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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The oncoprotein v-Myb activates transcription of Gremlin 2 during differentiation of the chicken neural crest to melanoblasts

ABSTRACT: The neural crest (NC) is a transient dynamic structure of ectodermal origin, found in early vertebrate embryos. The multipotential NC cells migrate along well defined routes, differentiate to various cells types including melanocytes and participate in the formation of various permanent tissues. Abnormal development of NC cells causes several human diseases M-bM-^@M-^S neurocristopathies. As there is only limited information about the molecular mechanisms controlling early events in melanocyte specification and development, we exploited the AMV v-Myb transcriptional regulator, which directs differentiation of in vitro chicken NC cells to the melanocyte lineage. This activity is strictly dependent on v-Myb specifically binding to the Myb recognition DNA element (MRE). The two tamoxifen-inducible v-myb alleles were constructed, one which recognizes the MRE and one which does not. These were activated in ex-ovo NC cells, and the expression profiles of resulting cells were analyzed using Affymetrix microarrays and RT-PCR. These approaches revealed up-regulation of the BMP antagonist gremlin 2 mRNA, and down-regulation of mRNAs encoding several epithelial genes including KRT19 as very early events following the activation of melanocyte differentiation by v-Myb. Comparison of gene expression profiles of chicken neural crest cells constitutively expressing 4-OH-tamoxifen inducible v-myb with mutated leucine zipper region or a version with an additional point mutation (N118D) in the DNA-binding domain. Three biological replicates were analyzed for each group.

ORGANISM(S): Gallus gallus

SUBMITTER: Vladimir Cermak

PROVIDER: E-GEOD-39346 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The oncoprotein v-Myb activates transcription of Gremlin 2 during differentiation of the chicken neural crest to melanoblasts

Project description:The neural crest (NC) is a transient dynamic structure of ectodermal origin, found in early vertebrate embryos. The multipotential NC cells migrate along well defined routes, differentiate to various cells types including melanocytes and participate in the formation of various permanent tissues. Abnormal development of NC cells causes several human diseases – neurocristopathies. As there is only limited information about the molecular mechanisms controlling early events in melanocyte specification and development, we exploited the AMV v-Myb transcriptional regulator, which directs differentiation of in vitro chicken NC cells to the melanocyte lineage. This activity is strictly dependent on v-Myb specifically binding to the Myb recognition DNA element (MRE). The two tamoxifen-inducible v-myb alleles were constructed, one which recognizes the MRE and one which does not. These were activated in ex-ovo NC cells, and the expression profiles of resulting cells were analyzed using Affymetrix microarrays and RT-PCR. These approaches revealed up-regulation of the BMP antagonist gremlin 2 mRNA, and down-regulation of mRNAs encoding several epithelial genes including KRT19 as very early events following the activation of melanocyte differentiation by v-Myb.

2012-07-14 | GSE39346 | GEO

Genome-wide analysis of differential gene expression in human embryonic stem cell-derived central nervous system, neural crest, and progenitor populations over time

Project description:Melanocytes are pigment-producing cells of neural crest origin responsible for protecting the skin against UV-irradiation. Melanocyte dysfunction leads to pigmentation defects including albinism, vitiligo, and piebaldism and is a key feature of systemic pathologies such as Hermansky-Pudlak (HP) and Chediak-Higashi (CH) Syndromes. Pluripotent stem cell technology offers a novel approach for studying human melanocyte development and disease. Here we report that timed exposure to activators of WNT, BMP and EDN3 signaling triggers the sequential induction of neural crest and melanocyte precursor fates under dual-SMAD inhibition conditions. Using a SOX10::GFP hESC reporter line, we demonstrate that the temporal onset of WNT activation is particularly critical for human neural crest induction. Surprisingly, suppression of BMP signaling does reduce neural crest yield. Subsequent differentiation of hESC-derived melanocyte precursors under defined conditions yields pure populations of pigmented cells matching the molecular and functional properties of adult melanocytes. Melanocytes from patient-specific iPSCs faithfully reproduce the ultrastructural features of the HP- and CH-specific pigmentation defects with minimal variability across lines. Our data define a highly specific requirement for WNT signaling during neural crest induction and enable the generation of pure populations of hiPSC-derived melanocytes for faithful modeling of human pigmentation disorders. Total RNA obtained from a timecourse of Dual SMAD Inhibition (DSi), Neural Crest (NC), and Melanocyte (BE) differentiation of human embryonic stem cells in triplicate.

