Table 1.
Gene ontology enrichment analysis for heat shock treated mice.
| comparison | regulation | genes | regulators (1: ChEA, 2: ENCODE) | pathways (1: WIKIPathways, 2: Reactome) | gene ontologies (biological process) | kinases | chromatin marks |
|---|---|---|---|---|---|---|---|
| WT control vs. HS | up | 570 | 1: CLOCK 315.2, HSF1 302.42, ESR1 210.21, TCFAP2C 149.06, PPARG 143.32: MYOD1 55.7, MYOG 42.06, HSF1 41.33, EP300 34.79, ZMIZ1 34.45 | 1: Adipogenesis 23.72, Diurnally Regulated Genes with Circadian Orthologs 9.86, MAPK Signaling Pathway 8.47, Aryl Hydrocarbon Receptor 6.672: Attenuation phase (of HSF1) 26.5, HSF1-dependent transactivation 23.52, Cellular response to heat stress 16.7 | response to topologically incorrect protein 39.17, protein refolding 28.18, regulation of p38MAPK cascade 21.76, cellular response to lipid 16.21, regulation of vasculature development 14.86 | IRAK4 122.8ILK 83.21IGF1R 56.46ITK 42.54EGFR 41.07 | H3K4me1 36.38H3K27me3 27.61H3K27ac 19.79 |
| down | 264 | 1: WT1 86.33, NANOG 81.37, POU5F1 80.23, EP300 66.67, ZFP281 63.942: MAZ 14.9, EP300 12.0, GATA2 10.61, MYOD1 10.53, TCF3 9.86 | 1: not significant2: Signaling by BMP 13.73, Defective SLC26A2 causes chondrodysplasias 7.29, Extracellular matrix organization 7.19, Defective EXT1 causes exostoses 1, TRPS2 and CHDS 7.18, Oncogene Induced Senescence 7.11 | cellular response to lipid 21.06, receptor protein serine/threonine kinase signaling pathway 18.85, BMP signaling pathway 18.08, positive regulation of endothelial cell migration 17.62, regulation of smooth muscle cell migration 15.15 | IRAK4 41.39FGFR1 31.01CDK8 19.9BMPR2 10.99KSR2 8.7 | H3K27me3 31.73H3K4me3 23.62H3K4me1 17.47 | |
| R6/2 control vs. HS | up | 89 | 1: CLOCK 69.16, STAT3 45.91, ESR1 40.48, SUZ12 34.81, EGR1 33.552: not significant | 1: Corticotropin-releasing hormone 7.05, AGE/RAGE pathway 6.15, Diurnally Regulated Genes with Circadian Orthologs 5.052: HSF1 activation 11.17, Attenuation phase (of HSF1) 11.09, HSF1-dependent transactivation 10.9, Cellular response to heat stress 8.24 | cellular response to lipid 15.92, cellular response to hormone stimulus 13.81, negative regulation of calcium ion transport 11.38, response to temperature stimulus 11.12, nitric oxide mediated signal transduction 10.37 | IRAK4 20.98AKT1 20.3RAF1 16.98CDK8 9.51ROCK1 8.63 | H3K9me3 13.86H3K27me3 10.28H3K4me1 10.24 |
| down | 20 | 1: EP300 19.44, KLF4 7.98, VDR 7.96, GATA2 7.00, DNAJC2 7.002: not significant | 1: Striated Muscle Contraction 13.98, Retinol metabolism 8.342: Striated Muscle Contraction 8.19, Signaling by Retinoic Acid 7.79 | actin-myosin filament sliding 17.2, negative regulation of cartilage development 13.33, response to leptin 5.41 | FGFR1 6.61AKT1 5.56 | not significant | |
| Hsf1 −/− control vs. HS | up | 239 | 1: ESR1 134.55, CLOCK 108.64, STAT3 91.19, MTF2 80.56, ZNF217 76.022: MYOD1 29.47, ESR1 21.0, STAT3 18.65, TCF12 18.6, RAD21 18.36 | 1: Adipogenesis 14.47, Oncostatin M Signaling Pathway 9.54, Spinal Cord Injury 9.08, Diurnally Regulated Genes with Circadian Orthologs 8.872: not significant | response to oxygen levels 13.14, regulation of heart contraction 12.63, negative regulation of phosphorylation 11.29, negative regulation of cell migration 10.48, Rho protein signal transduction 10.29 | IRAK4 70.63KSR1 35.67CDK8 27.78HUNK 23.99IGF1R 19.05 | H3K4me1 28.94H3K27me3 24.01H3K9me3 22.37 |
| down | 103 | 1: TCF3 41.25, PPARG 37.09, CLOCK 32.42, POU5F1 28.47, POU3F2 28.472: GATA2 5.63 | 1: Striated Muscle Contraction 17.28, PPAR signaling pathway 12.95, Adipogenesis genes 7.35, SIDS Susceptibility Pathways 5.782: Striated Muscle Contraction 14.29 | muscle filament sliding 24.95, circulatory system process 11.09, positive regulation of osteoclast differentiation 9.22, fat cell differentiation 8.75, lipid storage 8.65 | CDK8 24.31ILK 21.09FGFR1 20.89AKT2 12.6IRAK4 8.16 | H3K27me3 19.97H3K9me3 13.08H3K9ac 7.42 |
Upstream regulators were predicted using the ChIP-x Enrichment Analysis (1: ChEA) and ENCODE transcription factor ChIP-seq database 2015 (2: ENCODE).v Chromatin marks were predicted using the ENCODE histone modifications database 2015. Only the top non-redundant significantly enriched terms followed by their combined score are shown. See also Tables S1, S2, S5, S6 and S8.