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PHF3 regulates RNA stability through PHD and TLD domains - ChIPseq CNOT

ABSTRACT: PHF3 regulates RNA stability through PHD and TLD domains - ChIPseq CNOT

PROVIDER: PRJEB63536 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR11605604.fastq.gz	Fastqsanger.gz
	ERR11605605.fastq.gz	Fastqsanger.gz
	ERR11605606.fastq.gz	Fastqsanger.gz
	ERR11605607.fastq.gz	Fastqsanger.gz
	ERR11605608.fastq.gz	Fastqsanger.gz

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The SPOC proteins DIDO3 and PHF3 co-regulate gene expression and neuronal differentiation - RNAseq

Project description:Transcription is regulated by a multitude of activators and repressors, which bind to the RNA polymerase II (Pol II) machinery and modulate its progression. Death-inducer obliterator (DIDO) and PHD finger protein 3 (PHF3) are paralogue proteins that regulate transcription elongation by docking onto phosphorylated serine-2 in the C-terminal domain (CTD) of Pol II through their SPOC domains. Here we show that DIDO3 and PHF3 form a complex that bridges the Pol II elongation machinery with chromatin and RNA processing factors, and tethers Pol II in a phase-separated microenvironment. Their SPOC domains and C-terminal intrinsically disordered regions are critical for transcription regulation. PHF3 and DIDO exert cooperative and antagonistic effects on the expression of neuronal genes and are both essential for neuronal differentiation. The dataset contains RNAseq of HEK293 cells with various perturbations of PHF3 and DIDO1 genes.

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Project description:Transcription is regulated by a multitude of activators and repressors, which bind to the RNA polymerase II (Pol II) machinery and modulate its progression. Death-inducer obliterator (DIDO) and PHD finger protein 3 (PHF3) are paralogue proteins that regulate transcription elongation by docking onto phosphorylated serine-2 in the C-terminal domain (CTD) of Pol II through their SPOC domains. Here we show that DIDO3 and PHF3 form a complex that bridges the Pol II elongation machinery with chromatin and RNA processing factors, and tethers Pol II in a phase-separated microenvironment. Their SPOC domains and C-terminal intrinsically disordered regions are critical for transcription regulation. The dataset contains 3' Sequencing of WT, PHF3 KO, and PHF3 dSPOC mutant HEK293 cell line. Cytoplasmic and nuclear fractions were profiled separately.

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Project description:Transgenerational epigenetic inheritance (TEI), the transmission of epigenetic states between generations, has been observed in complex organisms ranging from plants to nematode worms, insects and mammals. One form of TEI that has been robustly studied is the inheritance of gene silencing. In Caenorhabditis elegans transgenerational gene silencing can be partitioned into three phases: the initiation of silencing, establishment of a heritable silencing signal within the parent individuals, and maintenance of this silencing signal within subsequent generations. Silencing involves nuclear and cytoplasmic components, and most genes involved in the process are linked to small RNA processing pathways. To date, two predicted histone methyltransferases have been implicated in the establishment of TEI, set-25 and set-32. Here, we demonstrate that the closely related paralogues set-9 and set-26 function in establishment and maintenance of TEI. We also identify a third related gene that lacks any predicted ordered domains; we name this gene intrinsically disordered protein-1 (idp-1). Strikingly, idp-1 also plays a role in establishment of TEI. SET-9 and SET-26 each contain a PHD finger and a SET domain. We show that the SET domains of SET-9 and SET-26 likely have no histone lysine methyltransferase activity, but that the PHD fingers bind trimethylated histone 3 lysine 4 (H3K4me3) in the absence of adjacent histone marks. We demonstrate that despite modelling data that suggests that set-9 and set-26 lack histone lysine methyltransferase activity, the function of both genes in TEI requires their PHD finger and SET domains. Our data confirm that the SET domain is functional and identifies three new chromatin factors required for epigenetic inheritance.

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