2013-06-01 | E-GEOD-45223 | biostudies-arrayexpress

Chicken neural crest and neural plate

Project description:Neural cest cells are a transient stem cell-like population appearing during vertebrate embryonic development. Generation of the cranial neural crest is known to require a balanced combination of FGF and BMP levels. However, it is poorly understood how the functions of such growth factors are controlled in the extracellular spaces. Here we identifiy the extracelluar matrix protein anosmin (Gga.14976.1.S1_at, clone ChEST132d10) as a novel molecule synthesized locally in the cranial neural crest of chicken embryos. Cranial neural folds (NF) and ventral neural plates (NP) were dissected from Hamburger & Hamilton stage 8 (HH8) embryos (80 to 14 embryos, n=4), and total RNA was analyzed using a GeneChip chicken genome arrays (Affymetrix)

2012-05-31 | E-GEOD-38381 | biostudies-arrayexpress

INK4A expression in leukemic cells transformed by the v-Myb oncoprotein depends on the integrity of the v-Myb leucine zipper region

Project description:The AMV v-Myb oncoprotein causes oncogenic transformation of myelomonocytic cells in vivo and in vitro. Its transforming capacity is strictly dependent upon the N-terminal DNA binding domain, the central transactivation region, and on the C-terminal domain containing a putative leucine zipper motif. While deletions in the central part of the leucine zipper region or point mutations of critical leucine residues abolish the leukemogenicity of the protein, a small deletion within the N-terminal part (deltaP mutant) preserves almost full in vitro transforming ability and only weakens the leukemogenic potential in vivo. We analyzed the gene expression profiles of ex vivo cultures transformed with either wild type or deltaP mutant of v-Myb. A few tens of genes were found to be significantly and reproducibly differentially expressed between the two cultures. Among them, the transcript of the CDKN2A gene, which is critically involved in the cell cycle progression regulation, showed higher expression in the deltaP mutant transformed cells. In mammals and also some avian species, there are two different mRNAs - ARF and INK4A – transcribed from the CDKN2A locus. It is known that in chickens the locus had been rearranged in evolution and only one mRNA is transcribed. We found that this mRNA encodes both ARF and INK4A and that the INK4A protein translation starts with a GUG codon downstream of the ARF AUG initiation codon and proceeds in a different reading frame. INK4A protein thus exists in chicken cells as well and its negative regulation by v-Myb is a part of the leukemic transformation mechanism. Comparison of expression profiles of chicken monoblasts transformed either by wild type v-myb or its mutated version designated deltaP. Three biological replicates were analyzed for each group.

2012-04-11 | E-GEOD-35413 | biostudies-arrayexpress

Genome-wide analysis of gene expression in human pluripotent stem cell-derived melanocyte progenitors, mature melanocytes, and disease-specific melanocytes

Project description:Melanocytes are pigment-producing cells of neural crest origin responsible for protecting the skin against UV-irradiation. Melanocyte dysfunction leads to pigmentation defects including albinism, vitiligo, and piebaldism and is a key feature of systemic pathologies such as Hermansky-Pudlak (HP) and Chediak-Higashi (CH) Syndromes. Pluripotent stem cell technology offers a novel approach for studying human melanocyte development and disease. Here we report that timed exposure to activators of WNT, BMP and EDN3 signaling triggers the sequential induction of neural crest and melanocyte precursor fates under dual-SMAD inhibition conditions. Using a SOX10::GFP hESC reporter line, we demonstrate that the temporal onset of WNT activation is particularly critical for human neural crest induction. Surprisingly, suppression of BMP signaling does reduce neural crest yield. Subsequent differentiation of hESC-derived melanocyte precursors under defined conditions yields pure populations of pigmented cells matching the molecular and functional properties of adult melanocytes. Melanocytes from patient-specific iPSCs faithfully reproduce the ultrastructural features of the HP- and CH-specific pigmentation defects with minimal variability across lines. Our data define a highly specific requirement for WNT signaling during neural crest induction and enable the generation of pure populations of hiPSC-derived melanocytes for faithful modeling of human pigmentation disorders. Total RNA obtained from embryonic stem cells (ESCs), ESC-derived melanocyte progenitors, ESC-derived mature melanocytes, primary melanocytes, and disease-specific induced pluripotent stem cell-derived melanocytes.

2013-06-01 | E-GEOD-45226 | biostudies-arrayexpress

expression profiles in the chicken PSM differentiation at Stage 12HH chicken embryo

Project description:To examine global gene expression profile of chicken early paraxial mesoderm differentiation, we microdissected stage 12HH chicken PSM regions into 20 pieces (10 pieces both left-right PSM), including the tail bud, the PSM and somites. We create microarray series using these fragments. Duplicated 10 fragmented tissues from stage 12 chicken PSM regions. contributor: IGBMC microarray facility

2015-12-09 | E-GEOD-75798 | biostudies-arrayexpress

CD11d is a novel antigen on chicken PBMC

Project description:Using Immunoprecipitation (IP) and mass spectrometry analysis, we aimed at identifying the target of a self-made monoclonal antibody to an unknown molecule on the outer membranes of chicken peripheral blood derived mononuclear cells (PBMC).

