Transcription factor PATZ1 promotes adipogenesis by controlling promoter regulatory loci of adipogenic factors [ChIPseq_D0_D5]
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ABSTRACT:
PROVIDER: PRJNA1141422 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30020784.fastq.gz | Fastqsanger.gz | |||
| SRR30020785.fastq.gz | Fastqsanger.gz | |||
| SRR30020786.fastq.gz | Fastqsanger.gz |
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Project description:White adipose tissue (WAT) plays a central role in lipid storage and systemic energy, lipid, and glucose homeostasis. Understanding the intricacies of adipocyte formation could inform therapies for obesity and metabolic disorders. We have identified the POZ/BTB and AT Hook Containing Zinc Finger 1 (PATZ1) protein as an adipogenic transcription factor through an unbiased high-throughput cDNA screen for transcriptional modulators of adipogenesis. PATZ1 is expressed by both human and mouse adipocyte precursor cells (APCs) and adipocytes, and in cell models, PATZ1 expression promotes adipogenesis through a mechanism dependent on protein-protein interaction and DNA binding. Both adipocyte-specific and APC-specific ablation of PATZ1 in mice leads to decreased fat mass and hypertrophied adipocytes. Genome-wide PATZ1 DNA binding analyses using ChIP-Seq suggest PATZ1 facilitates adipogenesis through interactions with transcription factor machinery at the promoter regions of critical early adipogenic factors and histone modifiers. Purification of the PATZ1 complex showed that General Transcription Factor 2I (GTF2I) associates with PATZ1 in a differentiation-dependent manner. Downregulation of GTF2I levels during adipogenesis markedly augments PATZ1 adipogenic function, suggesting a repressive interaction between GTF2I and PATZ1. These findings identify PATZ1 as a regulator of both adiposity and adipocyte differentiation programs and advance our understanding of the complex transcriptional mechanisms underlying adipose tissue development and homeostasis.
2024-07-29 | GSE273318 | GEO
Project description:White adipose tissue (WAT) plays a central role in lipid storage and systemic energy, lipid, and glucose homeostasis. Understanding the intricacies of adipocyte formation could inform therapies for obesity and metabolic disorders. We have identified the POZ/BTB and AT Hook Containing Zinc Finger 1 (PATZ1) protein as an adipogenic transcription factor through an unbiased high-throughput cDNA screen for transcriptional modulators of adipogenesis. PATZ1 is expressed by both human and mouse adipocyte precursor cells (APCs) and adipocytes, and in cell models, PATZ1 expression promotes adipogenesis through a mechanism dependent on protein-protein interaction and DNA binding. Both adipocyte-specific and APC-specific ablation of PATZ1 in mice leads to decreased fat mass and hypertrophied adipocytes. Genome-wide PATZ1 DNA binding analyses using ChIP-Seq suggest PATZ1 facilitates adipogenesis through interactions with transcription factor machinery at the promoter regions of critical early adipogenic factors and histone modifiers. Purification of the PATZ1 complex showed that General Transcription Factor 2I (GTF2I) associates with PATZ1 in a differentiation-dependent manner. Downregulation of GTF2I levels during adipogenesis markedly augments PATZ1 adipogenic function, suggesting a repressive interaction between GTF2I and PATZ1. These findings identify PATZ1 as a regulator of both adiposity and adipocyte differentiation programs and advance our understanding of the complex transcriptional mechanisms underlying adipose tissue development and homeostasis.
2024-07-29 | GSE273320 | GEO
Project description:White adipose tissue (WAT) plays a central role in lipid storage and systemic energy, lipid, and glucose homeostasis. Understanding the intricacies of adipocyte formation could inform therapies for obesity and metabolic disorders. We have identified the POZ/BTB and AT Hook Containing Zinc Finger 1 (PATZ1) protein as an adipogenic transcription factor through an unbiased high-throughput cDNA screen for transcriptional modulators of adipogenesis. PATZ1 is expressed by both human and mouse adipocyte precursor cells (APCs) and adipocytes, and in cell models, PATZ1 expression promotes adipogenesis through a mechanism dependent on protein-protein interaction and DNA binding. Both adipocyte-specific and APC-specific ablation of PATZ1 in mice leads to decreased fat mass and hypertrophied adipocytes. Genome-wide PATZ1 DNA binding analyses using ChIP-Seq suggest PATZ1 facilitates adipogenesis through interactions with transcription factor machinery at the promoter regions of critical early adipogenic factors and histone modifiers. Purification of the PATZ1 complex showed that General Transcription Factor 2I (GTF2I) associates with PATZ1 in a differentiation-dependent manner. Downregulation of GTF2I levels during adipogenesis markedly augments PATZ1 adipogenic function, suggesting a repressive interaction between GTF2I and PATZ1. These findings identify PATZ1 as a regulator of both adiposity and adipocyte differentiation programs and advance our understanding of the complex transcriptional mechanisms underlying adipose tissue development and homeostasis.
