metadata: run_metadata: 12 rows where experiment.library_layout = "PAIRED", technology = "bulk" and tissue

12 rows where experiment.library_layout = "PAIRED", technology = "bulk" and tissue_curation = "Skin"

descending

Link	rowid ▼	run.accession	experiment.accession	sample.accession	study.accession	bioproject	study.title	study.alias	study.type	study.abstract	study.PMIDs	sample.title	sample.alias	sample.attributes	GEOsample.title	GEOsample.dataprocessing	GEOsample.source	GEOsample.extractprotocol	GEOsample.characteristics	GEOsample.accession	experiment.title	experiment.alias	experiment.library_name	experiment.design_description	experiment.library_construction_protocol	experiment.library_strategy	experiment.library_source	experiment.library_selection	experiment.library_layout	experiment.platform	experiment.instrument_model	experiment.study_ref	run.attributes	run.filename	run.semantic_name	run.total_bases	run.total_spots	run.alias	run.read_lengths	run.base_counts	run.r1_length	run.r2_length	run.Acount	run.Ccount	run.Gcount	run.Tcount	run.Ncount	run.experiment	run.pool_member	submission.accession	submission.srasource	submission.bioprojectsource	seqdetective.n_mates	seqdetective.mapping_rate.mate1	seqdetective.mapping_rate.mate2	seqdetective.nofeature_rate.mate1	seqdetective.nofeature_rate.mate2	seqdetective.sparsity.mate1	seqdetective.sparsity.mate2	seqdetective.pos_strand_rate.mate1	seqdetective.pos_strand_rate.mate2	seqdetective.readlen.mate1	seqdetective.readlen.mate2	seqdetective.judgement.mate1	seqdetective.judgement.mate2	seqdetective.judgement.reason	platform_family	instrument_generation	read_bias	selection_class	prep_kit	sc_or_bulk	tech_class	technology	submission.bioprojectsource.country	earliest_date	devstage_curation	devstage_curation_coarse	tissue_curation	tissue_curation_coarse
33894	33894	SRR30866028	SRX26263941	SRS22803195	SRP536275	PRJNA1168148	Mgat4b mediated selective N glycosyl modification regulates melanocyte development and melanoma progression [bulk RNA seq]	GSE278653	Transcriptome Analysis	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. Overall design: To investigate the mechanisms that inhibit mutant cells from initiating melanoma in the absence of mgat4b we utilized mature melanophores and melanoma cells from the skin of five zebrafish including both MAZERATI wild type and MAZERATI zebrafish carrying mgat4b mutations. We then performed gene expression profiling analysis using data obtained from RNA seq of m…		m4b mut melanoma biol rep 2	GSM8552314	source name:skin\|tissue:skin\|cell type:melanoma\|genotype:mgat4b mutant\|treatment:MAZERATI\|geo loc name:missing\|collection date:missing	m4b mut melanoma biol rep 2	Raw fastq files were trimmed using trimmomatic to remove adaptors and retain high quality reads. The reads were then aligned with zebrafish reference assembly GRCz11 using STAR. Featurecounts was used to calculate raw counts from the aligned reads. Assembly: GRCz11 Supplementary files format and content: tab delimited text file including raw counts for each sample	skin	The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction	tissue:skin\|cell type:melanoma\|genotype:mgat4b mutant\|treatment:MAZERATI	GSM8552314	GSM8552314: m4b mut melanoma biol rep 2; Danio rerio; RNA Seq	GSM8552314 r1	GSM8552314	1	The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 2000	SRP536275		MKO2_S39_R1_001.fastq.gz MKO2_S39_R2_001.fastq.gz	fastq fastq	3705364625.0	14164066.0	GSM8552314 r1	0:126.72 1:134.89	A:785806700;C:949078797;G:1178279032;T:784972987;N:7227109	126	134	785806700	949078797	1178279032	784972987	7227109	SRX26263941	SRS22803195	SRA1984938	Pigment Cell Biology Lab, CSIR-IGIB	Pigment Cell Biology Lab, CSIR-IGIB												B	B	biological fallback assumption	illumina	nextseq_v2	unknown	cdna_unspecified	trueseq	sc_generic	bulk	bulk	India	2024-10-02	Undetermined	Undetermined	Skin	Surface Structure
