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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE193392 | GEO | 2022/06/23

REPOSITORIES: GEO

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PHF20 Activates Autophagy Genes through Enhancer Activation via H3K36me2 Binding Activity [ATAC-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 | GSE193215 | 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

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 [ATAC-seq]

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

| PRJNA795443 | 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]

| PRJNA795442 | ENA

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]

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PHF20 and PHF20L1 in NSL complex

2022-04-04 | PXD029258 | Pride

PHF20 readers link methylation of histone H3K4 and p53 with H4K16 acetylation

Project description:PHF20 is a core component of the lysine acetyltransferase complex MOF-NSL that produces the major epigenetic mark, H4K16ac, and is necessary for transcriptional regulation and DNA repair, however the role of PHF20 in the complex remains elusive. Here, we report on functional crosstalk between epigenetic readers of PHF20. We show that the PHF20 PHD finger recognizes dimethylated lysine 4 of histone H3 (H3K4me2) and represents first example of a native PHD reader selective for this modification. Biochemical and structural analyses illuminate the molecular mechanism underlying this function and explain the preference of Tudor2, another reader in PHF20, for dimethylated p53. Binding of the PHD finger to H3K4me2 is required for histone acetylation, accumulation of PHF20 at target genes, and transcriptional activation. Together, our findings establish a novel PHF20-mediated link between MOF HAT, p53 and H3K4me2-dependent cellular events and suggest a model for rapid spreading of H4K16ac-encriched open chromatin.

2017-05-22 | GSE82115 | GEO

Identification of genes and pathways that regulated by PHF20 via gene expression profile analysis in U87 cell with PHF20 silencing

Project description:Glioblastoma (GBM) is the most common tumor of the central nervous system with poor prognosis. PHF20 was highly expressed in primary human glioma specimens. However, the molecular mechanism of by which PHF20 regulated glioblastoma remains poorly understood. In the study, we investigate the gene expression profile of that regulated by PHF20 in U87 cells.

2017-10-31 | GSE93680 | GEO

Methyl-lysine readers PHF20 and PHF20L1 define two distinct NSL complexes

Project description:The methyl lysine readers PHF (plant homeodomain finger) 20 (PHF20) and its homolog PHF20 Like 1 (PHF20L1) are known components of the NSL (non-specific lethal) complex that regulates gene expression through its histone acetyltransferase activity. In the current model, both PHF homologs coexist in the same NSL complex although this was not formally tested; nor have the functions of PHF20 and PHF20L1 regarding NSL complex integrity and transcriptional regulation been investigated. Here we perform an in-depth biochemical and functional characterization of PHF20 and PHF20L1 in the context of the NSL complex. We identify the existence of two distinct NSL complexes that exclusively contain either PHF20 or PHF20L1; the two PHF homologs do not complex together in the same NSL species. Our data show that the C-terminal domains are essential for PHF20 and PHF20L1 to complex with NSL and the Tudor 2 domains of PHF20 and PHF20L1 are required for chromatin binding. The genome-wide landscape of PHF20/PHF20L1 binding to chromatin shows that they bind mostly to the same genomic regions, at promoters of highly expressed/housekeeping genes. Yet, deletion of PHF20 and PHF20L1 does not abrogate gene expression of the identified targets or impact the recruitment of NSL to the promoters of those genes, suggesting the existence of an alternative mechanism that compensates for the transcription of genes whose sustained expression is important for critical cellular functions.

2022-03-02 | GSE188601 | GEO

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