GSE107599
Epigenetic profiling of human HAP1 cells before and after nutrient deprivation
Autophagy is a lysosomal degradation pathway critical for maintaining cellular homeostasis and viability, and is predominantly regarded as a rapid and dynamic cytoplasmic process. To improve our understanding of the transcriptional and epigenetic events associated with autophagy, we performed genome-wide transcriptomic and epigenomic profiling after nutrient deprivation in human wildtype and autophagy-deficient cells. We observed that nutrient deprivation leads to the transcriptional induction of numerous autophagy-associated genes. These transcriptional changes are reflected at the epigenetic level (H3K4me3, H3K27ac, and H3K56ac) and are independent of autophagic flux. Overall design: Examination of H3K27ac, H3K56ac, H3K4me3 and RNA Polymerase II in HAP1 cells with and without amino acid + serum starvation (3h EBSS). Two replicates were included for each ChIP.