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RBBP5 is an epigenetic regulator of mammalian hepatic 12h oscillator [ChIP-seq]

ABSTRACT: RBBP5 is an epigenetic regulator of mammalian hepatic 12h oscillator [ChIP-seq]

PROVIDER: PRJNA1155193 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30504606.fastq.gz	Fastqsanger.gz
	SRR30504607.fastq.gz	Fastqsanger.gz
	SRR30504608.fastq.gz	Fastqsanger.gz
	SRR30504609.fastq.gz	Fastqsanger.gz
	SRR30504610.fastq.gz	Fastqsanger.gz

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RBBP5 is an epigenetic regulator of mammalian hepatic 12h oscillator [RNA-seq]

Project description:Proteostasis is vital for cellular health, with disruptions leading to pathologies including aging, neurodegeneration and metabolic disorders. Traditionally, proteotoxic stress responses were studied as acute reactions to various noxious factors; however, recent evidence reveals that many stress-response genes exhibit ~12-hour ultradian rhythms under physiological conditions in mammals. These rhythms, driven by an XBP1s-dependent 12h oscillator, are crucial for managing proteostasis. By exploring the chromatin landscape of the murine 12h hepatic oscillator, we identified RBBP5, a key subunit of the COMPASS complex, as an essential epigenetic regulator of proteostasis. RBBP5 is indispensable for regulating both the hepatic 12h oscillator and transcriptional response to acute proteotoxic stress, acting as a co-activator for master proteostasis transcription factor XBP1s. RBBP5 ablation leads to increased sensitivity to proteotoxic stress, chronic inflammation, and hepatic steatosis in mice, along with impaired autophagy and reduced cell survival in vitro. In humans, lower RBBP5 expression is associated with dampened adaptive stress-response gene expression and hepatic steatosis. Our findings establish RBBP5 as a critical regulator of proteostasis, essential for maintaining mammalian organismal health.

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RBBP5 is an epigenetic regulator of mammalian hepatic 12h oscillator [ChIP-seq]

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RBBP5 is an epigenetic regulator of mammalian hepatic 12h oscillator [RNA-seq]

Project description:RBBP5 is an epigenetic regulator of mammalian hepatic 12h oscillator [RNA-seq]

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Epigenetic regulation of global proteostasis dynamics by RBBP5 ensures mammalian organismal health

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Global Mapping at the Core of the Arabidopsis Circadian Clock Defines the Network Structure of the Oscillator

Project description:In many organisms, the circadian clock is composed of functionally coupled morning and evening oscillators that regulate the bouts of dawn and dusk activity. In Arabidopsis, oscillator coupling relies on a core loop in which the evening oscillator component TOC1 was proposed to activate a subset of morning-expressed oscillator genes. Our systems-biological approach overturns the current view of the Arabidopsis circadian clock showing that TOC1 does not function as an activator but as a timely-controlled general repressor of morning and evening oscillator components. Repression occurs through rhythmic binding to the promoters of all oscillator genes, suggesting a previously unexpected direct connection between the morning and evening loops. Examination of TOC1 genome-wide binding using TOC1 Minigene (TMG) seedlings expressing the genomic fragment of TOC1 fused to the Yellow Fluorescent Protein in a toc1-2 mutant background (TMG-YFP/toc1-2 seedlings) grown under LD cycles (12h light:12h dark).

2012-03-08 | E-GEOD-35952 | biostudies-arrayexpress

Functional study of Rbbp5 in preimplantation embryos

Project description:We performed RNA-sequencing, ChIP-sequncing and Brif-sequencing on Rbbp5 knockout (KO) and wild-type (WT) mouse ICM and E5.0 epiblast. Our results showed that Rbbp5 KO lead to significant reduction of H3K4me3 modification at early blastocyst stage. The change in H3K4me3 landscape occured before the transcriptome change. Moreover, Rbbp5 KO specifically affected epiblast lineages the most at late blastocyst stage and the KO embryos died at E5.5.

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Epigenetic regulation of global proteostasis dynamics by RBBP5 ensures mammalian organismal health

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Nuclear-localized HKDC1 promotes hepatocellular carcinoma through phosphorylating RBBP5 to activate H3K4me3

Project description:Histone methyltransferases KMT2A (also known as mixed lineage leukemia 1, MLL1) can convert H3K4me1 to H3K4me2 with limited activity. However, it fully trimethylates H3K4 when associated with core subunits, including WDR5, RBBP5, ASH2L, and DPY30. We demonstrated that HKDC1 binds and phosphorylates RBBP5, promoting the assembly of MLL1 complex and the activating H3K4me3. Here, we used CUT&Tag to study H3K4me3 levels of the promoter regions regulated by HKDC1 and RBBP5. We knocked down HKDC1 or RBBP5 in PLC cells and performed CUT&Tag assay.

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Nuclear-localized HKDC1 promotes hepatocellular carcinoma through phosphorylating RBBP5 to activate H3K4me3 [RNA-Seq]

Project description:Histone methyltransferases KMT2A (also known as mixed lineage leukemia 1, MLL1) can convert H3K4me1 to H3K4me2 with limited activity. However, it fully trimethylates H3K4 when associated with core subunits, including WDR5, RBBP5, ASH2L, and DPY30. We demonstrated that HKDC1 binds and phosphorylates RBBP5, promoting the assembly of MLL1 complex and the activating H3K4me3. Consequently, HKDC1 transcriptionally activates gene expression. We used CUT&Tag to study H3K4me3 levels of the promoter regions regulated by HKDC1 and RBBP5. Here, we also performed RNA-seq assay in PLC cells with HKDC1 or RBBP5 knocked down to study the role of HKDC1 and RBBP5 in regulating gene expression.

2025-01-12 | GSE275644 | GEO

Nuclear-localized HKDC1 promotes hepatocellular carcinoma through phosphorylating RBBP5 to upregulate H3K4me3

Project description:Metabolic enzymes play significant roles in the pathogenesis of various cancers through both canonical and noncanonical functions. Hexokinase domain-containing protein 1 (HKDC1) functions beyond glucose metabolism, but its underlying mechanisms in tumorigenesis are not fully understood. Here, we demonstrate that nuclear-localized HKDC1 acts as a protein kinase to promote hepatocellular carcinoma (HCC) cell proliferation. Mechanistically, HKDC1 phosphorylates RB binding protein 5 (RBBP5) at Ser497, which is crucial for MLL1 complex assembly and subsequent H3K4me3 modification. This leads to the transcriptional activation of mitosis-related genes, thereby driving cell cycle progression and proliferation. Notably, targeting HKDC1’s protein kinase activity, but not its hexokinase activity, blocks RBBP5 phosphorylation and suppresses tumor growth. Clinical analysis further reveals that RBBP5 phosphorylation positively correlates with HKDC1 levels and poor HCC prognosis. These findings highlight the protein kinase function of HKDC1 in the activation of H3K4me3, gene expression, and HCC progression.

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