33895	33895	SRR30866029	SRX26263940	SRS22803194	SRP536275	PRJNA1168148	Mgat4b mediated selective N glycosyl modification regulates melanocyte development and melanoma progression [bulk RNA seq]	GSE278653	Transcriptome Analysis	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. Overall design: To investigate the mechanisms that inhibit mutant cells from initiating melanoma in the absence of mgat4b we utilized mature melanophores and melanoma cells from the skin of five zebrafish including both MAZERATI wild type and MAZERATI zebrafish carrying mgat4b mutations. We then performed gene expression profiling analysis using data obtained from RNA seq of m…		m4b mut melanoma biol rep 1	GSM8552313	source name:skin\|tissue:skin\|cell type:melanoma\|genotype:mgat4b mutant\|treatment:MAZERATI\|geo loc name:missing\|collection date:missing	m4b mut melanoma biol rep 1	Raw fastq files were trimmed using trimmomatic to remove adaptors and retain high quality reads. The reads were then aligned with zebrafish reference assembly GRCz11 using STAR. Featurecounts was used to calculate raw counts from the aligned reads. Assembly: GRCz11 Supplementary files format and content: tab delimited text file including raw counts for each sample	skin	The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction	tissue:skin\|cell type:melanoma\|genotype:mgat4b mutant\|treatment:MAZERATI	GSM8552313	GSM8552313: m4b mut melanoma biol rep 1; Danio rerio; RNA Seq	GSM8552313 r1	GSM8552313	1	The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 2000	SRP536275		MKO1_S38_R1_001.fastq.gz MKO1_S38_R2_001.fastq.gz	fastq fastq	4779377372.0	18058294.0	GSM8552313 r1	0:128.72 1:135.94	A:1016908920;C:1236613888;G:1502465334;T:1018053808;N:5335422	128	135	1016908920	1236613888	1502465334	1018053808	5335422	SRX26263940	SRS22803194	SRA1984938	Pigment Cell Biology Lab, CSIR-IGIB	Pigment Cell Biology Lab, CSIR-IGIB												B	B	biological fallback assumption	illumina	nextseq_v2	unknown	cdna_unspecified	trueseq	sc_generic	bulk	bulk	India	2024-10-02	Undetermined	Undetermined	Skin	Surface Structure
33896	33896	SRR30866030	SRX26263939	SRS22803193	SRP536275	PRJNA1168148	Mgat4b mediated selective N glycosyl modification regulates melanocyte development and melanoma progression [bulk RNA seq]	GSE278653	Transcriptome Analysis	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. Overall design: To investigate the mechanisms that inhibit mutant cells from initiating melanoma in the absence of mgat4b we utilized mature melanophores and melanoma cells from the skin of five zebrafish including both MAZERATI wild type and MAZERATI zebrafish carrying mgat4b mutations. We then performed gene expression profiling analysis using data obtained from RNA seq of m…		wild type melanoma control biol rep 2	GSM8552312	source name:skin\|tissue:skin\|cell type:melanoma\|genotype:WT\|treatment:MAZERATI\|geo loc name:missing\|collection date:missing	wild type melanoma control biol rep 2	Raw fastq files were trimmed using trimmomatic to remove adaptors and retain high quality reads. The reads were then aligned with zebrafish reference assembly GRCz11 using STAR. Featurecounts was used to calculate raw counts from the aligned reads. Assembly: GRCz11 Supplementary files format and content: tab delimited text file including raw counts for each sample	skin	The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction	tissue:skin\|cell type:melanoma\|genotype:WT\|treatment:MAZERATI	GSM8552312	GSM8552312: wild type melanoma control biol rep 2; Danio rerio; RNA Seq	GSM8552312 r1	GSM8552312	1	The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 2000	SRP536275		EV2_S37_R1_001.fastq.gz EV2_S37_R2_001.fastq.gz	fastq fastq	5427379509.0	19981504.0	GSM8552312 r1	0:133.16 1:138.46	A:1136639418;C:1414638483;G:1736492639;T:1137614638;N:1994331	133	138	1136639418	1414638483	1736492639	1137614638	1994331	SRX26263939	SRS22803193	SRA1984938	Pigment Cell Biology Lab, CSIR-IGIB	Pigment Cell Biology Lab, CSIR-IGIB												B	B	biological fallback assumption	illumina	nextseq_v2	unknown	cdna_unspecified	trueseq	sc_generic	bulk	bulk	India	2024-10-02	Undetermined	Undetermined	Skin	Surface Structure
