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ZIC2 and ZIC3 promote SWI/SNF recruitment to safeguard progression towards human primed pluripotency [ATAC-Seq]

ABSTRACT: ZIC2 and ZIC3 are essential for acquisition and maintenance of primed pluripotency. In this study, we conducted ATAC-seq in single and compound knockout of ZIC2, ZIC3 and ZIC5 primed hESCs, naïve hESCs lacking ZIC3 that inducibly express ZIC2, naive hESCs that inducible express ZIC2 or ZIC3, ZIC3-depleted primed hESCs that were cultured in 5iLAF medium for six days and undergoing reversion to a naive state, naive hESCs expressing ectopic ZIC2 in the presence of a BRG1 PROTAC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE270948 | GEO | 2024/08/20

REPOSITORIES: GEO

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ZIC2 and ZIC3 promote SWI/SNF recruitment to safeguard progression towards human primed pluripotency [RNA-seq]

Project description:ZIC2 and ZIC3 are essential for acquisition and maintenance of primed pluripotency. In this study, we conducted next generation sequencing of polyA-enriched bulk RNA in single and compound knockouts of ZIC2, ZIC3 and ZIC5 primed hESCs, naïve hESCs lacking ZIC3 that inducibly express ZIC2, and primed hESCs that were cultured in 5iLAF medium for six days and undergoing reversion to a naive state.

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ZIC2 and ZIC3 promote SWI/SNF recruitment to safeguard progression towards human primed pluripotency [ChIP-seq]

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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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ZIC2 and ZIC3 promote SWI/SNF recruitment to safeguard progression towards human primed pluripotency

Project description:ZIC2 and ZIC3 promote SWI/SNF recruitment to safeguard progression towards human primed pluripotency

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ZIC2 and ZIC3 promote SWI/SNF recruitment to safeguard progression towards human primed pluripotency [ATAC-Seq]

Project description:ZIC2 and ZIC3 promote SWI/SNF recruitment to safeguard progression towards human primed pluripotency [ATAC-Seq]

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ZIC2 and ZIC3 promote SWI/SNF recruitment to safeguard progression towards human primed pluripotency [CUT&Tag]

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ZIC2 and ZIC3 promote SWI/SNF recruitment to safeguard progression towards human primed pluripotency [ChIP-seq]

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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.

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