Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
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

PubMed Disclaimer

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.
See this image and copyright information in PMC

Comment in

Comment on

References

    1. Martin BJE, et al. Transcription shapes genome-wide histone acetylation patterns. Nat. Commun. 2021;12:210. doi: 10.1038/s41467-020-20543-z. - DOI - PMC - PubMed
    1. Huber A, et al. Sch9 regulates ribosome biogenesis via Stb3, Dot6 and Tod6 and the histone deacetylase complex RPD3L. Embo J. 2011;30:3052–3064. doi: 10.1038/emboj.2011.221. - DOI - PMC - PubMed
    1. Humphrey EL, Shamji AF, Bernstein BE, Schreiber SL. Rpd3p relocation mediates a transcriptional response to rapamycin in yeast. Chem. Biol. 2004;11:295–299. doi: 10.1016/j.chembiol.2004.03.001. - DOI - PubMed
    1. Rohde JR, Cardenas ME. The tor pathway regulates gene expression by linking nutrient sensing to histone acetylation. Mol. Cell Biol. 2003;23:629–635. doi: 10.1128/MCB.23.2.629-635.2003. - DOI - PMC - PubMed
    1. Weiner A, et al. High-resolution chromatin dynamics during a yeast stress response. Mol. Cell. 2015;58:371–386. doi: 10.1016/j.molcel.2015.02.002. - DOI - PMC - PubMed