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ELL facilitates RNA Polymerase II mediated transcription of human epidermal proliferation genes

ABSTRACT: ELL facilitates RNA Polymerase II mediated transcription of human epidermal proliferation genes

PROVIDER: PRJNA655182 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12384500_1.fastq.gz	Fastqsanger.gz
	SRR12384500_2.fastq.gz	Fastqsanger.gz
	SRR12384501_1.fastq.gz	Fastqsanger.gz
	SRR12384501_2.fastq.gz	Fastqsanger.gz
	SRR12384502.fastq.gz	Fastqsanger.gz

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ELL facilitates RNA Polymerase II mediated transcription of human epidermal proliferation genes

Project description:ELL plays an essential role in human epidermal proliferation by binding to proliferation genes and facilitating the stabilization of RNA Polymerase II at the TSS to sustain their gene expression

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CDK12 maintains phosphorylation of RNA Polymerase II during epidermal differentiation

Project description:CDK12 plays an important role in regulating epidermal differntaition through maintaining the phosphorylation of RNA polymerase II levels in differentiation associated genes.

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High proliferation and delamination during skin epidermal stratification

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Intron looping is mediated during transcription by U1 snRNP and RNA polymerase II [RNA-Seq]

Project description:In the earliest step of spliceosome assembly, the two splice sites flanking an intron are brought into proximity by U1 snRNP and U2AF. The mechanism that facilitates this intron looping is poorly understood. Using a CRISPR interference-based approach to halt RNA polymerase II transcription in the middle of introns, we discovered that the 5 splice site base pairs with a U1 snRNA that is tethered to RNA polymerase II during intron synthesis. Correlation with splicing outcomes demonstrate that these associations are functional. The interactions between 5 splice sites, U1 snRNP, and elongating RNA polymerase II occurs genome-wide. Our findings reveal that during intron synthesis the upstream 5 splice site remains attached to the transcriptional machinery and is thus brought into proximity of the 3 splice site to enable rapid splicing.

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Intron looping is mediated during transcription by U1 snRNP and RNA polymerase II [RIP-seq]

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Intron looping is mediated by U1 snRNP and RNA polymerase II co-transcriptionally [ChIP-seq]

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TEAD1 and TEAD3 play redundant roles in human epidermal proliferation

Project description:TEAD1 and TEAD3 play redundant roles in human epidermal proliferation

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Regulation of epidermal differentiation through KDF1-mediated deubiquitination of IKKα

Project description:Progenitor cells at the basal layer of skin epidermis play an essential role in maintaining tissue homeostasis and enhancing wound repair in skin. The proliferation, differentiation, and cell death of epidermal progenitor cells have to be delicately regulated, as deregulation of this process can lead to many skin diseases, including skin cancers. However, the underlying molecular mechanisms involved in skin homeostasis remain poorly defined. In this study, with quantitative proteomics approach, we identified an important interaction between KDF1 (Keratinocyte Differentiation Factor 1) and IKKα (IκB kinase α) in differentiating skin keratinocytes. Ablation of either KDF1 or IKKα in mice leads to similar but striking abnormalities in skin development, particularly in skin epidermal differentiation. With biochemical and mouse genetics approach, we further demonstrate that the interaction of IKKα and KDF1 is essential for epidermal differentiation. To probe deeper into the mechanisms, we find that KDF1 associates with a deubiquitinating protease, USP7 (Ubiquitin Specific Peptidase 7), and KDF1 can regulate skin differentiation through deubiquitination and stabilization of IKKα. Taken together, our study unravels an important molecular mechanism underlying skin tissue homeostasis and epidermal differentiation.

2020-05-13 | PXD015673 | Pride

High proliferation and delamination during skin epidermal stratification

Project description:The development of complex stratified epithelial barriers in mammals is initiated from single-layered epithelia. How stratification is initiated and fueled are still open questions. Previous studies on skin epidermal stratification suggested a central role for perpendicular/asymmetric cell division orientation of the basal keratinocyte progenitors. Here, we use centrosomes, that organize the mitotic spindle, to test whether cell division orientation and stratification are linked. Genetically ablating centrosomes from the developing epidermis leads to the activation of the p53-, 53BP1- and USP28-dependent mitotic surveillance pathway causing a thinner epidermis and hair follicle arrest. The centrosome/p53-double mutant keratinocyte progenitors significantly alter their division orientation in the later stages without majorly affecting epidermal differentiation. Together with time-lapse imaging and tissue growth dynamics measurements, the data suggest that the first and major phase of epidermal development is boosted by high proliferation rates in both basal and suprabasally-committed keratinocytes as well as cell delamination, whereas the second phase maybe uncoupled from the division orientation of the basal progenitors. The data provide insights for tissue homeostasis and hyperproliferative diseases that may recapitulate developmental programs.

2021-04-02 | GSE161387 | GEO

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