Fig. 6: Ets1 transcriptionally suppresses mitochondrial coding genes and activates autophagy-related genes.

A Wild type 8- to 10-week-old C57/BL6j mice were kept either at room temperature (RT) or under cold stress (CS) for 7 days. Mature adipocytes separated from iWAT were used for ChIP-seq (Cut & Tag). B Normalized read count (average of reads signals across all genes) across gene body. C Venn diagram of peaks. D The IGV tool was used to visualize the binding peaks of Ets1 on the promoter region of autophagy-related and mitochondrial genes. Another Ets1 ChIP-seq that using SVF derived beige adipocyte were conducted and together analyzed (SVF adipo). E qPCR testing of the mRNA level of autophagy-related (left) and mitochondrial (right) genes, in the iWAT of 8- to 10-week-old EC+/+ or EA+/+ mice (n = 3 per group). F qPCR testing of the mRNA levels of autophagy-related (left) and mitochondrial (right) genes in 3T3L1 cells. Undifferentiated 3T3L1 cells were infected with either ad-Scramble or ad-shEts1 adenovirus; 48 h later, mRNA was collected and analyzed (n = 4 per group). G Promoter plasmid construction and the relative luciferase activity. Promoter regions of the mitochondrial clearance genes Atg9a and Atg10 and the biogenesis genes Sdhb and Uqcr10 were cloned, and the core sequence “GGA” in the predicted Ets1 binding sequence (EBS, black box) were point mutated to “GCA” (ΔEBS, red box). Promoter, Ets1 expression plasmid/vectors were co-transfected into 293 T cells, and luciferase activity was tested 24 h later (n = 5 per group). Data are means ± SEM. Two-sided Student’s t test was used to evaluate statistical significance. Source data are provided as a Source Data file.