33897	33897	SRR30866031	SRX26263938	SRS22803192	SRP536275	PRJNA1168148	Mgat4b mediated selective N glycosyl modification regulates melanocyte development and melanoma progression [bulk RNA seq]	GSE278653	Transcriptome Analysis	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. Overall design: To investigate the mechanisms that inhibit mutant cells from initiating melanoma in the absence of mgat4b we utilized mature melanophores and melanoma cells from the skin of five zebrafish including both MAZERATI wild type and MAZERATI zebrafish carrying mgat4b mutations. We then performed gene expression profiling analysis using data obtained from RNA seq of m…		wild type melanoma control biol rep 1	GSM8552311	source name:skin\|tissue:skin\|cell type:melanoma\|genotype:WT\|treatment:MAZERATI\|geo loc name:missing\|collection date:missing	wild type melanoma control biol rep 1	Raw fastq files were trimmed using trimmomatic to remove adaptors and retain high quality reads. The reads were then aligned with zebrafish reference assembly GRCz11 using STAR. Featurecounts was used to calculate raw counts from the aligned reads. Assembly: GRCz11 Supplementary files format and content: tab delimited text file including raw counts for each sample	skin	The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction	tissue:skin\|cell type:melanoma\|genotype:WT\|treatment:MAZERATI	GSM8552311	GSM8552311: wild type melanoma control biol rep 1; Danio rerio; RNA Seq	GSM8552311 r1	GSM8552311	1	The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 2000	SRP536275		EV1_S36_R1_001.fastq.gz EV1_S36_R2_001.fastq.gz	fastq fastq	5248108957.0	19087024.0	GSM8552311 r1	0:135.12 1:139.84	A:1112163842;C:1354895660;G:1658732932;T:1120342985;N:1973538	135	139	1112163842	1354895660	1658732932	1120342985	1973538	SRX26263938	SRS22803192	SRA1984938	Pigment Cell Biology Lab, CSIR-IGIB	Pigment Cell Biology Lab, CSIR-IGIB												B	B	biological fallback assumption	illumina	nextseq_v2	unknown	cdna_unspecified	trueseq	sc_generic	bulk	bulk	India	2024-10-02	Undetermined	Undetermined	Skin	Surface Structure
33898	33898	SRR30866032	SRX26263937	SRS22803191	SRP536275	PRJNA1168148	Mgat4b mediated selective N glycosyl modification regulates melanocyte development and melanoma progression [bulk RNA seq]	GSE278653	Transcriptome Analysis	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. Overall design: To investigate the mechanisms that inhibit mutant cells from initiating melanoma in the absence of mgat4b we utilized mature melanophores and melanoma cells from the skin of five zebrafish including both MAZERATI wild type and MAZERATI zebrafish carrying mgat4b mutations. We then performed gene expression profiling analysis using data obtained from RNA seq of m…		melanophore biol rep 2	GSM8552310	source name:skin\|tissue:skin\|cell type:melanophore\|genotype:WT\|treatment:No\|geo loc name:missing\|collection date:missing	melanophore biol rep 2	Raw fastq files were trimmed using trimmomatic to remove adaptors and retain high quality reads. The reads were then aligned with zebrafish reference assembly GRCz11 using STAR. Featurecounts was used to calculate raw counts from the aligned reads. Assembly: GRCz11 Supplementary files format and content: tab delimited text file including raw counts for each sample	skin	The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction	tissue:skin\|cell type:melanophore\|genotype:WT\|treatment:No	GSM8552310	GSM8552310: melanophore biol rep 2; Danio rerio; RNA Seq	GSM8552310 r1	GSM8552310	1	The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 2000	SRP536275		WT2_S41_R1_001.fastq.gz WT2_S41_R2_001.fastq.gz	fastq fastq	4636631881.0	16340506.0	GSM8552310 r1	0:140.47 1:143.28	A:1114533149;C:1104066636;G:1293649625;T:1122672029;N:1710442	140	143	1114533149	1104066636	1293649625	1122672029	1710442	SRX26263937	SRS22803191	SRA1984938	Pigment Cell Biology Lab, CSIR-IGIB	Pigment Cell Biology Lab, CSIR-IGIB												B	B	biological fallback assumption	illumina	nextseq_v2	unknown	cdna_unspecified	trueseq	sc_generic	bulk	bulk	India	2024-10-02	Undetermined	Undetermined	Skin	Surface Structure
33899	33899	SRR30866033	SRX26263936	SRS22803190	SRP536275	PRJNA1168148	Mgat4b mediated selective N glycosyl modification regulates melanocyte development and melanoma progression [bulk RNA seq]	GSE278653	Transcriptome Analysis	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. Overall design: To investigate the mechanisms that inhibit mutant cells from initiating melanoma in the absence of mgat4b we utilized mature melanophores and melanoma cells from the skin of five zebrafish including both MAZERATI wild type and MAZERATI zebrafish carrying mgat4b mutations. We then performed gene expression profiling analysis using data obtained from