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Gene expression analysis in mouse mature T-cells either upon knockdown of L3MBTL3 or rescue with RBPJ WT or F261A/A284V mutant

ABSTRACT: Gene expression analysis in mouse mature T-cells either upon knockdown of L3MBTL3 or rescue with RBPJ WT or F261A/A284V mutant

PROVIDER: PRJNA707592 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13899157.fastq.gz	Fastqsanger.gz
	SRR13899158.fastq.gz	Fastqsanger.gz
	SRR13899159.fastq.gz	Fastqsanger.gz
	SRR13899160.fastq.gz	Fastqsanger.gz
	SRR13899161.fastq.gz	Fastqsanger.gz

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Gene expression analysis in mouse mature T-cells either upon knockdown of L3MBTL3 or rescue with RBPJ WT or F261A/A284V mutant

Project description:We identified genes upregulated upon depletion of L3MBTL3 in mouse mature T-cells (MT). Additionally, we identified genes downregulated upon rescue with RBPJ WT but not with an L3MBTL3-interacting defecting mutant (F261A/A284V) in MT cells depleted of RBPJ using the CRISPR/Cas9 technology.

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RBPJ/CBF1 interacts with L3MBTL3/MBT1 to promote repression of Notch signaling via histone demethylase KDM1A/LSD1

Project description:Notch signaling is an evolutionarily conserved signal transduction pathway that is essential for metazoan development. At the molecular level, the key components of the Notch pathway are the NOTCH-family receptors, the ligands of the DSL (Delta, Serrate, Lag-2) family and the transcription factor CSL [CBF1/RBPJ, Su(H), Lag-1]. Upon ligand binding, the NOTCH Intra-Cellular Domain (NOTCH ICD) translocates into the nucleus and forms a complex with RBPJ to activate the transcription of target genes. In the absence of NOTCH ICD, RBPJ acts as a transcriptional repressor. Using a proteomic approach, we identified L3MBTL3 as a novel interactor of RBPJ. We discovered that L3MBTL3 competes with NOTCH ICD for binding to RBPJ. In the absence of NOTCH ICD, RBPJ recruits L3MBTL3 and its co-factor KDM1A [lysine (K)-specific demethylase 1A] to the promoters/enhancers of Notch target genes to promote H3K4me2 demethylation and transcriptional repression. In three distinct cell contexts in which Notch signaling governs cell fate, i.e., mature T-cells as well as brain and breast tumor cells, the loss of L3MBTL3 results in the de-repression of Notch target genes. Finally, the genetic analyses of the homologs of RBPJ and L3MBTL3 in Drosophila melanogaster and Caenorhabditis elegans demonstrate that the functional link between RBPJ/Su(H)/lag-1 and L3MBTL3/dL(3)mbt/lin-61 is evolutionarily conserved, thus identifying L3MBTL3 as a universal modulator of Notch signaling in metazoans.

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Analysis of the repressive activity of RBPJ in a mature T cell line

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Messenger RNA expression profiling in L3mbtl3 WT versus L3mbtl3 KO/+ mouse cerebella.

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The CBF1/L3MBTL3 axis promotes the repression of Notch signaling by the histone demethylase KDM1A

Project description:We performed ChIP-seq experiments to investigate on a genome-wide scale the co-localization of CBF1 (also known as RBPJ or CSL) and L3MBTL3 on chromatin in the MDA-MB-231 cell line. Analysis of the CBF1 and L3MBTL3 ChIP-seq experiments in the MDA-MB-231 cell line revealed a substantial and significant genome-wide co-localization on chromatin, in agreement with our hypothesis that CBF1 contributes to the recruitment of L3MBTL3 to chromatin.

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