Fig. 6: SET-26 and HCF-1 are unlikely to be major players in HDA-1’s recruitment to chromatin in somatic cells. | Nature Communications

Fig. 6: SET-26 and HCF-1 are unlikely to be major players in HDA-1’s recruitment to chromatin in somatic cells.

From: The chromatin factors SET-26 and HCF-1 oppose the histone deacetylase HDA-1 in longevity and gene regulation in C. elegans

Fig. 6

a Screenshot from IGV shows normalized somatic HDA-1 binding and peak calls in a portion of Chromosome I (captured by CUT&RUN of hda-1::gfp::ha worms, N = 2) in controls, set-26(-), or hcf-1(-) mutants grown on glp-1 RNAi. b Number of HDA-1 peaks called in combined replicates of controls, set-26(-), or hcf-1(-) mutants grown on glp-1 RNAi. c Metaplot (top) and heatmap (bottom) of z-scores representing normalized HDA-1 signal in somatic HDA-1 binding sites and surrounding 2 kb up- and downstream in either controls, set-26(-), or hcf-1(-) mutants grown on glp-1 RNAi. d, e Volcano plot of HDA-1 binding regions determined by DiffBind to be significantly different (pink, FDR < = 0.05) or unchanged (blue, FDR > 0.05) in (d) set-26(-) or (e) hcf-1(-) mutants compared to controls grown on glp-1 RNAi. DiffBind FDR values are calculated using DESeq2. f Venn diagram showing the genes with lower somatic HDA-1 binding in set-26(-) and hcf-1(-) mutants (identified in d, e) and the 6 and 27 genes that are commonly up- or downregulated, respectively, in set-26(-) and hcf-1(-) mutants as determined in Fig. 2a, b. Gene sets and differential peaks are provided in Supplementary Data 3 and 4.

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