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PRMT1 and CSNK1a1 control epidermal progenitor maintenance

ABSTRACT: PRMT1 and CSNK1a1 control epidermal progenitor maintenance

PROVIDER: PRJNA323472 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6666085.fastq.gz	Fastqsanger.gz
	SRR6666086.fastq.gz	Fastqsanger.gz
	SRR6666087.fastq.gz	Fastqsanger.gz
	SRR6666088.fastq.gz	Fastqsanger.gz

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PRMT1 and CSNK1a1 control epidermal progenitor maintenance (PRMT1/CSNK1a1 transcriptome profiling data sets)

Project description:PRMT1 and CSNK1a1 control epidermal progenitor maintenance (PRMT1/CSNK1a1 transcriptome profiling data sets)

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PRMT1 and CSNK1a1 control epidermal progenitor maintenance (PRMT1/CSNK1a1 transcriptome profiling data sets)

Project description:Here we determine the target gene sets controlled by PRMT1 or CSNK1a1 in maintaining the undifferentiated state of primary human keratinocytes.

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PRMT1 and CSNK1a1 control epidermal progenitor maintanence (PRMT1 ChIP-seq data set)

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PRMT1 and CSNK1a1 control epidermal progenitor maintenance

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AFF1-HEXIM1 cooperation suppresses rapid-response differentiation initiators to enforce epidermal progenitor maintenance

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AFF1-HEXIM1 cooperation suppresses rapid-response differentiation initiators to enforce epidermal progenitor maintenance

Project description:In this study we identified an essential role of the SEC, a crucial regulator of Pol II dynamics, in repressing differentiation for epidermal progenitor maintenance. This repression of differentiation is specifically mediated by the scaffold protein AFF1, but not AFF4. Mechanistically, we find that AFF1-SEC associates with the HEXIM1-containing inactive-PTEFb to directly repress a group of rapid-response genes, which feature robust Pol II pausing near their promoters in the progenitor state. De-repression of these genes occurs within 3 hours of SEC-PTEFb disruption by the peptidomimetic inhibitors. These rapid-response genes include the transcription factor ATF3. Increased ATF3 level is sufficient to promote the expression of key differentiation activators, such as PRDM1, OVOL1, GRHL3 and ZNF750. Furthermore, we find that the dissociation of inactivate P-TEFb from SEC mediates the earliest events of PKC signaling, in triggering epidermal differentiation.

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Project description:Transcriptional deregulation plays a major role in acute myeloid leukemia, identification of epigenetic modifying enzymes essential for the maintenance of oncogenic transcription programs holds the key to better understanding the biology and designing effective therapeutic strategies for the disease. Here we provide experimental evidence showing the functional involvement and therapeutic potentials of targeting PRMT1 with H4R3 methyltransferase activity in various MLL and non-MLL leukemias. PRMT1 is necessary but not sufficient for leukemic transformation, which requires co-recruitment of KDM4C with H3K9 demethylase activity by chimeric transcription factors to mediate epigenetic reprogramming. Inhibition of KDM4C/PRMT1 suppresses transcription and transformation ability of MLL fusions and MOZ-TIF2, revealing a novel and targetable epigenetic circuitry mediated by PRMT1 and KDM4C in acute leukemia.

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