Differential programs of melanocyte cell states
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA975369 | ENA |
REPOSITORIES: ENA
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Project description:This SuperSeries is composed of the SubSeries listed below.
2024-07-05 | GSE233198 | GEO
Project description:To elucidate mechanisms governing McSC self-renewal and differentiation we analyzed individual transcriptomes from thousands of melanocyte lineage cells during the regeneration process. We identified transcriptional signatures for McSCs, deciphered transcriptional changes and intermediate cell states during regeneration, and analyzed cell-cell signaling changes to discover mechanisms governing melanocyte regeneration.
2023-04-18 | GSE190115 | GEO
Project description:We sorted melanocyte nuclei from quiescent (telogen) skin, skin actively producing hair shafts (anagen), and skin exposed to UVB. With these sorted nuclei, we then utilized single-nucleus assay for transposase-accessible chromatin with high-throughput sequencing (snATAC-seq) and characterized three melanocyte lineages: quiescent McSCs (qMcSCs), activated McSCs (aMcSCs), and differentiated melanocytes (dMCs) that co-exist in all three skin conditions. Furthermore, we successfully identified differentially accessible genes and enriched transcription factor binding motifs for each melanocyte lineage. Our findings reveal potential gene regulators that determine these melanocyte cell states and provide new insights into how aMcSC chromatin states are regulated differently under divergent intrinsic and extrinsic cues. We also provide a publicly available online tool with a user-friendly interface to explore this comprehensive dataset, which will provide a resource for further studies on McSC regulation upon natural or UVB-mediated stem cell activation.
2023-07-18 | GSE232908 | GEO
Project description:Specification and differentiation of melanocytes is closely associated with their temporal localization. Melanocyte stem cells migrate extensively within defined trajectories before they undergo terminal differentiation to produce the photo-protective pigment, melanin. Cells adapt to the evolving developmental micro-environment via specialized cell surface receptors. To understand the responsive states and distinctive transcriptional states, fluorescently labeled melanocyte stem cells (24hpf and 34 hpf) or pigmented melanophores at 72hpf were isolated and their expression profiles were analysed as described below.
2024-07-01 | GSE189059 | GEO
Project description:Dissection of melanocyte stem cell transcriptomes during melanocyte regeneration in adult zebrafish
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Project description:The two most common melanoma histopathologic subtypes, superficial spreading (SSM) and nodular melanoma (NM), are believed to represent sequential phases of linear progression from radial to vertical growth. Studies suggest, however, that SSM and NM are biologically distinct. We utilized an integrative genomic approach to examine the possibility that SSM and NM are the result of independent pathways characterized by unique molecular alterations. Cell lines including SSM, NM, metastatic melanoma, and melanocyte controls were evaluated for copy number changes and differential mRNA expression using single nucleotide polymorphism array (SNP 6.0, Affymetrix) and gene array (U133A 2.0, Affymetrix). Data sets were integrated to identify copy number alterations that correlated with gene expression, and array results were validated using immunohistochemistry on human tissue microarrays (TMAs) and an external data set. The functional effect of genomic deletion was assessed by lentiviral overexpression. Integrative genomics revealed 8 genes in which NM/SSM-specific copy number alterations were correlated with NM/SSM differential gene expression (P<0.05, Spearman’s rank). Pathways analysis of differentially expressed genes (N=114) showed enrichment for metabolic-related processes. SSM-specific genomic deletions (DIS3, MTAP, G3BP2, SEC23IP, USO1) were verified in an expanded panel of cell lines, and forced overexpression of MTAP in SSM resulted in reduced cell growth. Metabolism-related gene ALDH7A1 was verified as overexpressed in NM using human TMAs.The identification of recurrent genomic deletions in SSM not present in NM challenges the linear model of melanoma progression and supports the unique molecular classification of SSM and NM. Gene expression profiling using Affymetrix U133A 2.0 arrays was performed on 18 melanoma cell lines including 2 primary superficial spreading melanoma, 2 primary nodular melanoma, 2 metastatic nodular melanoma, and 12 metastatic cell lines. Four melanocyte control lines were also evaluated including 2 immortalized melanocyte cell lines (Hermes 1 and 2B) and 2 normal melanocyte lines cultured from neonatal foreskin (HEM-N and HEM-LP).
2010-12-01 | E-GEOD-22301 | biostudies-arrayexpress
Project description:The epigenetic repressor BMI1 plays an integral role in promoting the self-renewal and proliferation of many adult stem cell populations, and also tumor types, primarily through silencing the Cdkn2a locus, which encodes the tumor suppressors p16Ink4a and p19Arf. However, in cutaneous melanoma, BMI1 drives epithelial-mesenchymal transition programs, and thus metastasis, while having little impact on proliferation or primary tumor growth. This raised questions about the requirement and role for BMI1 in melanocyte stem cell (MeSC) biology. Here, we demonstrate that murine melanocyte-specific Bmi1 deletion causes premature hair greying, which results from gradual MeSC loss. We establish that MeSC loss begins in the second hair cycle and is accompanied by melanocyte depletion. RNA-seq of MeSCs revealed that Bmi1 deletion induces transcriptional upregulation of p16Ink4a and p19Arf, mirroring the central role of BMI1 in other stem cell contexts. Additionally, the glutathione S-transferase enzymes Gsta1 and Gsta2 are downregulated by BMI1 loss, raising the possibility that MeSCs could be susceptible to oxidative stress. Accordingly, treatment with the antioxidant N-acetyl cysteine (NAC) partially rescued melanocyte expansion. Together, our data establish a critical role for BMI1 in MeSC maintenance that reflect a partial role for suppression of oxidative stress, and likely transcriptional repression of Cdkn2a.
2024-01-28 | GSE194373 | GEO
Project description:FOXP2 regulates differential transcriptional programs in human subplate
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Project description:Using ChIP-seq for p300 and H3K4me1, we identified 2,489 putative melanocyte enhancer loci in the mouse genome. We demonstrated that these putative enhancers are evolutionarily constrained, enriched for sequence motifs predicted to bind key melanocyte transcription factors, located near genes relevant to melanocyte biology, and capable of driving reporter gene expression with high frequency in cultured melanocytes and in melanocytes of transgenic zebrafish. ChIP-seq for EP300 and H3K4me1 in the mouse melanocyte cell line melan-a.
2012-09-14 | E-GEOD-38498 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE33092: Oncogenic BRAFV600E remodels the melanocyte transcriptome and induces BLNCR1 to regulate melanoma cell migration [HT-seq] GSE37132: Oncogenic BRAFV600E remodels the melanocyte transcriptome and induces BLNCR1 to regulate melanoma cell migration [Affymetrix] Refer to individual Series
2012-04-27 | E-GEOD-37169 | biostudies-arrayexpress