RNA seq of m…		melanophore biol rep 1	GSM8552309	source name:skin\|tissue:skin\|cell type:melanophore\|genotype:WT\|treatment:No\|geo loc name:missing\|collection date:missing	melanophore biol rep 1	Raw fastq files were trimmed using trimmomatic to remove adaptors and retain high quality reads. The reads were then aligned with zebrafish reference assembly GRCz11 using STAR. Featurecounts was used to calculate raw counts from the aligned reads. Assembly: GRCz11 Supplementary files format and content: tab delimited text file including raw counts for each sample	skin	The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction	tissue:skin\|cell type:melanophore\|genotype:WT\|treatment:No	GSM8552309	GSM8552309: melanophore biol rep 1; Danio rerio; RNA Seq	GSM8552309 r1	GSM8552309	1	The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	NextSeq 2000	SRP536275		WT1_S40_R1_001.fastq.gz WT1_S40_R2_001.fastq.gz	fastq fastq	5185761246.0	18118534.0	GSM8552309 r1	0:141.81 1:144.40	A:1231235669;C:1235759770;G:1476864583;T:1240636871;N:1264353	141	144	1231235669	1235759770	1476864583	1240636871	1264353	SRX26263936	SRS22803190	SRA1984938	Pigment Cell Biology Lab, CSIR-IGIB	Pigment Cell Biology Lab, CSIR-IGIB												B	B	biological fallback assumption	illumina	nextseq_v2	unknown	cdna_unspecified	trueseq	sc_generic	bulk	bulk	India	2024-10-02	Undetermined	Undetermined	Skin	Surface Structure
69552	69552	SRR18901596	SRX14979865	SRS12729755	SRP371883	PRJNA831276	Lipid droplets are a metabolic vulnerability in melanoma	GSE201378	Transcriptome Analysis	Melanoma exhibits numerous transcriptional cell states including neural crest like cells as well as pigmented melanocytic cells. How these different cell states relate to distinct tumorigenic phenotypes remains unclear. Here we use a zebrafish melanoma model to identify a transcriptional program linking the melanocytic cell state to a dependence on lipid droplets the specialized organelle responsible for lipid storage. Single cell RNA sequencing of these tumors show a concordance between genes regulating pigmentation and those involved in lipid and oxidative metabolism. This state is conserved across human melanoma cell lines and patient tumors. This melanocytic state demonstrates increased fatty acid uptake an increased number of lipid droplets and dependence upon fatty acid oxidative metabolism. Genetic and pharmacologic suppression of lipid droplet production is sufficient to disrupt cell cycle progression and slow melanoma growth in vivo. Because the melanocytic cell state is linked to poor outcomes in patients these data indicate a metabolic vulnerability in melanoma that depends on the lipid droplet organelle. Overall design: Expression profiling by high throughput sequencing of zebrafish melanoma	pubmed:37268606	sgDGAT1a 3 bulk RNAseq	GSM6062270	source name:Skin\|tissue:Skin\|cell type:melanoma\|genotype:DGAT1a knockout	sgDGAT1a 3 bulk RNAseq	Sequencing reads underwent quality control with FASTQC 0.11.9 trimming with TRIMMOMATIC 14.0.1 and aligned using Salmon 1.4.0 to the danio rerio GRCz11. Data analysis was conducted in R version 4.0.5. Differential expression and normalized counts were calculated using DESeq2 1.30.1 using default parameters. Normalized counts derived from DESeq2 processing. Data was processed using R version 4.0.5 and Seurat version 4.0.2. Cells with fewer than 200 unique genes and mitochondrial genes above 30% were filtered. Expression data was normalized using SCTransform with principal component analysis and UMAP dimensionality reduction performed at default parameters. Clustering was performed using the Seurat function FindClusters with resolution of 0.4. Cluster annotation for zebrafish cell type specific marker genes as done previously using FindAllMarkers. Assembly: GRCz11	Skin	Zebrafish tumors were dissected and sorted for tdTomato+ cells using the BD FACSAria cell sorter. Library construction followed the SMARTer Universal Low Input RNA Kit for Sequencing Takara according to manufacturer's instructions.	tissue:Skin\|cell type:melanoma\|genotype:DGAT1a knockout	GSM6062270	GSM6062270: sgDGAT1a 3 bulk RNAseq; Danio rerio; RNA Seq	GSM6062270 r1	GSM6062270	1	Zebrafish tumors were dissected and sorted for tdTomato+ cells using the BD FACSAria cell sorter. Library construction followed the SMARTer Universal Low Input RNA Kit for Sequencing Takara according to manufacturer's instructions.