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PHF20 Activates Autophagy Genes through Enhancer Activation via H3K36me2 Binding Activity

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE193393 | GEO | 2022/06/23

REPOSITORIES: GEO

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

Project description:Autophagy is a catabolic pathway that maintains cellular homeostasis under various stress conditions, including nutrient-deprived conditions. To elevate autophagic flux to a sufficient level under stress conditions, transcriptional activation of autophagy genes occurs to replenish autophagy components. Here, using combination of RNA-seq, ATAC-seq and ChIP-seq, we demonstrated found that plant homeodomain finger protein 20 (Phf20PHF20), which is an epigenetic reader possessing methyl binding activity, plays a key role in controlling the expression of autophagy genes. PHF20 activates autophagy genes through enhancer activation via H3K36me2 binding activity as an epigenetic reader and that our findings emphasize the importance of nuclear regulation of autophagy.

2022-06-23 | GSE193392 | GEO

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

2022-06-23 | GSE193217 | GEO

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

2022-06-23 | GSE193215 | GEO

PHF20 Activates Autophagy Genes through Enhancer Activation via H3K36me2 Binding Activity

Project description:PHF20 Activates Autophagy Genes through Enhancer Activation via H3K36me2 Binding Activity

| PRJNA796013 | ENA

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

Project description:PHF20 Activates Autophagy Genes through Enhancer Activation via H3K36me2 Binding Activity [ChIP-seq]

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

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

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

Project description:PHF20 Activates Autophagy Genes through Enhancer Activation via H3K36me2 Binding Activity [RNA-seq]

| PRJNA796017 | ENA

PHF20 is crucial for epigenetic control of starvation-induced autophagy through enhancer activation.

Project description:Autophagy is a catabolic pathway that maintains cellular homeostasis under various stress conditions, including conditions of nutrient deprivation. To elevate autophagic flux to a sufficient level under stress conditions, transcriptional activation of autophagy genes occurs to replenish autophagy components. Thus, the transcriptional and epigenetic control of the genes regulating autophagy is essential for cellular homeostasis. Here, we applied integrated transcriptomic and epigenomic profiling to reveal the roles of plant homeodomain finger protein 20 (PHF20), which is an epigenetic reader possessing methyl binding activity, in controlling the expression of autophagy genes. Phf20 deficiency led to impaired autophagic flux and autophagy gene expression under glucose starvation. Interestingly, the genome-wide characterization of chromatin states by Assay for Transposase-Accessible Chromatin (ATAC)-sequencing revealed that the PHF20-dependent chromatin remodelling occurs in enhancers that are co-occupied by dimethylated lysine 36 on histone H3 (H3K36me2). Importantly, the recognition of H3K36me2 by PHF20 was found to be highly correlated with increased levels of H3K4me1/2 at the enhancer regions. Collectively, these results indicate that PHF20 regulates autophagy genes through enhancer activation via H3K36me2 recognition as an epigenetic reader. Our findings emphasize the importance of nuclear events in the regulation of autophagy.

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w09, a novel autophagy enhancer, induces autophagy-dependent cell apoptosis via activation of the EGFR-mediated RAS-RAF1-MAP2K-MAPK1/3 pathway.

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PAX8 activates metabolic genes via enhancer elements in Renal Cell Carcinoma.

Project description:Transcription factor networks shape the gene expression programs responsible for normal cell identity and pathogenic state. Using Core Regulatory Circuitry analysis (CRC), we identify PAX8 as a candidate oncogene in Renal Cell Carcinoma (RCC) cells. Validation of large-scale functional genomic screens confirms that PAX8 silencing leads to decreased proliferation of RCC cell lines. Epigenomic analyses of PAX8-dependent cistrome demonstrate that PAX8 largely occupies active enhancer elements controlling genes involved in various metabolic pathways. We selected the ferroxidase Ceruloplasmin (CP) as an exemplary gene to dissect PAX8 molecular functions. PAX8 recruits histone acetylation activity at bound enhancers looping onto the CP promoter. Importantly, CP expression correlates with sensitivity to PAX8 silencing and identifies a subset of RCC cases with poor survival. Our data identifies PAX8 as a candidate oncogene in RCC and provides a potential biomarker to monitor its activity.

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