Induction of dorsal mesodermal genes by pinhead and chordin
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA707043 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13866614_1.fastq.gz | Fastqsanger.gz | |||
| SRR13866614_2.fastq.gz | Fastqsanger.gz | |||
| SRR13866615_1.fastq.gz | Fastqsanger.gz | |||
| SRR13866615_2.fastq.gz | Fastqsanger.gz | |||
| SRR13866616_1.fastq.gz | Fastqsanger.gz |
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Project description:Xenopus embryonic ectodermal cells are responsive to various inducing factors. Mesoderm is specified and patterned by extracellular factors including FGF, Nodal, BMP and Wnt families. Pinhead is another secreted protein implicated in mesoderm formation. We found that Pinhead physically interacts with and antagonizes ADMP (anti-dorsalizing morphogenetic protein) that acts as BMP-like protein to promote ventral mesoderm formation. ADMP and BMPs have been shown to cooperate to activate phospho-Smad1 signaling to lead to ventral mesoderm development. Since Chordin is a BMP antagonist, we hypothesized that Pinhead together with Chordin can promote downregulation of phospho-Smad1 signaling that leads to dorsal mesoderm development. RNA sequencing revealed that Pinhead and Chordin synergize in dorsal mesoderm formation in ectodermal explants.
2021-04-19 | GSE168370 | GEO
Project description:RNA sequencing has allowed high-throughput screening of differential gene expression in many tissues and organisms. Xenopus laevis is a classical embryological and cell-free extract model system, but its genomic sequence had been lacking due to difficulties arising from allotetraploidy. There is currently much excitement surrounding the release of the completed X. laevis genome (version 9.1) by the Joint Genome Institute (JGI), which provides a platform for genome-wide studies. Here we present a deep RNA-seq dataset of transcripts expressed in dorsal and ventral lips of the early Xenopus gastrula embryo using the new genomic information, which was further annotated by blast searches against the human proteome. Overall, our findings confirm previous results from differential screenings using other methods that uncovered classical dorsal genes such as Chordin, Noggin and Cerberus, as well as ventral genes such as Sizzled, Ventx, Wnt8 and BAMBI. Complete transcriptome-wide Excel files of mRNAs suitable for data mining are presented, which include many novel dorsal- and ventral-specific genes. RNA-seq was very quantitative and reproducible, and allowed us to define dorsal and ventral signatures useful for gene set expression analyses (GSEA). As an example of a new gene, we present here data on an organizer-specific secreted protein tyrosine kinase known as Pkdcc (protein kinase domain containing, cytoplasmic) or Vlk (vertebrate lonesome kinase). Overexpression experiments indicate that Pkdcc can act as a negative regulator of Wnt/ β-catenin signaling independently of its kinase activity. We conclude that RNA-seq in combination with the Xenopus laevis complete genome now available provides a powerful tool for unraveling cell-cell signaling pathways during embryonic induction.
2016-06-20 | GSE75278 | GEO
Project description:We aimed to identify genes that are inhibited by Kctd15 overexpression during neural crest (NC) induction. Injection of RNAs encoding Wnt3a and chordin into the embryo followed by animal cap explant culture leads to the induction of NC marker genes as well as additional genes expressed in the neural plate border. Our previous study indicated that co-injection of kctd15 inhibits the induction of these markers. We injected four sets of RNAs, lacZ as control (L), wnt3a+chd (WC), wnt3a+chd+kctd15 (WCK), and kctd15 (K). After evaluation of marker gene expression with RT-PCR, we prepared probes with same RNA extract for Affymetrix DNA microarray. The hybridization, washing and scanning were perfomed following the manual from Affymetrix. Partek Genomics Suite was employed for data analysis. Xenopus embryos were injected with mRNAs at two-cell stage. When developing to stage 9, the animal caps were dissected for RNA extraction and hybridization on Affymetrix microarrays. According to the mRNAs injected, the animal caps (AC) were divided into four groups, including (1) AC injected with lacZ; (2) AC injected with kctd15; (3) AC injected with chordin and wnt3a; (4) AC injected with chordin, wnt3a and kctd15. The injected animal caps were cultured till stage 15 and then collected for RT-PCR and microarray assay. Each group had three repeats.
