Journal
AUTOPHAGY
Volume 15, Issue 1, Pages 98-112Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2018.1509608
Keywords
Autophagy; ChIP-seq; EGR1; nutrient-deprivation; RNA-seq
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Funding
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek [91615113, 022.004.018]
- Wilhelmina Children's Hospital
- Marie Sklodowska-Curie Cofund [713660]
- Marie Sklodowska-Curie ITN [765912]
- Reumafonds [14-3-201]
- ZonMw [016.130.606]
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Macroautophagy (hereafter 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 increase our understanding of the transcriptional and epigenetic events associated with autophagy, we performed extensive genome-wide transcriptomic and epigenomic profiling after nutrient deprivation in human autophagy-proficient 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. As a proof of principle that this resource can be used to identify novel autophagy regulators, we followed up on one identified target: EGR1 (early growth response 1), which indeed appears to be a central transcriptional regulator of autophagy by affecting autophagy-associated gene expression and autophagic flux. Taken together, these data stress the relevance of transcriptional and epigenetic regulation of autophagy and can be used as a resource to identify (novel) factors involved in autophagy regulation.
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