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Paired Box 9 (PAX9), the RNA polymerase II transcription factor, regulates human ribosome biogenesis and craniofacial development (RNA-seq)

ABSTRACT: Paired Box 9 (PAX9), the RNA polymerase II transcription factor, regulates human ribosome biogenesis and craniofacial development (RNA-seq)

PROVIDER: PRJNA645430 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12195317.fastq.gz	Fastqsanger.gz
	SRR12195318.fastq.gz	Fastqsanger.gz
	SRR12195319.fastq.gz	Fastqsanger.gz
	SRR12195320.fastq.gz	Fastqsanger.gz
	SRR12195321.fastq.gz	Fastqsanger.gz

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Paired Box 9 (PAX9), the RNA polymerase II transcription factor, regulates human ribosome biogenesis and craniofacial development (RNA-seq)

Project description:We investigated the role of Paired Box 9 in regulating the transcription of mRNAs required for human ribosome biogenesis and craniofacial development.

2020-08-31 | GSE154216 | GEO

Paired Box 9 (PAX9), the RNA polymerase II transcription factor, regulates human ribosome biogenesis and craniofacial development (RNAPII ChIP-seq)

Project description:We investigated the role of Paired Box 9 in regulating the transcription of mRNAs required for human ribosome biogenesis and craniofacial development.

2020-08-31 | GSE154760 | GEO

Paired Box 9 (PAX9), the RNA polymerase II transcription factor, regulates human ribosome biogenesis and craniofacial development

Project description:Paired Box 9 (PAX9), the RNA polymerase II transcription factor, regulates human ribosome biogenesis and craniofacial development

| PRJNA647393 | ENA

Paired Box 9 (PAX9), the RNA polymerase II transcription factor, regulates human ribosome biogenesis and craniofacial development (RNAPII ChIP-seq)

Project description:Paired Box 9 (PAX9), the RNA polymerase II transcription factor, regulates human ribosome biogenesis and craniofacial development (RNAPII ChIP-seq)

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Paired Box 9 (PAX9), the RNA polymerase II transcription factor, regulates human ribosome biogenesis and craniofacial development.

Project description:Dysregulation of ribosome production can lead to a number of developmental disorders called ribosomopathies. Despite the ubiquitous requirement for these cellular machines used in protein synthesis, ribosomopathies manifest in a tissue-specific manner, with many affecting the development of the face. Here we reveal yet another connection between craniofacial development and making ribosomes through the protein Paired Box 9 (PAX9). PAX9 functions as an RNA Polymerase II transcription factor to regulate the expression of proteins required for craniofacial and tooth development in humans. We now expand this function of PAX9 by demonstrating that PAX9 acts outside of the cell nucleolus to regulate the levels of proteins critical for building the small subunit of the ribosome. This function of PAX9 is conserved to the organism Xenopus tropicalis, an established model for human ribosomopathies. Depletion of pax9 leads to craniofacial defects due to abnormalities in neural crest development, a result consistent with that found for depletion of other ribosome biogenesis factors. This work highlights an unexpected layer of how the making of ribosomes is regulated in human cells and during embryonic development.

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Paired Box 9 (PAX9), the RNA polymerase II transcription factor, regulates human ribosome biogenesis and craniofacial development

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-08-31 | GSE154764 | GEO

PAX9 determines epigenetic state transition and cell fate in small cell lung cancer

Project description:Small cell lung cancer (SCLC) is a more aggressive and deadlier form of lung cancer with limited effective therapies currently available. By utilizing a genome-wide CRISPR-Cas9 dropout screen, we have identified the Paired box protein 9 (PAX9) as an essential factor for the cell viability of SCLC-A type, which accounts for approximately 70% of all SCLC. PAX9 is transcriptionally driven by the BAP1/ASXL3/BRD4 epigenetic axis and is overexpressed in human malignant SCLC tumor samples. Genome-wide studies have revealed that PAX9 occupies distal enhancer elements and represses gene expression by restricting enhancer activity. Genetic depletion of PAX9 leads to a dramatic induction of a primed-active enhancer transition, resulting in an increased expression of a large number of neural differentiation and tumor-suppressive genes in multiple SCLC cell lines. Mechanistically, PAX9 interacts and co-functions with the Nucleosome Remodeling and Deacetylase (NuRD) complex at enhancers and they repress the nearby gene expression, which could be rescued by pharmacological HDAC inhibition. Overall, this study provides mechanistic insight into the oncogenic function of the PAX9/NuRD complex epigenetic axis in human SCLC and suggests that re-activation of the primed enhancers may have therapeutic efficacy in treating SCLC-A type cancers expressing high levels of PAX9.

2021-08-03 | GSE164247 | GEO

A Developmental Genomic Analysis of Pax1 and Pax9 in Embryonic Intervertebral Disc Development

Project description:Pax1 and Pax9 play redundant, synergistic functions in the patterning and differentiation of the sclerotomal cells that give rise to the vertebral bodies and intervertebral discs (IVD) of the axial skeleton. Gene expression profiling of an enriched population of Pax1/Pax9-expressing cells of the embryonic IVD revealed that Pax1 and Pax9 regulate cell proliferation, cartilage development, collagen fibrillogenesis and other processes vital in early IVD morphogenesis. Twenty-nine of the Pax1/Pax9 targets are also associated with axial skeletal defects that phenocopy Pax1/Pax9-deficient mice. Pax1 likely auto-regulates itself and is up-regulated in the absence of Pax9, clarifying how it compensates for the loss of Pax9, while Pax9 is unaffected by the loss of Pax1. Pax1 and Pax9 positively regulate several of the cartilage development genes known to be regulated by the “Sox trio” (Sox5/Sox6/Sox9).

2017-08-25 | GSE63017 | GEO

Differential gene expression between wild type and Pax9-null pharyngeal arch tissue

Project description:The aim of this study was to identify differentially expressed genes within the pharyngeal arches of Pax9-null embryos at E9.5. Mice null for Pax9 die in the neonatal period with complex cardiovascular defects, caused by abnormal morphogenesis of the pharyngeal arch arteries.

2019-08-28 | GSE128087 | GEO

Esophageal epithelium of WT mice; Esophageal epithelium of Pax9 KO mice

Project description:To study if the Pax9 gene plays an important role in the mouse model.

2018-03-16 | GSE96735 | GEO