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Genome binding/occupancy profiling of PHF23 and changes in H3K27ac based on the presence of PHF23

ABSTRACT: Autophagy is a conserved self-digestion pathway essential for maintaining cellular homeostasis and catabolism. Under normal conditions, autophagic activity remains minimal but is rapidly upregulated in response to stresses such as nutrient deprivation. While the transcriptional and epigenetic activation of autophagy under nutrient deprived condition has been widely studied, less is known about the repression mechanisms of autophagy under normal conditions. Here, we identify PHF23 as an epigenetic repressor of autophagy through a CRISPR interference (CRISPRi) screening. PHF23 inhibits the expression of autophagy genes by recruiting the NuRD complex and reducing chromatin accessibility, particularly at enhancer regions. This repressive function of PHF23 requires an intact PHD domain and is attenuated under amino acid starvation or mTOR inhibition conditions. Notably, inhibiting PHF23 enhances the autophagic clearance of pathological protein aggregates including Tau and a1 antitrypsin Z variant (ATZ), underscoring its potential as a therapeutic target in diseases characterized by proteotoxic stress.

ORGANISM(S): Homo sapiens

PROVIDER: GSE300094 | GEO | 2025/12/17

REPOSITORIES: GEO

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chromatin accessibility profiling by ATAC-seq based on the presence of PHF23

Project description:Autophagy is a conserved self-digestion pathway essential for maintaining cellular homeostasis and catabolism. Under normal conditions, autophagic activity remains minimal but is rapidly upregulated in response to stresses such as nutrient deprivation. While the transcriptional and epigenetic activation of autophagy under nutrient deprived condition has been widely studied, less is known about the repression mechanisms of autophagy under normal conditions. Here, we identify PHF23 as an epigenetic repressor of autophagy through a CRISPR interference (CRISPRi) screening. PHF23 inhibits the expression of autophagy genes by recruiting the NuRD complex and reducing chromatin accessibility, particularly at enhancer regions. This repressive function of PHF23 requires an intact PHD domain and is attenuated under amino acid starvation or mTOR inhibition conditions. Notably, inhibiting PHF23 enhances the autophagic clearance of pathological protein aggregates including Tau and a1 antitrypsin Z variant (ATZ), underscoring its potential as a therapeutic target in diseases characterized by proteotoxic stress.

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PHF20 Activates Autophagy Genes through Enhancer Activation via H3K36me2 Binding Activity [ATAC-seq]

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Project description:Autophagy, a catabolic process to remove unnecessary or dysfunctional cells, is triggered by various signals including nutrient starvation. Depending on the type of the nutrient deficiency, diverse sensing mechanisms and pathways are used for autophagy, suggesting subsequent nutrient dependent transcriptional regulation. Still, however, our knowledge about nutrient specific transcriptional regulation during autophagy is limited. To understand nutrient type dependent transcriptional mechanisms during autophagy, we performed single cell RNA sequencing (scRNAseq) for the mouse embryonic fibroblasts (MEFs) before and after applying glucose- (GS) as well as amino acid starvation (AAS). Trajectory analysis using scRNAseq identified sequential induction of potential transcriptional regulators for each deficiency condition. Gene regulatory rules inferred using TENET newly identified CCAAT/enhancer binding protein γ (C/EBPγ) regulates autophagy processes specifically to AAS condition. Strikingly, knockdown of C/EBPγ attenuated the autophagic process only in the AAS condition. Cell biological and biochemical studies validated that C/EBPγ plays a switching role for ATF4 to activate autophagy genes under AAS, but not under GS. Together, our data identified C/EBPγ as a previously unidentified key regulator under amino acid starvation-induced autophagy.

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