Transcriptional and epigenetic profiling of nutrient-deprived cells to identify novel regulators of autophagy

Autophagy. 2019 Jan;15(1):98-112. doi: 10.1080/15548627.2018.1509608. Epub 2018 Sep 11.

Abstract

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.

Keywords: Autophagy; ChIP-seq; EGR1; RNA-seq; nutrient-deprivation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Autophagy / physiology*
  • Early Growth Response Protein 1 / genetics
  • Early Growth Response Protein 1 / metabolism*
  • Epigenesis, Genetic*
  • Gene Expression Profiling*
  • Gene Expression Regulation
  • HEK293 Cells
  • Humans
  • Lysosomes / metabolism*
  • Nutrients

Substances

  • Early Growth Response Protein 1

Grants and funding

This work was supported by the Nederlandse Organisatie voor Wetenschappelijk Onderzoek [022.004.018];Nederlandse Organisatie voor Wetenschappelijk Onderzoek [91615113];Wilhelmina Children’s Hospital;Marie Skłodowska-Curie Cofund [713660];Marie Skłodowska-Curie ITN [765912];Reumafonds [14-3-201];ZonMw [016.130.606].