Mapping out genome wide binding sites of Prox1 by CUT&RUN approach in mouse cochlea
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA609690 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11214002_1.fastq.gz | Fastqsanger.gz | |||
| SRR11214002_2.fastq.gz | Fastqsanger.gz | |||
| SRR11214003_1.fastq.gz | Fastqsanger.gz | |||
| SRR11214003_2.fastq.gz | Fastqsanger.gz | |||
| SRR11214004_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:The homeobox transcription factor Prox1 is critical for organogenesis including brain, retina, liver and pancreas and lymphatic system. Prox1 is transiently expressed in mouse cochlear hair cells (HCs) and supporting cells (SCs), however, it remains elusive about its in vivo DNA binding site and roles during cochlear development. Here, by using fresh cochlear tissues and Prox1 antibody, we firstly mapped out the genome-wide binding sites of Prox1 via Cleavage Under Targets and Release Using Nuclease (CUT&RUN). Gene function enrichment analysis suggests several potential functions of Prox1, one of which is regulating cell cycle progression. Secondly, to validate our CUT&RUN data, we further performed in vivo prox1 gain-of-function studies through genetic approaches. Onset of ectopic Prox1 at early embryonic otocyst leads to shorter cochlea with density of HCs and SCs distribution, suggesting a precocious cell cycle exit of cochlear sensory progenitor cells. These findings highlight the power of CUT&RUN in mapping DNA binding sites even in tissues (i.e. cochlea) with rare cells, as well as providing the first genetic evidence to support roles of Prox1 in regulating progenitor pools of cochlear progenitors.
2021-08-06 | GSE146191 | GEO
Project description:Transcriptome analysis of P16 cochlea from wild type and miR-183/96 Knock out mice Gene expression analysis of miR-183/96 KO cochlea revealed a set of hair cell-relevant differentially expressed genes that could adversely impact hair cell physiology and contribute to the observed phenotype.
2018-05-01 | GSE106599 | GEO
Project description:We report CUT&RUN experiments to profile the genomic binding dynamics of V5-tagged Prox1 in isolated aortic valve cells from 1 month old NFATc1enCre Prox1 KI/+ mice or H3K27ac in isolated aortic valve endothelial cells from 1 month old wildtype mice.
2023-06-29 | GSE231336 | GEO
Project description:Gene expression profiling of miR-183/96 knock out mouse cochlea
| PRJNA417332 | ENA
Project description:Control or A2V+CD40 treated Prox1-proficient (AP) and Prox1-deficient (APP) tumors
2020-02-04 | GSE124716 | GEO
Project description:Our work describes the application of mass spectrometry-based label-free quantitative proteomics for the identification of differentially expressed proteins between different-aged cochlea. We report proteins exclusively present as well as up- and downregulated in the cochlear sensory epithelium at significant developmental stages. Additionally, we report proteins exclusively present on P3 that were recently identified in the cochlea for the first time. We use bioinformatics to provide insight on biological functions and potential primary and secondary partners of the differentially expressed proteins. This study provides the first differentially expressed proteome in the mammalian cochlea at significant developmental stages; before hearing, during the onset of hearing, and when hearing is fully developed. We believe that these results will provide insights into the function of proteins that change during development and identify potential protein biomarkers related to hearing impairments.
2018-08-29 | PXD001973 | Pride
Project description:Oncogenic mutations in Kras initiate neoplastic transformation in the pancreas through a process that hijacks the activity of developmental regulators and induces an inflammatory microenvironment. We report that the homeodomain transcription factor Prox1 is a novel component of a progenitor signature that is activated in acinar cells undergoing dedifferentiation and ductal metaplasia conversion. Also, the conditional deletion of a single Prox1 allele markedly accelerates early transformation and significantly enhances features of inflammation in pancreatic tissues carrying a Kras oncogene. By using in vitro and in silico approaches, we demonstrate that Prox1 negatively regulates the expression of proinflammatory genes and genes implicated in malignant transformation in pancreatic cells. Microrrays were used to identify gene expression profiles and pathways that are differentially activated after enforced expression of PROX1 in the PROX1-negative human pancreatic ductal adenocarcinoma (PDAC) cell line Capan1. MSCV retroviral transduction was used to generate Capan1 cells that ectopically express PROX1 and selected for puromycin resistance. Three independent transductions with control virus (MSCV_puro) and 3 independent transductions with Prox1-cDNA virus (MSCV_PROX1_puro) were conducted for these experiments.