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Project description:In early embryonic development, the organiser functions in multiple developmental processes, including neural induction, dorsoventral patterning of the mesoderm, and formation of the axial mesoderm. Chordin is a central molecule for the activity of the Spemann’s organiser and abundantly secreted from the Spemann’s organiser in Xenopus laevis. However, so far, a whole picture of the gene expression profile regulated by Chordin has not been examined. Here, we perform microarray analysis of chordin overexpression and identify fam46a as an upregulated gene. We demonstrate that fam46a is essential for Xenopus laevis early embryonic development as well as gene induction during cell differentiation in mammalian cell culture models. fam46a is preferentially expressed in tissues with high secretory ability. In Xenopus laevis, fam46a is required for normal neural tube closure and expression of epidermal markers, neural markers and mesodermal markers. In the human Caco-2 cell model, FAM46A is localised in the nucleus and cytoplasm, and regulates gene induction during cell differentiation. In the mouse intestinal organoid model, Fam46a is required for survival of organoids as well as enterocyte differentiation. These results indicate that fam46a is a regulator for gene expression in secretory cells during cell differentiation in early embryonic development and adult homeostasis.
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Project description:In early embryonic development, the organiser functions in multiple developmental processes, including neural induction, dorsoventral patterning of the mesoderm, and formation of the axial mesoderm. Chordin is a central molecule for the activity of the Spemann’s organiser and abundantly secreted from the Spemann’s organiser in Xenopus laevis. However, so far, a whole picture of the gene expression profile regulated by Chordin has not been examined. Here, we perform microarray analysis of chordin overexpression and identify fam46a as an upregulated gene. We demonstrate that fam46a is essential for Xenopus laevis early embryonic development as well as gene induction during cell differentiation in mammalian cell culture models. fam46a is preferentially expressed in tissues with high secretory ability. In Xenopus laevis, fam46a is required for normal neural tube closure and expression of epidermal markers, neural markers and mesodermal markers. In the human Caco-2 cell model, FAM46A is localised in the nucleus and cytoplasm, and regulates gene induction during cell differentiation. In the mouse intestinal organoid model, Fam46a is required for survival of organoids as well as enterocyte differentiation. These results indicate that fam46a is a regulator for gene expression in secretory cells during cell differentiation in early embryonic development and adult homeostasis.
2023-11-21 | GSE108686 | GEO
Project description:In early embryonic development, the organiser functions in multiple developmental processes, including neural induction, dorsoventral patterning of the mesoderm, and formation of the axial mesoderm. Chordin is a central molecule for the activity of the Spemann’s organiser and abundantly secreted from the Spemann’s organiser in Xenopus laevis. However, so far, a whole picture of the gene expression profile regulated by Chordin has not been examined. Here, we perform microarray analysis of chordin overexpression and identify fam46a as an upregulated gene. We demonstrate that fam46a is essential for Xenopus laevis early embryonic development as well as gene induction during cell differentiation in mammalian cell culture models. fam46a is preferentially expressed in tissues with high secretory ability. In Xenopus laevis, fam46a is required for normal neural tube closure and expression of epidermal markers, neural markers and mesodermal markers. In the human Caco-2 cell model, FAM46A is localised in the nucleus and cytoplasm, and regulates gene induction during cell differentiation. In the mouse intestinal organoid model, Fam46a is required for survival of organoids as well as enterocyte differentiation. These results indicate that fam46a is a regulator for gene expression in secretory cells during cell differentiation in early embryonic development and adult homeostasis.
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Project description:The pathways used by cells to transition between pluripotent and tissue-specific states are incompletely understood. Here we show that the widely-expressed transcription factor Oct1/Pou2f1 activates silent, developmental lineage-appropriate genes to “canalize” developmental progression. Using Oct1 inducible knockout embryonic stem cells, we show that that Oct1 deficiency impairs mesodermal and terminal muscle differentiation in a manner that can be rescued by Oct1 retroviral expression. We show that mesoderm-specific genes are not correctly induced early in the differentiation timecourse. Oct1-deficient cells lose temporal coherence in the induction of lineage-specific genes and show inappropriate developmental lineage branching, resulting in poorly differentiated cells states retaining epithelial characteristics. In embryonic stem cells, Oct1 co-binds with Oct4 to genes critical for mesoderm induction, and continues to bind these genes during differentiation. Oct1 binding events are enriched at the termini of chromatin loops, including loops gained with differentiation. The Utx/Kdm6a histone lysine demethylase also binds to many of these genes, and using a prototypic Pax3 gene we show that Oct1 recruits Utx to remove inhibitory H3K27me3 marks and activate expression. The specificity of the ubiquitous Oct1 protein for mesodermal genes can be explained by cooperative interactions with lineage-driving Smad transcription factors, as we show that Smad and Oct binding sites frequently coexist mesoderm-specific genes, and that Oct1 and Smad3 act cooperatively at the Myog enhancer. Overall, these results identify Oct1 as a key mediator of the induction of mesoderm lineage-specific genes.
