Comparative analysis of the molecular mechanisms of melanocyte regeneration and melanoma using the zebrafish model
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ABSTRACT:
PROVIDER: PRJEB49404 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR7720650_1.fastq.gz | Fastqsanger.gz | |||
| ERR7720650_2.fastq.gz | Fastqsanger.gz | |||
| ERR7720660_1.fastq.gz | Fastqsanger.gz | |||
| ERR7720660_2.fastq.gz | Fastqsanger.gz | |||
| ERR7720651_1.fastq.gz | Fastqsanger.gz |
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Project description:Zebrafish have the ability to regenerate many organs and tissues including the melanocytes which are elements of the skin. RNA sequencing (RNA-Seq) is a high-throughput sequencing method facilitating transcript identification and quantification of gene expression in a precise manner. The development of RNA-Seq technologies and their extensive data-analysis methods make an investigation of regulatory genes and functional gene annotations possible under specific conditions. Here, we aim to perform large-scale comparative deep transcriptome profiling of regeneration versus cancer in the following two cellular contexts: The skin melanocytes, which can substantially regenerate in mammals and melanoma which is the type of cancer that begins in the melanocytes.
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Project description:Dysregulated melanocyte state transitions are a pivotal driver of melanoma development, highlighting the need to identify key regulators of these processes. Understanding these factors is key to know how normal melanocyte functions and shift towards initiation of melanoma. Our study identifies Mgat4b, a glycosyl transferase involved in selective N-glycan branching enriched in pigment progenitors, as a key regulator of directional melanocyte migration and establishment of Melanocyte stem cell (McSC) pool during early development in zebrafish and mammalian melanocytes. Single cell RNA sequencing analysis in zebrafish upon targeted disruption of Mgat4b reveals that a subset of melanocytes marked by aberrant galectin expression are impaired in migration and are lost. Lectin binding proteomic analysis reveals the glycosylation of key melanocyte proteins Gpnmb, Kit, and Tyrp1 to be under the control of Mgat4b. Additionally, mislocalization of Gamma catenin (Jup) explains the observed defects in cell adhesion and migration to be regulated by mgat4b but not its isozyme mgat4a. Our meta-analysis further revealed that melanoma patients with both the BrafV600E mutation and elevated Mgat4b levels have significantly worse survival outcomes compared to those with only the BrafV600E mutation. By leveraging the MAZERATI platform to model BrafV600E driver mutation in vivo, we show that Mgat4b mutant cells fail to aggregate and initiate tumors. Our study underscores the importance of selective N-glycan branching in both melanocyte development and melanoma initiation, suggesting a Mitf controlled Mgat4b as a promising therapeutic target for melanoma treatment.
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Project description:Dysregulated melanocyte state transitions are a pivotal driver of melanoma development, highlighting the need to identify key regulators of these processes. Understanding these factors is key to know how normal melanocyte functions and shift towards initiation of melanoma. Our study identifies Mgat4b, a glycosyl transferase involved in selective N-glycan branching enriched in pigment progenitors, as a key regulator of directional melanocyte migration and establishment of Melanocyte stem cell (McSC) pool during early development in zebrafish and mammalian melanocytes. Single cell RNA sequencing analysis in zebrafish upon targeted disruption of Mgat4b reveals that a subset of melanocytes marked by aberrant galectin expression are impaired in migration and are lost. Lectin binding proteomic analysis reveals the glycosylation of key melanocyte proteins Gpnmb, Kit, and Tyrp1 to be under the control of Mgat4b. Additionally, mislocalization of Gamma catenin (Jup) explains the observed defects in cell adhesion and migration to be regulated by mgat4b but not its isozyme mgat4a. Our meta-analysis further revealed that melanoma patients with both the BrafV600E mutation and elevated Mgat4b levels have significantly worse survival outcomes compared to those with only the BrafV600E mutation. By leveraging the MAZERATI platform to model BrafV600E driver mutation in vivo, we show that Mgat4b mutant cells fail to aggregate and initiate tumors. Our study underscores the importance of selective N-glycan branching in both melanocyte development and melanoma initiation, suggesting a Mitf controlled Mgat4b as a promising therapeutic target for melanoma treatment.
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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).
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Project description:Ischemic cardiopathy is the leading cause of death in the world, for which efficient regenerative therapy is not currently available. In mammals, after a myocardial infarction episode, the damaged myocardium is replaced by scar tissue featuring collagen deposition and tissue remodelling with negligible cardiomyocyte proliferation. Zebrafish, in contrast, display an extensive regenerative capacity as they are able to restore completely lost cardiac tissue after partial ventricular amputation. Due to the lack of genetic lineage tracing evidence, it is not yet clear if new cardiomyocytes arise from existing contractile cells or from an uncharacterised set of progenitors cells. Nonetheless, several genes and molecules have been shown to participate in this process, some of them being cardiomyocyte mitogens in vitro. Though questions as what are the early signals that drive the regenerative response and what is the relative role of each cardiac cell in this process still need to be answered, the zebrafish is emerging as a very valuable tool to understand heart regeneration and devise strategies that may be of potential value to treat human cardiac disease. Here, we performed a genome-wide transcriptome profile analysis focusing on the early time points of zebrafish heart regeneration and compared our results with those of previously published data. Our analyses confirmed the differential expression of several transcripts, and identified additional genes the expression of which is differentially regulated during zebrafish heart regeneration. We validated the microarray data by conventional and/or quantitative RT-PCR. For a subset of these genes, their expression pattern was analyzed by in situ hybridization and shown to be upregulated in the regenerating area of the heart. The specific role of these new transcripts during zebrafish heart regeneration was further investigated ex vivo using primary cultures of zebrafish cardiomyocytes and/or epicardial cells. Our results offer new insights into the biology of heart regeneration in the zebrafish and, together with future experiments in mammals, may be of potential interest for clinical applications. In order to study zebrafish heart regeneration, a time course experiment was realized where amputated heart regenerating were compared to control heart. Samples in triplicate were extracted at 1, 3, 5 and 7 days post-amputation.
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