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq 6000	SRP371883	loader:fastq load.py	DGAT1a_3_R1.fastq.gz DGAT1a_3_R2.fastq.gz	fastq fastq	6999632088.0	34651644.0	GSM6062270 r1	0:101 1:101	A:1966677410;C:1379731640;G:1488012081;T:2165132052;N:78905	101	101	1966677410	1379731640	1488012081	2165132052	78905	SRX14979865	SRS12729755	SRA1408865	Richard M. White, Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center	Richard M. White, Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center	2	0.92364	0.83987	0.12298	0.10958	0.7289	0.75205	0.55329	0.53686	101	101	B	B	biological fallback assumption	illumina	novaseq_era	full_length	cdna_unspecified	smarter	sc_generic	bulk	bulk	United States	2022-04-23	Undetermined	Undetermined	Skin	Surface Structure
69553	69553	SRR18901597	SRX14979864	SRS12729754	SRP371883	PRJNA831276	Lipid droplets are a metabolic vulnerability in melanoma	GSE201378	Transcriptome Analysis	Melanoma exhibits numerous transcriptional cell states including neural crest like cells as well as pigmented melanocytic cells. How these different cell states relate to distinct tumorigenic phenotypes remains unclear. Here we use a zebrafish melanoma model to identify a transcriptional program linking the melanocytic cell state to a dependence on lipid droplets the specialized organelle responsible for lipid storage. Single cell RNA sequencing of these tumors show a concordance between genes regulating pigmentation and those involved in lipid and oxidative metabolism. This state is conserved across human melanoma cell lines and patient tumors. This melanocytic state demonstrates increased fatty acid uptake an increased number of lipid droplets and dependence upon fatty acid oxidative metabolism. Genetic and pharmacologic suppression of lipid droplet production is sufficient to disrupt cell cycle progression and slow melanoma growth in vivo. Because the melanocytic cell state is linked to poor outcomes in patients these data indicate a metabolic vulnerability in melanoma that depends on the lipid droplet organelle. Overall design: Expression profiling by high throughput sequencing of zebrafish melanoma	pubmed:37268606	sgDGAT1a 2 bulk RNAseq	GSM6062269	source name:Skin\|tissue:Skin\|cell type:melanoma\|genotype:DGAT1a knockout	sgDGAT1a 2 bulk RNAseq	Sequencing reads underwent quality control with FASTQC 0.11.9 trimming with TRIMMOMATIC 14.0.1 and aligned using Salmon 1.4.0 to the danio rerio GRCz11. Data analysis was conducted in R version 4.0.5. Differential expression and normalized counts were calculated using DESeq2 1.30.1 using default parameters. Normalized counts derived from DESeq2 processing. Data was processed using R version 4.0.5 and Seurat version 4.0.2. Cells with fewer than 200 unique genes and mitochondrial genes above 30% were filtered. Expression data was normalized using SCTransform with principal component analysis and UMAP dimensionality reduction performed at default parameters. Clustering was performed using the Seurat function FindClusters with resolution of 0.4. Cluster annotation for zebrafish cell type specific marker genes as done previously using FindAllMarkers. Assembly: GRCz11	Skin	Zebrafish tumors were dissected and sorted for tdTomato+ cells using the BD FACSAria cell sorter. Library construction followed the SMARTer Universal Low Input RNA Kit for Sequencing Takara according to manufacturer's instructions.	tissue:Skin\|cell type:melanoma\|genotype:DGAT1a knockout	GSM6062269	GSM6062269: sgDGAT1a 2 bulk RNAseq; Danio rerio; RNA Seq	GSM6062269 r1	GSM6062269	1	Zebrafish tumors were dissected and sorted for tdTomato+ cells using the BD FACSAria cell sorter. Library construction followed the SMARTer Universal Low Input RNA Kit for Sequencing Takara according to manufacturer's instructions.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq 6000	SRP371883	loader:fastq load.py	DGAT1a_2_R1.fastq.gz DGAT1a_2_R2.fastq.gz	fastq fastq	8251144500.0	40847250.0	GSM6062269 r1	0:101 1:101	A:2347333328;C:1614724681;G:1750159235;T:2538833381;N:93875	101	101	2347333328	1614724681	1750159235	2538833381	93875	SRX14979864	SRS12729754	SRA1408865	Richard M. White, Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center	Richard M. White, Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center	2	0.91689	0.85062	0.17154	0.15832	0.7135	0.73357	0.55242	0.53573	101	101	B	B	biological fallback assumption	illumina	novaseq_era	full_length	cdna_unspecified	smarter	sc_generic	bulk	bulk	United States	2022-04-23	Undetermined	Undetermined	Skin	Surface Structure
