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A genome-wide long noncoding RNA CRISPRi screen identifies PRANCR as a novel regulator of epidermal homeostasis

ABSTRACT: A genome-wide long noncoding RNA CRISPRi screen identifies PRANCR as a novel regulator of epidermal homeostasis

PROVIDER: PRJNA516223 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8467690.fastq.gz	Fastqsanger.gz
	SRR8467691.fastq.gz	Fastqsanger.gz
	SRR8467682.fastq.gz	Fastqsanger.gz
	SRR8467692.fastq.gz	Fastqsanger.gz
	SRR8467683.fastq.gz	Fastqsanger.gz

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A genome-wide long noncoding RNA CRISPRi screen identifies PRANCR as a novel regulator of epidermal homeostasis

Project description:Long noncoding RNAs (lncRNAs) are a major component of the noncoding genome, but their functions in human development and disease are still incompletely understood. CRISPR interference screens allow for systematic identification of functional lncRNAs that regulate fundamental biological processes such as tissue development and homeostasis. We identified 2,263 lncRNAs transcribed in human epidermis, and performed a comprehensive CRISPR interference screen against all these elements in primary human epidermal progenitors. Our screen identified 209 lncRNAs controlling epidermal progenitor renewal, with the majority (94%) being positive regulators of proliferation. To validate the results, we performed deeper characterization of a novel lncRNA identified from this screen, PRANCR (LINC01481), using RNA interference-mediated transcript knockdown and phenotype analysis in organotypic human tissue. PRANCR depletion inhibited progenitor proliferation through a G2/M cell cycle arrest, reduced clonogenic potential, and impaired functional epidermal stratification. Transcriptome and computational analysis indicated that PRANCR governs progenitor renewal by controlling the expression of 1,136 genes in trans, in part via the p53-E2F4-CHR pathway. This pathway controls the expression of G2/M cell cycle genes and is a novel mechanism of regulating cell proliferation in epidermal progenitors.

2019-11-07 | GSE125400 | GEO

A genome-wide long noncoding RNA CRISPRi screen identifies <i>PRANCR</i> as a novel regulator of epidermal homeostasis.

Project description:Genome-wide association studies indicate that many disease susceptibility regions reside in non-protein-coding regions of the genome. Long noncoding RNAs (lncRNAs) are a major component of the noncoding genome, but their biological impacts are not fully understood. Here, we performed a CRISPR interference (CRISPRi) screen on 2263 epidermis-expressed lncRNAs and identified nine novel candidate lncRNAs regulating keratinocyte proliferation. We further characterized a top hit from the screen, progenitor renewal associated non-coding RNA (PRANCR), using RNA interference-mediated knockdown and phenotypic analysis in organotypic human tissue. PRANCR regulates keratinocyte proliferation, cell cycle progression, and clonogenicity. PRANCR-deficient epidermis displayed impaired stratification with reduced expression of differentiation genes that are altered in human skin diseases, including keratins 1 and 10, filaggrin, and loricrin. Transcriptome analysis showed that PRANCR controls the expression of 1136 genes, with strong enrichment for late cell cycle genes containing a CHR promoter element. In addition, PRANCR depletion led to increased levels of both total and nuclear CDKN1A (also known as p21), which is known to govern both keratinocyte proliferation and differentiation. Collectively, these data show that PRANCR is a novel lncRNA regulating epidermal homeostasis and identify other lncRNA candidates that may have roles in this process as well.

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CRISPRi screen of prostate cancer associated risk cis-regulatory elements [CRISPRi]

Project description:CRISPRi screen of prostate cancer associated risk cis-regulatory elements [CRISPRi]

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Genome-wide CRISPRi screen for myriocin sensitivity

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Genome-wide CRISPRi screen for myriocin sensitivity

Project description:To delineate cellular pathways underlying cell growth in the absence of sphingolipid syntehsis, we performed a genome-wide CRISPRi screen to identify genetic modifiers of myriocin sensitivity in human K562 cells.

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Bioinformatics and single-cell CRISPRi-based screen reveals effector genes and implicates multi-tissue etiology for BMD [scCRISPR screen]

Project description:To nominate identify tissues relevant to the etiology of bone mineral density we generated ATAC-seq in pediatric hMSC-osteoblasts, hFOB 1.19 cells (hFOBs), osteoclasts, and primary chondrocytes. Leveraging the results of this experiment, we designed a CRISPRi screen in hFOBs with scRNA-seq expression read out. The targets selected for the screen were informed by newly generated Capture-C and bulk RNA-seq from hFOBs.

2024-04-17 | GSE261283 | GEO

CRISPRi Screen of Long Non-coding RNAs Identifies LINC03045 Regulating Glioblastoma Invasion

Project description:Introduction: Glioblastoma (GBM) invasion studies have focused on coding genes, while few studies evaluate long non-coding RNAs (lncRNAs), transcripts without protein-coding potential, for role in GBM invasion. We leveraged CRISPR-interference (CRISPRi) to evaluate invasive function of GBM-associated lncRNAs in an unbiased functional screen, characterizing and exploring the mechanism of identified candidates. Methods: We implemented a CRISPRi lncRNA loss-of-function screen evaluating association of lncRNA knockdown (KD) with invasion capacity in Matrigel. Top screen candidates were validated using CRISPRi and oligonucleotide(ASO)-mediated knockdown in three tumor lines. Clinical relevance of candidates was assessed via The Cancer Genome Atlas(TCGA) and Genotype-Tissue Expression(GTEx) survival analysis. Mediators of lncRNA effect were identified via differential expression analysis following lncRNA KD and assessed for tumor invasion using knockdown and rescue experiments. Results: Forty-eight lncRNAs were significantly associated with 33-83% decrease in invasion (p<0.01) upon knockdown. The top candidate, LINC03045, identified from effect size and p-value, demonstrated 82.7% decrease in tumor cell invasion upon knockdown, while LINC03045 expression was significantly associated with patient survival and tumor grade(p<0.0001). RNAseq analysis of LINC03045 knockdown revealed that WASF3, previously implicated in tumor invasion studies, was highly correlated with lncRNA expression, while WASF3 KD was associated with significant decrease in invasion. Finally, WASF3 overexpression demonstrated rescue of invasive function lost with LINC03045 KD. Conclusion: CRISPRi screening identified LINC03045, a previously unannotated lncRNA, as critical to GBM invasion. Gene expression is significantly associated with tumor grade and survival. RNA-seq and mechanistic studies suggest that this novel lncRNA may regulate invasion via WASF3.

2024-06-03 | GSE268342 | GEO

CRISPRi screen of prostate cancer associated risk cis-regulatory elements

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The phosphatase regulator NIPP1 controls epidermal homeostasis

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