2016-02-11 | E-GEOD-58547 | biostudies-arrayexpress
Project description:Accumulation of excess nutrients hampers proper liver function and is linked to non-alcoholic fatty liver disease (NAFLD) in obesity. However, the signals responsible for an impaired adaptation of hepatocytes to obesogenic dietary cues remain still largely unknown. Post-translational modification by the Small Ubiquitin-like Modifier (SUMO), allows for adynamic regulation of numerous processes including transcriptional reprograming. We demonstrate that specific SUMOylation of transcription factor Prox1 represents a nutrient-sensitive determinant of hepatic fasting metabolism. Prox1 was highly SUMOylated on lysine 556 in the liver of ad libitum and re-fed mice, while this modification was abolished upon fasting. In the context of diet-induced obesity, Prox1 SUMOylation became less sensitive to fasting cues. The hepatocyte-selective knock-in of a SUMOylation-deficient Prox1 mutant into mice fed a high-fat/high-fructose diet led to a reduction of systemic cholesterol levels, associated with the induction of liver bile acid detoxifying pathways during fasting. The generation of tools to maintain the nutrient-sensitive SUMO-switch on Prox1 may thus contribute to the development of “fasting-based” approaches for the preservation of metabolic health.
2023-10-24 | PXD041329 | Pride
Project description:During central nervous system (CNS) development, proper and timely induction of axon elongation is critical for generating functional, mature neurons and neuronal networks. Despite the wealth of information on the action of extracellular cues, little is known about the intrinsic gene regulatory factors that control this developmental decision. Here we report the identification of Prox1, a homeobox transcription factor, as a key player in inhibiting axon elongation. Although Prox1 promotes acquisition of early neuronal identity and is expressed in nascent post-mitotic neurons, it is heavily down-regulated in the majority of terminally differentiated neurons, indicating a regulatory role in delaying axon outgrowth in newly formed neurons. Consistently, we show that Prox1 is sufficient to inhibit neurite extension in neuroblastoma cell lines. Furthermore, shRNA-mediated knock-down of Prox1 in Neuro2A cells induces the extension of neurites. More importantly, Prox1 overexpression suppresses axon elongation in primary neuronal cultures as well as in the developing mouse brain, while Prox1 knock-down promotes axon outgrowth. Mechanistically, RNA-Seq analysis reveals that Prox1 affects critical pathways for neuronal maturation and neurite extension. Interestingly, Prox1 strongly inhibits many components of Ca2+ signaling pathway, an important mediator of axon extension and neuronal maturation. In accordance, Prox1 represses Ca2+ entry upon KCl-mediated depolarization and reduce CREB phosphorylation. These observations suggest that Prox1 acts as a potent suppressor of axon elongation by inhibiting Ca2+ signaling pathway. This action may provide the appropriate time window for nascent neurons to find the correct position in the CNS prior to initiation of axon elongation.
2020-12-31 | GSE158904 | GEO
Project description:Human thyroid cancer cell line BCPAP was engineered for doxycyclin-mediated inducible expressoin of Prox1 and next generation sequcing was performed to study the transcriptional regulation by Prox1 BCPAP cells were infected with rTTA2 lentivirus. The resulting cell populations were then stably transfected either with pIRES-hygromycin vector (Clontech) to generate BCPAP-Ctr cells, or with Flag-PROX1-IRES-hygromycin vector to generate BCPAP-Prx cells. PROX1 expression was induced or not in BCPAP-Ctr and BCPAP-Prx cells with 0.5 µg/ml doxycycline (Dox) for 48 hours and the total RNA samples were collected for sequencing.
2016-03-02 | E-GEOD-75059 | biostudies-arrayexpress