69554	69554	SRR18901598	SRX14979863	SRS12729783	SRP371883	PRJNA831276	Lipid droplets are a metabolic vulnerability in melanoma	GSE201378	Transcriptome Analysis	Melanoma exhibits numerous transcriptional cell states including neural crest like cells as well as pigmented melanocytic cells. How these different cell states relate to distinct tumorigenic phenotypes remains unclear. Here we use a zebrafish melanoma model to identify a transcriptional program linking the melanocytic cell state to a dependence on lipid droplets the specialized organelle responsible for lipid storage. Single cell RNA sequencing of these tumors show a concordance between genes regulating pigmentation and those involved in lipid and oxidative metabolism. This state is conserved across human melanoma cell lines and patient tumors. This melanocytic state demonstrates increased fatty acid uptake an increased number of lipid droplets and dependence upon fatty acid oxidative metabolism. Genetic and pharmacologic suppression of lipid droplet production is sufficient to disrupt cell cycle progression and slow melanoma growth in vivo. Because the melanocytic cell state is linked to poor outcomes in patients these data indicate a metabolic vulnerability in melanoma that depends on the lipid droplet organelle. Overall design: Expression profiling by high throughput sequencing of zebrafish melanoma	pubmed:37268606	sgDGAT1a 1 bulk RNAseq	GSM6062268	source name:Skin\|tissue:Skin\|cell type:melanoma\|genotype:DGAT1a knockout	sgDGAT1a 1 bulk RNAseq	Sequencing reads underwent quality control with FASTQC 0.11.9 trimming with TRIMMOMATIC 14.0.1 and aligned using Salmon 1.4.0 to the danio rerio GRCz11. Data analysis was conducted in R version 4.0.5. Differential expression and normalized counts were calculated using DESeq2 1.30.1 using default parameters. Normalized counts derived from DESeq2 processing. Data was processed using R version 4.0.5 and Seurat version 4.0.2. Cells with fewer than 200 unique genes and mitochondrial genes above 30% were filtered. Expression data was normalized using SCTransform with principal component analysis and UMAP dimensionality reduction performed at default parameters. Clustering was performed using the Seurat function FindClusters with resolution of 0.4. Cluster annotation for zebrafish cell type specific marker genes as done previously using FindAllMarkers. Assembly: GRCz11	Skin	Zebrafish tumors were dissected and sorted for tdTomato+ cells using the BD FACSAria cell sorter. Library construction followed the SMARTer Universal Low Input RNA Kit for Sequencing Takara according to manufacturer's instructions.	tissue:Skin\|cell type:melanoma\|genotype:DGAT1a knockout	GSM6062268	GSM6062268: sgDGAT1a 1 bulk RNAseq; Danio rerio; RNA Seq	GSM6062268 r1	GSM6062268	1	Zebrafish tumors were dissected and sorted for tdTomato+ cells using the BD FACSAria cell sorter. Library construction followed the SMARTer Universal Low Input RNA Kit for Sequencing Takara according to manufacturer's instructions.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq 6000	SRP371883	loader:fastq load.py	DGAT1a_1_R1.fastq.gz DGAT1a_1_R2.fastq.gz	fastq fastq	18660768484.0	92380042.0	GSM6062268 r1	0:101 1:101	A:5305116678;C:3630125100;G:3862694653;T:5862619976;N:212077	101	101	5305116678	3630125100	3862694653	5862619976	212077	SRX14979863	SRS12729783	SRA1408865	Richard M. White, Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center	Richard M. White, Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center	2	0.91727	0.83321	0.16534	0.14775	0.71037	0.73594	0.53932	0.52443	101	101	B	B	biological fallback assumption	illumina	novaseq_era	full_length	cdna_unspecified	smarter	sc_generic	bulk	bulk	United States	2022-04-23	Undetermined	Undetermined	Skin	Surface Structure