2024-07-29 | GSE273317 | GEO
Project description:White adipose tissue (WAT) plays a central role in lipid storage and systemic energy, lipid, and glucose homeostasis. Understanding the intricacies of adipocyte formation could inform therapies for obesity and metabolic disorders. We have identified the POZ/BTB and AT Hook Containing Zinc Finger 1 (PATZ1) protein as an adipogenic transcription factor through an unbiased high-throughput cDNA screen for transcriptional modulators of adipogenesis. PATZ1 is expressed by both human and mouse adipocyte precursor cells (APCs) and adipocytes, and in cell models, PATZ1 expression promotes adipogenesis through a mechanism dependent on protein-protein interaction and DNA binding. Both adipocyte-specific and APC-specific ablation of PATZ1 in mice leads to decreased fat mass and hypertrophied adipocytes. Genome-wide PATZ1 DNA binding analyses using ChIP-Seq suggest PATZ1 facilitates adipogenesis through interactions with transcription factor machinery at the promoter regions of critical early adipogenic factors and histone modifiers. Purification of the PATZ1 complex showed that General Transcription Factor 2I (GTF2I) associates with PATZ1 in a differentiation-dependent manner. Downregulation of GTF2I levels during adipogenesis markedly augments PATZ1 adipogenic function, suggesting a repressive interaction between GTF2I and PATZ1. These findings identify PATZ1 as a regulator of both adiposity and adipocyte differentiation programs and advance our understanding of the complex transcriptional mechanisms underlying adipose tissue development and homeostasis.
2024-07-29 | GSE273319 | GEO
Project description:Transcription factor PATZ1 promotes adipogenesis by controlling promoter regulatory loci of adipogenic factors [ChIPreChIPseq_D0_D5]
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Project description:Transcription factor PATZ1 promotes adipogenesis by controlling promoter regulatory loci of adipogenic factors [RNA-seq]
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Project description:Transcription factor PATZ1 promotes adipogenesis by controlling promoter regulatory loci of adipogenic factors [ChIPseq_D-2_D0_D5_D8]
| PRJNA1141421 | ENA
Project description:White adipose tissue (WAT) is essential for lipid storage and systemic energy homeostasis. Understanding adipocyte formation and stability is key to developing therapies for obesity and metabolic disorders. Through a high-throughput cDNA screen, we identified PATZ1, a POZ/BTB and AT-Hook Containing Zinc Finger 1 protein, as an important adipogenic transcription factor. PATZ1 is expressed in human and mouse adipocyte precursor cells (APCs) and adipocytes. In cellular models, PATZ1 promotes adipogenesis via protein-protein interactions and DNA binding. PATZ1 ablation in mouse adipocytes and APCs leads to a reduced APC pool, decreased fat mass, and hypertrophied adipocytes. ChIP-Seq and RNA-seq analyses show that PATZ1 supports adipogenesis by interacting with transcriptional machinery at the promoter regions of key early adipogenic factors. Mass-spec results show that PATZ1 associates with GTF2I, with GTF2I modulating PATZ1's function during differentiation. These findings underscore PATZ1's regulatory role in adipocyte differentiation and adiposity, offering insights into adipose tissue development.
| S-EPMC11447024 | biostudies-literature
Project description:Bone marrow stromal cells (BMSCs) were isolated from the femora and tibiae of irtTA-GBD*-TAg transgenic mice. Using cellular cloning we established skeletal progenitors with unipotent osteogenic and adipogenic properties. Previous RNA-seq analysis of more progenitor types revealed differential expression in members of the Interferon-gamma (IFNγ) signaling pathway. Treatment of adipogenic progenitors with IFNγ inhibited adipogenesis and promoted osteogenesis. RNA-seq analysis of osteogenic, adipogenic and IFNγ treated adipogenic clones revealed factors controlling the osteogenic versus adipogenic commitment of bone marrow skeletal progenitors.
2018-07-02 | GSE114475 | GEO
Project description:Liver cancer is the third most common cause of cancer death in the world. POZ/BTB and AT-hook-containing zinc finger protein 1 (PATZ1) is a transcription factor associated with various cancers. However, the role of PATZ1 in cancer progression remains controversial. Here we report that PATZ1 regulates cell proliferation by directly regulating CDKN1B (p27) in hepatocellular carcinoma HepG2 cells. PATZ1 level was found to be ectopically expressed in hepatocellular carcinoma cells compared to normal primary human hepatocytes, thus affirming its relevance in liver cancer. Our gene expression microarray and PATZ1 ChIP-seq analysis further revealed strong enrichment in gene ontology terms related to cellular proliferation. Importantly, siRNA-mediated PATZ1 knockdown in HepG2 cells led to an increased rate of colony formation, elevated Ki-67 expression and greater S phase entry. Furthermore, the increased cancer cell proliferation was accompanied with suppressed expression of the cyclin-dependent kinase inhibitor CDKN1B. Consistently, PATZ1 binds to the genomic loci flanking the transcriptional start site of CDKN1B and positively regulates its promoter activity. Additionally, we found that PATZ1 associates with p53 and the absence of p53 abrogated the PATZ1-mediated regulation of CDKN1B expression. In conclusion, our study provides novel mechanistic insights into the role of PATZ1 in liver cancer progression, thereby providing a promising therapeutic intervention to alleviate tumor burden in liver cancer.
2020-12-31 | GSE114030 | GEO