Fig. 7

Integration of –omics data sets with a previous definition of HS memory genes. As described previously, 1–1-1 genes are upregulated at 4 h, 28 h, and 52 h after ACC, 1–1-0 genes are upregulated at 4 h and 28 h after ACC, and 1–0-0 genes are upregulated only at 4 h [22]. a, b 1–1-1 genes are enriched in cclusters c7 and c12 (*p < 0.01, Fisher’s exact test, Additional File 2: Supplementary Data 1). The fraction of memory genes across cclusters (a) and the number of 1–1-1 genes per cluster (b) is indicated. c, d 1–1-1 genes are enriched in rclusters r8, r11, r14, and r15 (*p < 0.01, Fisher’s exact test, Additional File 2: Supplementary Data 1). Fraction of memory genes across rclusters (c) and the number of 1–1-1 genes per rcluster (d) is indicated. e 1–1-1 genes have a low basal expression level. Density plot representing the basal expression of 1–1-1, 1–1-0 and 1–0-0 genes. f 1–1-1 genes show increased binding (CPM) of HSFA2 and HSFA3 after ACC. Empirical cumulative distribution function of HSFA2- and HSFA3-binding at the indicated time points after ACC. The distribution of values for 1–1-1 genes was significantly different to that of the other three groups for HSFA2 at 4 h and for HSFA3 at 4 h and 28 h (KS-test, p < 0.05). g 1–1-1 genes are not enriched in any histone modification. Enrichment of histone modifications at memory genes of different categories. Gene bodies ± 500 bp are shown; gene models were scaled between transcriptional start site (TSS) and transcriptional termination site (TTS). n, number of genes per group. Histone modification ChIP-seq data were reanalyzed from [42]. h Venn diagrams illustrate the overlap between HSFA2/HSFA3 target genes according to binding (c7, c12, c14) and expression (r11, r14, 15) and 1–1-1, 1–1-0, 1–0-0 genes, respectively