69555	69555	SRR18901599	SRX14979862	SRS12729753	SRP371883	PRJNA831276	Lipid droplets are a metabolic vulnerability in melanoma	GSE201378	Transcriptome Analysis	Melanoma exhibits numerous transcriptional cell states including neural crest like cells as well as pigmented melanocytic cells. How these different cell states relate to distinct tumorigenic phenotypes remains unclear. Here we use a zebrafish melanoma model to identify a transcriptional program linking the melanocytic cell state to a dependence on lipid droplets the specialized organelle responsible for lipid storage. Single cell RNA sequencing of these tumors show a concordance between genes regulating pigmentation and those involved in lipid and oxidative metabolism. This state is conserved across human melanoma cell lines and patient tumors. This melanocytic state demonstrates increased fatty acid uptake an increased number of lipid droplets and dependence upon fatty acid oxidative metabolism. Genetic and pharmacologic suppression of lipid droplet production is sufficient to disrupt cell cycle progression and slow melanoma growth in vivo. Because the melanocytic cell state is linked to poor outcomes in patients these data indicate a metabolic vulnerability in melanoma that depends on the lipid droplet organelle. Overall design: Expression profiling by high throughput sequencing of zebrafish melanoma	pubmed:37268606	sgNT 3 bulk RNAseq	GSM6062267	source name:Skin\|tissue:Skin\|cell type:melanoma\|genotype:WT	sgNT 3 bulk RNAseq	Sequencing reads underwent quality control with FASTQC 0.11.9 trimming with TRIMMOMATIC 14.0.1 and aligned using Salmon 1.4.0 to the danio rerio GRCz11. Data analysis was conducted in R version 4.0.5. Differential expression and normalized counts were calculated using DESeq2 1.30.1 using default parameters. Normalized counts derived from DESeq2 processing. Data was processed using R version 4.0.5 and Seurat version 4.0.2. Cells with fewer than 200 unique genes and mitochondrial genes above 30% were filtered. Expression data was normalized using SCTransform with principal component analysis and UMAP dimensionality reduction performed at default parameters. Clustering was performed using the Seurat function FindClusters with resolution of 0.4. Cluster annotation for zebrafish cell type specific marker genes as done previously using FindAllMarkers. Assembly: GRCz11	Skin	Zebrafish tumors were dissected and sorted for tdTomato+ cells using the BD FACSAria cell sorter. Library construction followed the SMARTer Universal Low Input RNA Kit for Sequencing Takara according to manufacturer's instructions.	tissue:Skin\|cell type:melanoma\|genotype:WT	GSM6062267	GSM6062267: sgNT 3 bulk RNAseq; Danio rerio; RNA Seq	GSM6062267 r1	GSM6062267	1	Zebrafish tumors were dissected and sorted for tdTomato+ cells using the BD FACSAria cell sorter. Library construction followed the SMARTer Universal Low Input RNA Kit for Sequencing Takara according to manufacturer's instructions.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq 6000	SRP371883	loader:fastq load.py	NT_3_R1.fastq.gz NT_3_R2.fastq.gz	fastq fastq	11541383120.0	57135560.0	GSM6062267 r1	0:101 1:101	A:3251133156;C:2311327780;G:2454133526;T:3524658644;N:130014	101	101	3251133156	2311327780	2454133526	3524658644	130014	SRX14979862	SRS12729753	SRA1408865	Richard M. White, Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center	Richard M. White, Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center	2	0.91632	0.84851	0.15351	0.14147	0.71366	0.73294	0.51256	0.49995	101	101	B	B	biological fallback assumption	illumina	novaseq_era	full_length	cdna_unspecified	smarter	sc_generic	bulk	bulk	United States	2022-04-23	Undetermined	Undetermined	Skin	Surface Structure