2022-11-26 | GSE207828 | GEO
Project description:The pathways used by cells to transition from undifferentiated, pluripotent gene expression programs into cell type-specific gene expression programs are incompletely understood. Here we show that the transcription factor Oct1/Pou2f1 recruits histone lysine demethylase complexes to allow for correct induction of silent, developmental lineage-specific genes and “canalize” developmental progression. Using mesodermal differentiation of inducible-conditional Oct1 knockout embryonic stem cells and single-cell gene expression profiling, we show that the potential to progress efficiently through mesodermal development is impaired in the Oct1 deficient condition. Oct1 deficient cells fail to form late presomitic mesoderm and early somite stage populations, and show “leaky” developmental trajectories with inappropriate lineage branching and accumulation of poorly differentiated cells that retain gene expression and metabolic hallmarks of pluripotency. Oct1 directly binds and regulates genes critical for developmental regulation, including genes encoding mesoderm-specific master regulators and components of chromatin regulatory complexes. Cells lacking Oct1 fail to positively resolve gene bivalency and activate gene expression by removing inhibitory H3K27me3 chromatin marks at mesoderm-specific genes. The Oct1 protein interacts with and recruits UTX to lineage-specific bivalent/poised targets, explaining the failure of Oct1 deficient cells to remove H3K27me3. Ectopic Oct1 expression improves the ability of cells to differentiate accurately under mesoderm lineage-inducing conditions.
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Project description:The pathways used by cells to transition from undifferentiated, pluripotent gene expression programs into cell type-specific gene expression programs are incompletely understood. Here we show that the transcription factor Oct1/Pou2f1 recruits histone lysine demethylase complexes to allow for correct induction of silent, developmental lineage-specific genes and “canalize” developmental progression. Using mesodermal differentiation of inducible-conditional Oct1 knockout embryonic stem cells and single-cell gene expression profiling, we show that the potential to progress efficiently through mesodermal development is impaired in the Oct1 deficient condition. Oct1 deficient cells fail to form late presomitic mesoderm and early somite stage populations, and show “leaky” developmental trajectories with inappropriate lineage branching and accumulation of poorly differentiated cells that retain gene expression and metabolic hallmarks of pluripotency. Oct1 directly binds and regulates genes critical for developmental regulation, including genes encoding mesoderm-specific master regulators and components of chromatin regulatory complexes. Cells lacking Oct1 fail to positively resolve gene bivalency and activate gene expression by removing inhibitory H3K27me3 chromatin marks at mesoderm-specific genes. The Oct1 protein interacts with and recruits UTX to lineage-specific bivalent/poised targets, explaining the failure of Oct1 deficient cells to remove H3K27me3. Ectopic Oct1 expression improves the ability of cells to differentiate accurately under mesoderm lineage-inducing conditions.
2022-11-26 | GSE160941 | GEO
Project description:Our understanding of how mesodermal tissue is formed, has been limited by the absence of specific and reliable markers of early mesoderm commitment. We report that mesoderm commitment from human embryonic stem cells (hESC) is initiated by Epithelial to Mesenchymal transition (EMT) as shown by gene expression profiling and by reciprocal changes in expression of the cell surface proteins, EpCAM/CD326 and NCAM/CD56. Molecular and functional assays reveal that CD326negCD56+ cells, generated from hESC in the presence of activin A, BMP4, VEGF and FGF2, represent a novel, multi-potent mesoderm-committed progenitor population. CD326negCD56+ progenitors are unique in their ability to generate all mesodermal lineages including hematopoietic, endothelial, mesenchymal (bone, cartilage, fat, fibroblast), smooth muscle and cardiomyocytes, while lacking the pluripotency of hESC. CD326negCD56+ cells are the precursors of previously reported, more lineage-restricted mesodermal progenitors. These findings present a novel approach to study how germ layer specification is regulated, and offer a unique target for tissue engineering. We used microarrays to compare gene expression profile of early mesodermal progenitors with undifferentiated hESC (H9 line). Mesoderm induction from hESC was initiatiated with combination of morphogens and growth factors including activin A, bone morphogenic protein 4, basic fibroblast growth factor and vascular endothelial growth factor. Proposed mesodermal progenitor population was isolated by FACS on day 3.5 of culture based on the presence of CD56 expression and the absenbce of CD326 expression.
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