Analysis of ARID3A and ARID3B regulated genes by RNA-seq
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ABSTRACT:
PROVIDER: PRJNA529973 | ENA |
REPOSITORIES: ENA
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Project description:Previous studies in the mouse indicated that Arid3a plays a critical role in the first cell fate decision required for generation of trophectoderm (TE). Here, we demonstrate that Arid3a is widely expressed during mouse and human placentation and essential for early embryonic viability. Arid3a is located within trophoblast giant cells and other trophoblast-derived cell subtypes in the junctional and labyrinth zones of the placenta. Conventional Arid3a knockout embryos suffer restricted intrauterine growth with sever defects in placental structural organization. Arid3a null placentas show aberrant expression of subtype-specific markers as well as significant alteration in inflammatory response-related genes, cytokines and chemokines. We provide evidence that BMP4-mediated induction of trophoblast stem (TS)-like cells from human induced pluripotent (iPS) stem cells results in ARID3A upregulation and cytoplasmic to nuclear translocation. Overexpression of ARID3A in human iPS and BMP4-mediated TS-like cells up-regulated TE markers, whereas pluripotent markers were down-regulated. Our results indicate that the roles of Arid3a are conserved and essential for mammalian placental development through regulation of both intrinsic and extrinsic developmental programs. Placentas of E10.5 and E11.5 wild type (WT) and Arid3a-/- mice were generated by deep sequencing, using Illumina
2016-07-01 | E-GEOD-79638 | biostudies-arrayexpress
Project description:Previous studies in the mouse indicated that Arid3a plays a critical role in the first cell fate decision required for generation of trophectoderm (TE). Here, we demonstrate that Arid3a is widely expressed during mouse and human placentation and essential for early embryonic viability. Arid3a is located within trophoblast giant cells and other trophoblast-derived cell subtypes in the junctional and labyrinth zones of the placenta. Conventional Arid3a knockout embryos suffer restricted intrauterine growth with sever defects in placental structural organization. Arid3a null placentas show aberrant expression of subtype-specific markers as well as significant alteration in inflammatory response-related genes, cytokines and chemokines. We provide evidence that BMP4-mediated induction of trophoblast stem (TS)-like cells from human induced pluripotent (iPS) stem cells results in ARID3A upregulation and cytoplasmic to nuclear translocation. Overexpression of ARID3A in human iPS and BMP4-mediated TS-like cells up-regulated TE markers, whereas pluripotent markers were down-regulated. Our results indicate that the roles of Arid3a are conserved and essential for mammalian placental development through regulation of both intrinsic and extrinsic developmental programs.
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Project description:In this study we assayed for genome-wide localization of ARID3B and KDM4C enrichment in control and ARID3B-knockout OECM1 cells. The expression of the embryonic stem cell (ESC) signature in cancer cells indicates the coordinated regulation of the stemness genes in cancer stem cells, which are responsible for cancer initiation and dissemination. let-7 family microRNAs are crucial regulators for stem cell differentiation. In cancer cells, let-7 suppresses cancer stemness through targeting different oncogenes such as c-Myc, RAS, and HMGA2. However, most let-7 target genes are oncogenes rather than stemness factors, and the mechanism of let-7-repressed stemness is unclear. Here we demonstrate that let-7 supresses the formation of AT-rich interacting domain 3B (ARID3B) complex through targeting the expression of ARID3B, the interacting partner ARID3A, and importin 9. ARID3B complex recruits histone demethylase 4C (KDM4C) to the regulatory region of stemness genes for reducing histone 3 lysine 9 trimethylation, resulting in an open configuration of the chromatin of stemness genes. In cancer tissues, ARID3B expression correlates with the nuclear ARID3A expression and a worse prognosis. This result highlights the role of let-7 in regulating stemness through histone modifications.
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Project description:The purpose of this study was to decipher the molecular function of ARID3A. We leveraged gene expression (RNA-Seq) and chromatin profiling (ATAC-Seq and CUT&RUN) to evaluate gene expression changes upon restoring Arid3a expression in the context of the Gata1s mutation and miR-125b overexpression
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Project description:Microarray analyses for the identification of differences in gene expression patterns have increased our understanding of the molecular mechanism of ARID3B in HNSCC.We used gene expression analysis data from FaDu-ARID3B and FaDu-pCDH to identify differentially expressed probes. The expression of the embryonic stem cell (ESC) signature in cancer cells indicates the coordinated regulation of the stemness genes in cancer stem cells, which are responsible for cancer initiation and dissemination. let-7 family microRNAs are crucial regulators for stem cell differentiation. In cancer cells, let-7 suppresses cancer stemness through targeting different oncogenes such as c-Myc, RAS, and HMGA2. However, most let-7 target genes are oncogenes rather than stemness factors, and the mechanism of let-7-repressed stemness is unclear. Here we demonstrate that let-7 supresses the formation of AT-rich interacting domain 3B (ARID3B) complex through targeting the expression of ARID3B, the interacting partner ARID3A, and importin 9. ARID3B complex recruits histone demethylase 4C (KDM4C) to the regulatory region of stemness genes for reducing histone 3 lysine 9 trimethylation, resulting in an open configuration of the chromatin of stemness genes. In cancer tissues, ARID3B expression correlates with the nuclear ARID3A expression and a worse prognosis. This result highlights the role of let-7 in regulating stemness through histone modifications.
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Project description:Arid3a, a transcription factor known for its requirement in B-lymphocyte development, has been recently identified as a member of ES cell pluripotency network. Arid3a is moderately expressed in ES cells, and its expression is gradually increased during differentiation. Since Arid3a shows the highest expression in placenta, we hypothesized that Arid3a may play important roles in TE development. We report that Arid3a is a central regulator of both TE-specific and pluripotency-associated gene expression during ES cell differentiation. While dispensable for self-renewal, we observed that knockdown of Arid3a delays differentiation of ES cells. Induction of Arid3a leads ES cells to promote differentiation, specifically towards TE lineage. Moreover, these Arid3a-overexpressing cells maintained in TE culture media are sufficient to generate functional trophoblast stem-like cells, suggesting roles of Arid3a in TE differentiation. By integrative analyses using the chromosomal targets of Arid3a with expression profiling, we revealed the dual roles of Arid3a, as a direct activator of TE-specific genes and a repressor of pluripotency-associated genes. We further revealed the repressive roles of Arid3a are mediated by histone deacetylases (HDACs). Taken together, our results demonstrate that Arid3a is a critical novel regulator in TE lineage specification. Arid3a ChIP was performed using bioChIP-sequencing. Control ChIP-sequencing was performed using BirA cells. HDAC1 ChIP was performed as native antibody ChIP-sequencing.
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