,10-pt treatment. The ChIP-seq signal is quantified in a region delimited as the 100 bp region upstream and downstream of the Epl1 signal peak defined by Martin et al.. Asterisks show significant difference according to the Wilcoxon test (*P < 0.05, **P < 0.01, ***P < 0.001, ns not significant). D Most significant motifs found in genes at which Epl1 binding increases (>1,2-fold) or decreases (<0,8-fold) after 1,10-pt treatment. E values and the TF associated with the consensus binding motif identified by MEME are indicated. E Genome browser tracks showing Epl1, Rap1 and Tbf1 ChIP-seq read counts at the promoter regions (roughly demarcated by dotted lines) of the indicated genes before (t = 0) or 15 min after 1,10-pt treatment. Raw data are from Martin et al., Knight et al., and Preti et al. and for Epl1, Rap1, and Tbf1 ChIP-seq, respectively.
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