Plag1 in the mouse Epididymis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA590199 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10486715_1.fastq.gz | Fastqsanger.gz | |||
| SRR10486715_2.fastq.gz | Fastqsanger.gz | |||
| SRR10486716_1.fastq.gz | Fastqsanger.gz | |||
| SRR10486716_2.fastq.gz | Fastqsanger.gz | |||
| SRR10486717_1.fastq.gz | Fastqsanger.gz |
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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
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
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
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
Project description:To characterize genome-wide chromatin occupancy of the transcription factor PLAG1-S that could contribute to transient ex vivo expansion of human cord-blood (CB) derived HSC we performed CUT&RUN. 3 pools of Lin-CD34+ CB cells transduced to overexpress 3xFLAG-PLAG1-S were used for anti-FLAG or anti-IgG control enrichment of specific PLAG1-S DNA binding sites.
2022-12-01 | GSE181975 | GEO
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.
2010-08-01 | GSE16679 | GEO
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
Project description:The wild-type p53-induced phosphatase 1 (WIP1) frustrated mice exhibited defects in reproductive organs. This study aimed to understand how Wip1 deficiency affects the spermatogenesis or maturation. We employed the Wip1-/- mouse model and conducted a gel-free iTRAQ LC-MS/MS based quantitative proteomics analysis of whole epididymis including the sperms and somatic tissue. A total of 8763 proteins were identified, of which 91 were significantly differentially expressed proteins (DEPs) in the Wip1 depleted mice. Four DEPs (PRM2, ODF1, PIWIL1 and KLHL10) were confirmed with western blotting. The DEPs enriched in biological process of reproduction were identified by GO analysis and further confirmed in the mouse phenotype database. Pathway analysis suggested that Smac/Diablo-mediated apoptosis pathway and SERPINA3-mediated inflammatory process might contribute to the atrophy and the marked sperm decrease in epididymis. Network analysis of productivity related DEPs revealed possible interactions that WIP1 might affect the sperm maturation by decreasing the outer dense fiber protein 1 (ODF1) and protamine-2 (PRM2), and increasing the PIWIL1/MIWI through p53. PRM2 was down-regulated and PIWIL1 was up-regulated by immunohistochemistry staining. It was further confirmed that the spermatid deficiency began from the testis observed by HE staining. Therefore, WIP1 disruption caused the deficiency of spermatogenesis potentially through regulating the expression of the above DEPs and pathways.
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Project description:Genomic profiling of K562 cells resistant to imatinib as well as imatinib resistant CML patients harboured a recurrent chromosomal amplification in 8q11.2-12.1. Gene encoding PLAG1, a transcription factor associated with cancers and chemo resistance, resides on this locus and was found to be amplified in resistant cells. Upon PLAG1 knockdown we observed a decrease in imatinib resistance, and to understand the molecular events underlying PLAG1-mediated imatinib resistance, RNA sequencing was carried out. Imatinib-resistant K562 cells were transfected with lentiviral particles containing shRNA against PLAG1 and lentiviral particles containing pLKO.1-empty vectors. Monoclonal populations were established. Total RNA sequencing was performed. For QC, RNA samples were quantified using the Qubit RNA BR Assay kit (Invitrogen, Cat# Q10211). RNA purity was checked using QIAxpert, and RNA integrity was assessed on TapeStation using High Sensitivity RNA ScreenTape® (Agilent, Cat# 5067-5579). QC passed RNA samples were subjected to the library preparation, and NEB Ultra RNA-Seq Library Prep kit protocol (Cat# E7530L) was used and sequenced on Illumina NovaSeq 6000 instrument. Transcriptomic analysis identified several genes down-regulated upon PLAG1 knockdown which were further investigated.
2024-01-01 | E-MTAB-11893 | biostudies-arrayexpress
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.
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