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ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE248528 | GEO | 2024/10/23

REPOSITORIES: GEO

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ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [CUT&Tag]

Project description:N6-methyladenonsine (m6A) modification locates ubiquitously in mammalian mRNA, and profoundly impacts various physiological processes and pathogenesis. However, the precise involvement of m6A in early endoderm development has yet to be fully elucidated. Here, we reported that depletion of the m6A demethylase ALKBH5 in human embryonic stem cells (hESCs) severely impaired definitive endoderm (DE) differentiation. Within this process, ALKBH5-/- hESCs failed to undergo the primitive streak (PS) intermediate transition, which is considered as a prelude to endoderm specification. Mechanistically, we demonstrated that ALKBH5 deficiency induced m6A hypermethylation around the 3’ untranslated region (3’UTR) of GATA6 transcripts and destabilized GATA6 mRNA in a YTHDF2-dependent manner. Moreover, dysregulation of GATA6 expression ablated its occupancy with critical regulators of Wnt/β-catenin signaling pathway, thereby disrupting the signaling logic underlying DE formation. Overall, our findings unveil a mechanism whereby the ALKBH5-GATA6-WNT/β-catenin axis modulates human in vitro DE induction, and present novel insights on m6A modification in early embryonic development.

2024-10-23 | GSE248527 | GEO

ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [meRIP-seq]

2024-10-23 | GSE248526 | GEO

ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [RNA-seq]

2024-10-23 | GSE248525 | GEO

ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis.

Project description:ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis.

| PRJNA1044426 | ENA

ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [RNA-seq]

Project description:ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [RNA-seq]

| PRJNA1044427 | ENA

ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [CUT&Tag]

Project description:ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [CUT&Tag]

| PRJNA1044428 | ENA

ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [meRIP-seq]

Project description:ALKBH5 modulates endoderm fate diversion from hESCs through the ALKBH5-GATA6-WNT/β-catenin regulatory axis [meRIP-seq]

| PRJNA1044429 | ENA

GATA6 levels modulate primitive endoderm cell fate choice and timing in the mouse blastocyst.

Project description:Cells of the inner cell mass (ICM) of the mouse blastocyst differentiate into the pluripotent epiblast or the primitive endoderm (PrE), marked by the transcription factors NANOG and GATA6, respectively. To investigate the mechanistic regulation of this process, we applied an unbiased, quantitative, single-cell-resolution image analysis pipeline to analyze embryos lacking or exhibiting reduced levels of GATA6. We find that Gata6 mutants exhibit a complete absence of PrE and demonstrate that GATA6 levels regulate the timing and speed of lineage commitment within the ICM. Furthermore, we show that GATA6 is necessary for PrE specification by FGF signaling and propose a model where interactions between NANOG, GATA6, and the FGF/ERK pathway determine ICM cell fate. This study provides a framework for quantitative analyses of mammalian embryos and establishes GATA6 as a nodal point in the gene regulatory network driving ICM lineage specification.

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GATA6-AS1 Regulates GATA6 Expression to Modulate Human Endoderm Differentiation.

Project description:Transcriptome analysis has uncovered a series of long noncoding RNAs (lncRNAs) transcribed during cell differentiation, but how lncRNA is integrated with known transcriptional regulatory network is poorly understood. Here, we utilize human definitive endoderm differentiation as a model system and decipher the functional interaction between lncRNA and key transcriptional factor. We have identified GATA6-AS1, an lncRNA divergently transcribed from the GATA6 locus, is highly expressed during endoderm differentiation. Knockdown of GATA6-AS1 in human pluripotent stem cells has no influence on morphology and pluripotency; however, GATA6-AS1 depletion causes the deficiency of definitive endoderm differentiation. GATA6-AS1 positively regulates the expression of endoderm key factor GATA6. Further investigation shows GATA6-AS1 interacts with SMAD2/3 and activates the transcription of GATA6. In addition, overexpression of GATA6 is able to rescue the defect of endoderm differentiation due to the absence of GATA6-AS1, suggesting that GATA6 is the functional target of GATA6-AS1 during endoderm differentiation. Ultimately, our study reveals that GATA6-AS1 is necessary for human endoderm specification and reveals the underlying mechanism between GATA6-AS1 and GATA6.

| S-EPMC7486217 | biostudies-literature

GATA6 defines endoderm fate by controlling chromatin accessibility during differentiation of human-induced pluripotent stem cells.

Project description:In addition to driving specific gene expression profiles, transcriptional regulators are becoming increasingly recognized for their capacity to modulate chromatin structure. GATA6 is essential for the formation of definitive endoderm; however, the molecular basis defining the importance of GATA6 to endoderm commitment is poorly understood. The members of the GATA family of transcription factors have the capacity to bind and alter the accessibility of chromatin. Using pluripotent stem cells as a model of human development, we reveal that GATA6 is integral to the establishment of the endoderm enhancer network via the induction of chromatin accessibility and histone modifications. We additionally identify the chromatin-modifying complexes that interact with GATA6, defining the putative mechanisms by which GATA6 modulates chromatin architecture. The identified GATA6-dependent processes further our knowledge of the molecular mechanisms that underpin cell-fate decisions during formative development.

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