Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA146581 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In differentiated mouse ESCs, most of the nodal/activin responsive genes are dependent on both Smad4 and Trim33, some are solely dependent on Smad4, and some are dependent on Trim33. Ebs at Day2.5 from WT, Smad4 null, and Trim33 knock-down ESCs, were treated with activin or SB 431542 for 2 h.
2012-01-09 | E-GEOD-32903 | biostudies-arrayexpress
Project description:In differentiated mouse ESCs, most of the nodal/activin responsive genes are dependent on both Smad4 and Trim33, some are solely dependent on Smad4, and some are dependent on Trim33.
2012-01-09 | GSE32903 | GEO
Project description:The epigenome of a cell is established and maintained by chromatin modifiers and remodelers, which are recruited to the chromatin by specific transcription factors. In this report, we show that nodal cross-talks with the epigenome through TRIM33-H3K18ac to mediate mesendodermal genes expression. The chromatin accessibility at mesendodermal genes depends on TRIM33. Moreover, histone acetylation is essential for TRIM33 recruitment to many nodal target genes involved in mesendodermal differentiation. The distribution pattern of the H3K18ac mark changes from foci to expanded domains at the mesendodermal genes promoter during embryonic stem cells (ESCs) differentiation to embryoid bodies (EBs). This could be the cue to facilitate TRIM33 colocalized with Smad2/3 at chromatin in EBs but not in ESCs. TRIM33 interacts with the H3K18ac “writer” p300 dependent on nodal signaling, providing a positive feedback to promote activation of mesendodermal genes and association with HDAC1 plays a negative role in activation of mesendodermal genes.
2019-06-01 | GSE115169 | GEO
Project description:TRIM33 is a chromatin reader required for nodal signaling during mesendoderm differentiation, although differences in its function between mouse embryonic stem cells (mESCs) and differentiated mesendoderm cells are unknown. Here, we found that TRIM33 co-condenses with PML nuclear bodies (NBs) via liquid-liquid phase separation specifically in mESCs to mediate nodal signaling-directed transcription of Lefty1/2. Our findings show that TRIM33 puncta formation depends on the presence of PML NBs. TurboID proximity labeling further revealed that PML NBs recruit distinct sets of client proteins in NaAsO2-treated, untreated mESCs, and differentiated cells. TRIM33 and PML co-regulate Lefty1/2 expression, while PML NBs directly associate with the Lefty1/2 loci and regulate a gene cluster that includes Lefty1/2 loci specifically in mESCs. Moreover, TRIM33 association with chromatin depends on PML NBs. Thus, PML NBs serve as a hub for transcriptional regulation of Lefty1/2 by TRIM33 and other pluripotency factors in mESCs.
2022-12-08 | GSE199737 | GEO
Project description:TRIM33 is a chromatin reader required for nodal signaling during mesendoderm differentiation, although differences in its function between mouse embryonic stem cells (mESCs) and differentiated mesendoderm cells are unknown. Here, we found that TRIM33 co-condenses with PML nuclear bodies (NBs) via liquid-liquid phase separation specifically in mESCs to mediate nodal signaling-directed transcription of Lefty1/2. Our findings show that TRIM33 puncta formation depends on the presence of PML NBs. TurboID proximity labeling further revealed that PML NBs recruit distinct sets of client proteins in NaAsO2-treated, untreated mESCs, and differentiated cells. TRIM33 and PML co-regulate Lefty1/2 expression, while PML NBs directly associate with the Lefty1/2 loci and regulate a gene cluster that includes Lefty1/2 loci specifically in mESCs. Moreover, TRIM33 association with chromatin depends on PML NBs. Thus, PML NBs serve as a hub for transcriptional regulation of Lefty1/2 by TRIM33 and other pluripotency factors in mESCs.
2022-12-08 | GSE199736 | GEO
Project description:Cardiac mesoderm, a precursor for all cardiovascular lineages, is a promising cell source for basic research and clinical applications. BMP/Nodal/Wnt signaling induces cardiac mesoderm in embryonic stem cells (ESCs); however the molecular mechanism is unclear and the differentiation protocols are labor-intensive. Identification of a master regulator that induces cardiac mesoderm is needed. Here we found that Tbx6 directly reprogrammed mouse fibroblasts into cardiac mesoderm-like cells, which differentiated into cardiomyocytes and smooth muscle cells with addition of lineage-specific transcription factors. In mouse ESCs, BMP/Activin (Nodal) induced Tbx6 in cardiac mesoderm, while inhibition of Tbx6 blocked differentiation into cardiac mesoderm and cardiomyocytes. Conversely, transient expression of Tbx6 induced cardiac mesoderm in ESCs without exogenous factors, and generated all cardiovascular lineages. Mechanistically, Tbx6 directly upregulated Mesp1, inhibited Sox2, and activated BMP/Nodal/Wnt signaling to induce cardiac mesoderm. Thus, Tbx6 acts as a key regulator for cardiac mesoderm induction, and our findings provide new insights into the mechanism of cardiovascular differentiation.
2018-10-19 | GSE89820 | GEO
Project description:To explore the molecular basis of functional differences observed between Nodal versus Activin-derived endoderm, we compared their respective gene expression profiles. Sox17-GFP mouse ES cells were differentiated in the presence of Nodal or Activin for 7 days, after which GFP(+) cells were purified by FACs. Undifferentiated ES cells were also included for comparison as a control. Results indicate that the two endoderm populations are nearly identical at the level of global transcription. Subtle differences suggest a difference in the degree of endoderm progression. Total RNA obtained from SOX17-GFP (+) mouse ES cells, Sox17-GFP treated with Nodal, Sox17-GFP treated with Activin. Two replicates for each sample; Sample data table contains average values of two replicates. The non_normalized.txt file contains individual signal values for each replicate.
2013-01-01 | E-GEOD-41086 | biostudies-arrayexpress
Project description:Activin/Nodal signaling in mouse embryonic stem cells
| PRJNA119997 | ENA
Project description:Over the past years, microRNAs (miRNAs) have emerged as crucial factors that regulate self-renewal and differentiation of embryonic stem cells (ESCs). Although much is known about their role in maintaining ESC pluripotency, the mechanisms by which they affect cell fate decisions remain poorly understood. By performing deep sequencing to profile miRNAs expression in mouse ESCs (mESCs) and differentiated embryoid bodies (EBs), we identified four differentially expressed miRNAs. Among them, miR-191 and miR-16-1 are highly expressed in ESCs and repress Smad2, the most essential mediator of Activin-Nodal signaling, resulting in the inhibition of mesendoderm formation. miR-23a, which is also downregulated in the differentiated state, suppresses differentiation towards the endoderm and ectoderm lineages. We further identified miR-421 as a differentiation-associated regulator through the direct repression of core pluripotency transcription factor Oct4 and BMP-signaling components, Smad5 and Id2. Collectively, our findings uncover a regulatory network between the studied miRNAs and both branches of TGF-β/BMP signaling pathways revealing their importance for ESC lineage decisions. miRNA profiles of ESCs and differentiated EBs D8 were generated by deep sequencing, in duplicate, using ION TORRENT PGM platform
2016-02-11 | E-GEOD-76375 | biostudies-arrayexpress