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ZIC2 Is Required For Nodal Expression And The Establishment Of Left-Sided Identity

ABSTRACT: The purpose of this study was to identify putative downstream targets of the transcription factor ZIC2 in the mouse embryo. The results indicate loss of NODAL pathway expression, consistent with the observed phenotype of right isomerism in heart, lungs and viscera.

ORGANISM(S): Mus musculus

PROVIDER: GSE106350 | GEO | 2017/10/31

SECONDARY ACCESSION(S): PRJNA416367

REPOSITORIES: GEO

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ZIC2 Is Required For Nodal Expression And The Establishment Of Left-Sided Identity

Project description:ZIC2 Is Required For Nodal Expression And The Establishment Of Left-Sided Identity

| PRJNA416367 | ENA

A Requirement for Zic2 in the Regulation of Nodal Expression Underlies the Establishment of Left-Sided Identity.

Project description: Not available

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Transient Nodal signalling in left precursors coordinates opposed asymmetries shaping the heart loop

Project description:The secreted factor Nodal has been shown to be a major left determinant. Although it is associated with severe congenital heart defects, its role in heart morphogenesis has remained poorly understood. Here, we report that Nodal is transiently active in precursors of the mouse heart tube poles, before the morphological changes of heart looping. In conditional mutants, we show that Nodal is not required to initiate asymmetric morphogenesis. We provide evidence of a heart-specific random generator of asymmetry that is independent of Nodal. Using 3D quantifications and simulations, we demonstrate that Nodal functions as a bias of this mechanism: it is required to amplify and coordinate opposed left-right asymmetries at the heart tube poles, thus generating a robust helical shape. We identify downstream effectors of Nodal signalling, regulating asymmetries in cell proliferation, cell differentiation and extra-cellular matrix composition. Our work provides novel insight into how Nodal regulates asymmetric organogenesis.

2020-11-09 | GSE148123 | GEO

Zic2, an enhancer-binding factor required for embryonic stem cell specification

Project description:The Zinc finger protein of the cerebellum 2 (Zic2) is one of the vertebrate homologs of the Drosophila pair-rule gene odd-paired (opa). Our molecular and biochemical studies have demonstrated that Zic2 to preferentially bind to transcriptional enhancers and functions as a cofactor that interacts with the NuRD complex in ES cells. Detailed genome-wide studies demonstrate that Zic2 function with Mbd3/NuRD in regulating the chromatin state and transcriptional output of genes linked to differentiation. Zic2 is dispensable for the selfrenewal of ES cells but is required for proper differentiation, similar to what has been previously reported for Mbd3/NuRD. Our study identifies Zic2 as a key factor in the execution of the pluripotency program with Mbd3/NuRD in ES cells. ChIP-seq of Zic2, Chd4, Mbd3 and Zic3 in mES cells. ChIP-seq of H3K27me3, H3K27ac, H3K4me3, H3K4me1 and PolII in mES cells after Zic2 shRNA and non-targeting shRNA. RNA-seq of mES cells after Zic2, Zic3, Mbd3 and Mta2 shRNA and non-targeting shRNA.

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Identification of ZIC2 target genes in human pancreatic cancer cell lines PANC-1 and KP-4

Project description:PANC-1Tet/ZIC2 and PANC-1Tet/empty were established from human pancreatic cancer cell line PANC-1. PANC-1Tet/ZIC2 cells express FLAG-tagged human ZIC2 on the withdrawal of DOX. On the other hand, PANC-1Tet/empty was transfected an empty vector for the control experiment. To identify ZIC2 target genes, total RNAs were purified from the cells before and 48 hours after the DOX withdrawal. Gene expression profiles were analyzed by AGILENT human 4x44k cDNA microarray. As well as ZIC2-inducible system, we performed ZIC2-knockdown experiments in PANC-1 human pancreatic cancer cells. After 96 hours transfection of siRNAs for ZIC2 and its control, total RNAs were purified and gene expression profiles were analyzed by AGILENT human 4x44k cDNA microarray. ZIC2 target genes were identified in PANC-1 cells. Gene expression profiles of PANC-1Tet/ZIC2 and PANC-1Tet/empty cells were analyzed by AGILENT human 4x44k cDNA microarray before and 48 hours after the DOX withdrawal. As well as ZIC2-inducible system, gene expression profiles of control- and ZIC2-knocdown PANC-1 cells were also analyzed by AGILENT human 4x44k cDNA microarray.

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Resolving the Difference Between Left-sided and Right-sided Colorectal Cancer by Single-cell Sequencing

Project description:Colorectal cancers (CRCs) exhibit differences in incidence, pathogenesis, molecular pathways and outcome depending on the location of the tumor. The transcriptomes of 27,927 single human CRC cells, from three left-sided and three right-sided CRC patients were profiled by scRNA-seq. Right-sided CRC harbors a significant proportion of exhausted CD8 T cells of a highly migratory nature. One cluster of cells from left-sided CRC exhibiting states preceding exhaustion and a high ratio of “pre-exhausted” to exhausted T cells were favorable prognostic markers. Notably, we identified a novel RBP4+ NTS+ subpopulation of cancer cells that exclusively expands in left-sided CRC. Tregs from left-sided CRC showed higher levels of immunotherapy-related genes than those from right-sided CRC, indicating that left-sided CRC may have increased responsiveness to immunotherapy. Antibody-dependent cellular phagocytosis (ADCP) and antibody-dependent cellular cytotoxicity (ADCC) induced by M2-like macrophages were more pronounced in left-sided CRC and correlated with a good prognosis in CRC.

2021-11-15 | GSE188711 | GEO

Transcription factor ZIC2 regulates tumorigenic phenotypes in epithelial ovarian cancer in a context-dependent manner

Project description:Transcription factor ZIC2 plays a pro-tumorigenic role in several human cancers. Herein, we demonstrate that elevated ZIC2 expression was associated with lower overall and post-progression survival of epithelial ovarian cancer (EOC) patients. Knockout of ZIC2 in EOC cells attenuated tumorigenic phenotypes in vitro and in vivo, indicating a pro-tumorigenic role for ZIC2 in EOC. On the other hand, however, overexpression of ZIC2 in EOC cells that do not express endogenous ZIC2 promoted cell migration and sphere formation, but inhibited cell growth and colony formation in vitro and tumor growth in vivo, indicating a context-dependent function for ZIC2 in EOC. Transcriptomic study showed that ZIC2-regulated genes were involved in multiple biological processes and signaling pathways associated with tumor progression and that ZIC2 regulated common or distinct genes in ZIC2 knockout and overexpression models, which explains the consistency and discrepancy in ZIC2 functions observed in the two models. In conclusion, our findings reveal a context-dependent role for ZIC2 in regulating tumorigenic phenotypes in EOC, providing evidence that ZIC2 can be a potential therapeutic target for EOCs that express a high level of ZIC2.

2024-05-01 | GSE227395 | GEO

ZIC2 ChIP-Seq in KSHV latent and lytic reactivated BCBL-1 cells

Project description:ZIC2 is required for the maintenance of KSHV latency in human host cells. To understand the molecular action of ZIC2, we map ZIC2 binding sites across the KSHV genome in BCBL-1 cells using ChIP-Seq analysis.

2017-08-25 | GSE102462 | GEO

Zic2, an enhancer-binding factor required for embryonic stem cell specification

2015-02-23 | GSE61188 | GEO

Identification of ZIC2 target genes in human pancreatic cancer cell lines PANC-1 and KP-4

2014-04-14 | GSE39704 | GEO