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PLAG1 and USF2 Co-regulate Expression of Musashi-2 in Human Hematopoietic Stem and Progenitor Cells

ABSTRACT: PLAG1 and USF2 Co-regulate Expression of Musashi-2 in Human Hematopoietic Stem and Progenitor Cells

PROVIDER: PRJNA437125 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6810050.fastq.gz	Fastqsanger.gz
	SRR6810060.fastq.gz	Fastqsanger.gz
	SRR6810051.fastq.gz	Fastqsanger.gz
	SRR6810052.fastq.gz	Fastqsanger.gz
	SRR6810053.fastq.gz	Fastqsanger.gz

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Similar Datasets

PLAG1 and USF2 Co-regulate Expression of Musashi-2 in Human Hematopoietic Stem and Progenitor Cells

Project description:MSI2, which is expressed predominantly in hematopoietic stem and progenitor cells (HSPCs), enforces HSPC expansion when overexpressed and is upregulated in myeloid leukemias indicating its regulated transcription is critical to balanced self-renewal and leukemia restraint. Despite this, little is understood of the factors that enforce appropriate physiological levels of MSI2 in the blood system. Here we define a promoter region that reports on endogenous expression of MSI2 and identify USF2 and PLAG1 as transcription factors whose promoter binding drives reporter activity. We show that these factors co-regulate, and are required for, efficient transactivation of endogenous MSI2. Coincident overexpression of USF2 and PLAG1 in primitive cord blood cells enhanced MSI2 transcription and yielded cellular phenotypes, including expansion of CD34+ cells in vitro, consistent with that achieved by direct MSI2 overexpression. Global ChIP-seq analyses confirm a preferential co-binding of PLAG1 and USF2 at the promoter of MSI2, as well as regulatory regions corresponding to genes with roles in HSPC homeostasis. PLAG1 and USF2 cooperation is thus an important contributor to stem cell-specific expression of MSI2 and represents novel HSPC-specific transcriptional circuitry.

2018-03-15 | GSE111469 | GEO

PLAG1 and USF2 Co-regulate Expression of Musashi-2 in Human Hematopoietic Stem and Progenitor Cells.

Project description:MSI2, which is expressed predominantly in hematopoietic stem and progenitor cells (HSPCs), enforces HSPC expansion when overexpressed and is upregulated in myeloid leukemias, indicating its regulated transcription is critical to balanced self-renewal and leukemia restraint. Despite this, little is understood of the factors that enforce appropriate physiological levels of MSI2 in the blood system. Here, we define a promoter region that reports on endogenous expression of MSI2 and identify USF2 and PLAG1 as transcription factors whose promoter binding drives reporter activity. We show that these factors co-regulate, and are required for, efficient transactivation of endogenous MSI2. Coincident overexpression of USF2 and PLAG1 in primitive cord blood cells enhanced MSI2 transcription and yielded cellular phenotypes, including expansion of CD34+ cells in vitro, consistent with that achieved by direct MSI2 overexpression. Global chromatin immunoprecipitation sequencing analyses confirm a preferential co-binding of PLAG1 and USF2 at the promoter of MSI2, as well as regulatory regions corresponding to genes with roles in HSPC homeostasis. PLAG1 and USF2 cooperation is thus an important contributor to stem cell-specific expression of MSI2 and HSPC-specific transcriptional circuitry.

| S-EPMC5998603 | biostudies-literature

Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia

Project description:The goal of this study is to develop a Plag1 signature and determine how its overexpression contributes to leukemogenesis. To study this, we transduced an immortalized (but not transformed) cell line (derived from Gata1s mutant fetal liver progenitor through insertional mutagenesis) by Plag1-expressing retrovirus. This turned a non-transformed cell line to a leukemogenic cell line. To study whether Plag1 overexpression led to deregulation of signaling pathways that may contribute to leukemic transformation, we generated microarray gene expression profiles of this cell line transduced with either Plag1 or the empty vector. We generated gene expression profiles by microarray from stable cell lines transduced with either the empty vector or the Plag1-expressing vector.

