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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 [ChIP-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.

2024-10-10 | GSE276157 | GEO

RBBP5 is an epigenetic regulator of mammalian hepatic 12h oscillator [RNA-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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The SET1/COMPASS subunit RBBP5 orchestrates epigenetic control of global proteostasis and the 12h oscillator to safeguard metabolic and cellular homeostasis

Project description:Proteostasis is vital for cellular health, with disruptions leading to aging, neurodegeneration and metabolic disorders. Traditionally, proteotoxic stress responses were studied as acute reactions to various noxious factors; however, recent evidence reveals that many proteostasis genes exhibit ~12h ultradian rhythms under physiological conditions in mammals, driven by an XBP1s-dependent 12h oscillator. By examining the chromatin landscape of this oscillator, we identified RBBP5 as an essential epigenetic regulator of global proteostasis dynamics. Mechanistically, as the core subunit of the SET1/COMPASS complex, RBBP5 co-activates XBP1s to facilitate dynamic proteostasis gene expression by marking promoter-proximal H3K4me3, which further recruits the Integrator Complex and SWI/SNF chromatin remodelers. Functionally, RBBP5 is indispensable for regulating both the 12h oscillator and acute transcriptional response to various proteotoxic stresses, including ER stress and nutrient deprivation. RBBP5 ablation causes increased susceptibility 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 reduced adaptive stress-response gene expression and hepatic steatosis. Our findings not only highlight a previously unrecognized epigenetic timing mechanism distinct from circadian regulation but also establish RBBP5 as a central regulator of proteostasis, essential for cellular resilience and organismal health.

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

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The SET1/COMPASS subunit RBBP5 orchestrates epigenetic control of global proteostasis and the 12h oscillator to safeguard metabolic and cellular homeostasis

Project description:The SET1/COMPASS subunit RBBP5 orchestrates epigenetic control of global proteostasis and the 12h oscillator to safeguard metabolic and cellular homeostasis

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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).

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

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

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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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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.

2025-01-12 | GSE275531 | GEO

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