2020-06-18 | PXD017248 | Pride

Chromatin remodellers Brg1 and Bptf are required for normal gene expression and progression of oncogenic Braf-driven mouse melanoma [ChIP-seq]

Project description:Somatic oncogenic mutation of BRAF coupled with inactivation of PTEN constitute a frequent combination of genomic alterations driving development of human melanoma. Mice genetically engineered to conditionally express oncogenic BrafV600E and inactivate Pten in melanocytes following tamoxifen treatment rapidly develop melanoma. While early stage melanomas comprised melanin-pigmented Mitf and Dct-expressing cells, expression of these and other melanocyte identity genes was lost in later stage tumours that showed histological and molecular characteristics of de-differentiated neural crest type cells. Melanocyte identity genes displayed loss of active chromatin marks and RNA polymerase II and gain of heterochromatin marks indicating epigenetic reprogramming during tumour progression. Nevertheless, late stage tumour cells grown in culture re-expressed Mitf and melanocyte markers and Mitf together with Sox10 co-regulated a large number of genes essential for their growth. In this melanoma model, somatic inactivation that the catalytic Brg1 (Smarca4) subunit of the SWI/SNF complex and the scaffolding Bptf subunit of the NuRF delayed tumour formation and deregulated large and overlapping gene expression programs essential for normal tumour cell growth. Moreover, we show that Brg1 and Bptf co-regulated many genes together with Mitf and Sox10. Together these transcription factors and chromatin remodelling complexes orchestrate essential gene expression programs in mouse melanoma cells

2019-04-17 | GSE100998 | GEO

From pioneer to repressor: Bimodal foxd3 activity dynamically remodels neural crest regulatory landscape in vivo

Project description:The neural crest (NC) is a transient embryonic stem cell population characterised by its multipotency and broad developmental potential. Here, we perform NC-specific transcriptional and epigenomic profiling of foxd3-mutant versus wild-type cells in vivo to define the gene regulatory circuits controlling NC specification. Together with global binding analysis obtained by foxd3 biotin-ChIP and single cell profiles of foxd3-expressing premigratory NC, our analysis shows that during early steps of NC formation, foxd3 acts globally as a pioneer factor to prime the onset of genes regulating NC specification and migration by re-arranging the chromatin landscape, opening cis-regulatory elements and reshuffling nucleosomes. Strikingly, foxd3 then gradually switches from an activator to its previously well-described role as a transcriptional repressor. Taken together, these results demonstrate that foxd3 acts bimodally in the neural crest as a switch from ‘permissive’ to ‘repressive’ nucleosome/chromatin organisation to maintain multipotency and define cell fates.

2018-12-07 | GSE106676 | GEO

A Robust Method To Derive Functional Neural Crest Cells From Human Pluripotent Stem Cells

Project description:Neural crest (NC) cells contribute to the development of many complex tissues. The abnormal development of NC cells accounts for a number of congenital birth defects. Generating NC cells, and more specifically NC subpopulations such as cranial, cardiac, and trunk NC cells from human induced pluripotent stem (iPS) cells and human embryonic stem (ES) cells presents a valuable tool to model and study human NC development and disease. Here we provide a robust, efficient, and reproducible protocol for the differentiation of human iPS and ES cells into NC cells. The protocol has been validated in multiple human pluripotent stem cell lines and yields relatively pure NC cell populations in eight days. The resulting cells can be propagated and retain NC marker expression over multiple passages. The NC cells show proper cell specification and can develop into NC-derived cell lineages including smooth muscle cells, peripheral neurons, and Schwann cells. Additionally, the NC cells are functional and migrate to appropriate chemoattractants such as SDF-1, Fgf8b, BMP2, and Wnt3a. Importantly, this method generates all NC subpopulations (cranial, cardiac, and trunk) providing a great advantage to readily available NC differentiation methods. Neural crest cells derived from human induced pluripotent stem cells were profiled using Affymetrix Gene 1.0 arrays to identify differential gene expression changes and alternative exons from the open-source software AltAnalyze. An FDR adjusted emperical Bayes moderated t-test p < 0.05 was used to identify differentially expressed Ensembl genes and GO-Elite used to identify biologically relevant, Ontology, pathway and gene-set categories. Alternative exons were obtained using the FIRMA analysis option and default thresholds. Other array neural crest array and RNA-Seq dataset were compared to this to identify common and distinct regulatory mechanisms.

2013-08-16 | E-GEOD-44727 | biostudies-arrayexpress

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