2010-08-01 | E-GEOD-16679 | biostudies-arrayexpress

RNA-seq of Lin-CD34+ cord-blood cells expressing shRNA against PLAG1 or control [KD]

Project description:To characterize transcriptional changes associated with loss of the transcription factor PLAG1-S that could contribute to PLAG1 essentiality in long-term human HSC we performed RNA-seq of 2 pools of Lin-CD34+ cord-blood derived hematopoietic stem and progenitor cells 72 hours following lentiviral introduction of shRNA against PLAG1 or non-targeting control.

2022-12-01 | GSE181991 | GEO

Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia

2010-08-01 | GSE16679 | GEO

Plag1 in the mouse Epididymis

Project description:RNA sequencing of Plag1 mouse epididymides. 5 each of Plag1 WT, HET and KO whole epididymis tissues were sequenced.

2019-11-19 | GSE140576 | GEO

Microarray analysis of differential gene expression of whole testis extracts from transgenic Musashi-2 and transgenic Musashi-1 over-expression mice

2014-07-12 | GSE59358 | GEO

Microarray analysis of differential gene expression of whole testis extracts from transgenic Musashi-2 and transgenic Musashi-1 over-expression mice

Project description:Analysis of testis-specific over-expression of Musashi-1 and Musashi-2 at gene expression level. The hypothesis tested in the present study was that testis-specific over-expression of Musashi-1/Musashi-2 would result in differential gene expression profiles from the Wildtype control. Results provide important information of the genes affected by Musashi-2 overexpression during spermatogenesis. Total RNA obtained from whole adult testis of transgenic testis-specfic Musashi-1 and Musashi-2 overexpression mice compared to Wildtype (control) littermates. 4 replicates, 16 samples, 2 comparisons: Wt (Musashi-1) vs. TgMsi1 & Wt (Musashi-2) vs. TgMsi2

2014-07-12 | E-GEOD-59358 | biostudies-arrayexpress

Maternal Plag1 deficiency delays two-cell stage embryo development and embryonic genome activation [Embryos]

Project description:Pleomorphic adenoma gene 1 (PLAG1) encodes a transcription factor involved in cancer and growth. We study the role of PLAG1 in preimplantation embryos using STRT RNA-seq of single embryos from wild type and knockout mothers (both mated with wild type studs). The lack of maternal Plag1 led to delayed mouse 2-cell stage embryo development, compensatory expression of Plag1 from the paternal allele, and dysregulation of 1,089 genes. Half of these genes displayed a pattern of delayed activation and play roles in ribosome biogenesis and protein synthesis. These mouse genes further showed a significant overlap with human EGA genes with similar ontology, and an enrichment of the PLAG1 de novo motif. We conclude that Plag1 affects EGA through retrotransposons influencing ribosomes and protein synthesis, a mechanism that might also explain its roles in cancer and growth

2019-06-20 | GSE111039 | GEO

Maternal Plag1 deficiency delays two-cell stage embryo development and embryonic genome activation [Uterus]

Project description:Pleomorphic adenoma gene 1 (PLAG1) encodes a transcription factor involved in cancer and growth. We study the role of PLAG1 in female reproductive tract and preimplantation embryos using STRT RNA-seq of single embryos from wild type and knockout mothers (both mated with wild type studs). We did not find significant effects in ovaries or uterus. The lack of maternal Plag1 led to delayed mouse 2-cell stage embryo development, compensatory expression of Plag1 from the paternal allele, and dysregulation of 1,089 genes. Half of these genes displayed a pattern of delayed activation and play roles in ribosome biogenesis and protein synthesis. These mouse genes further showed a significant overlap with human EGA genes with similar ontology, and an enrichment of the PLAG1 de novo motif. We conclude that Plag1 affects EGA through retrotransposons influencing ribosomes and protein synthesis, a mechanism that might also explain its roles in cancer and growth

2019-06-20 | GSE111035 | GEO

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