69556	69556	SRR18901600	SRX14979861	SRS12729752	SRP371883	PRJNA831276	Lipid droplets are a metabolic vulnerability in melanoma	GSE201378	Transcriptome Analysis	Melanoma exhibits numerous transcriptional cell states including neural crest like cells as well as pigmented melanocytic cells. How these different cell states relate to distinct tumorigenic phenotypes remains unclear. Here we use a zebrafish melanoma model to identify a transcriptional program linking the melanocytic cell state to a dependence on lipid droplets the specialized organelle responsible for lipid storage. Single cell RNA sequencing of these tumors show a concordance between genes regulating pigmentation and those involved in lipid and oxidative metabolism. This state is conserved across human melanoma cell lines and patient tumors. This melanocytic state demonstrates increased fatty acid uptake an increased number of lipid droplets and dependence upon fatty acid oxidative metabolism. Genetic and pharmacologic suppression of lipid droplet production is sufficient to disrupt cell cycle progression and slow melanoma growth in vivo. Because the melanocytic cell state is linked to poor outcomes in patients these data indicate a metabolic vulnerability in melanoma that depends on the lipid droplet organelle. Overall design: Expression profiling by high throughput sequencing of zebrafish melanoma	pubmed:37268606	sgNT 2 bulk RNAseq	GSM6062266	source name:Skin\|tissue:Skin\|cell type:melanoma\|genotype:WT	sgNT 2 bulk RNAseq	Sequencing reads underwent quality control with FASTQC 0.11.9 trimming with TRIMMOMATIC 14.0.1 and aligned using Salmon 1.4.0 to the danio rerio GRCz11. Data analysis was conducted in R version 4.0.5. Differential expression and normalized counts were calculated using DESeq2 1.30.1 using default parameters. Normalized counts derived from DESeq2 processing. Data was processed using R version 4.0.5 and Seurat version 4.0.2. Cells with fewer than 200 unique genes and mitochondrial genes above 30% were filtered. Expression data was normalized using SCTransform with principal component analysis and UMAP dimensionality reduction performed at default parameters. Clustering was performed using the Seurat function FindClusters with resolution of 0.4. Cluster annotation for zebrafish cell type specific marker genes as done previously using FindAllMarkers. Assembly: GRCz11	Skin	Zebrafish tumors were dissected and sorted for tdTomato+ cells using the BD FACSAria cell sorter. Library construction followed the SMARTer Universal Low Input RNA Kit for Sequencing Takara according to manufacturer's instructions.	tissue:Skin\|cell type:melanoma\|genotype:WT	GSM6062266	GSM6062266: sgNT 2 bulk RNAseq; Danio rerio; RNA Seq	GSM6062266 r1	GSM6062266	1	Zebrafish tumors were dissected and sorted for tdTomato+ cells using the BD FACSAria cell sorter. Library construction followed the SMARTer Universal Low Input RNA Kit for Sequencing Takara according to manufacturer's instructions.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq 6000	SRP371883	loader:fastq load.py	NT_2_R1.fastq.gz NT_2_R2.fastq.gz	fastq fastq	12944530468.0	64081834.0	GSM6062266 r1	0:101 1:101	A:3642085778;C:2657512300;G:2804491849;T:3840293107;N:147434	101	101	3642085778	2657512300	2804491849	3840293107	147434	SRX14979861	SRS12729752	SRA1408865	Richard M. White, Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center	Richard M. White, Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center	2	0.91453	0.86557	0.10035	0.0905	0.73261	0.7428	0.52684	0.51769	101	101	B	B	biological fallback assumption	illumina	novaseq_era	full_length	cdna_unspecified	smarter	sc_generic	bulk	bulk	United States	2022-04-23	Undetermined	Undetermined	Skin	Surface Structure
69557	69557	SRR18901601	SRX14979860	SRS12729751	SRP371883	PRJNA831276	Lipid droplets are a metabolic vulnerability in melanoma	GSE201378	Transcriptome Analysis	Melanoma exhibits numerous transcriptional cell states including neural crest like cells as well as pigmented melanocytic cells. How these different cell states relate to distinct tumorigenic phenotypes remains unclear. Here we use a zebrafish melanoma model to identify a transcriptional program linking the melanocytic cell state to a dependence on lipid droplets the specialized organelle responsible for lipid storage. Single cell RNA sequencing of these tumors show a concordance between genes regulating pigmentation and those involved in lipid and oxidative metabolism. This state is conserved across human melanoma cell lines and patient tumors. This melanocytic state demonstrates increased fatty acid uptake an increased number of lipid droplets and dependence upon fatty acid oxidative metabolism. Genetic and pharmacologic suppression of lipid droplet production is sufficient to disrupt cell cycle progression and slow melanoma growth in vivo. Because the melanocytic cell state is linked to poor outcomes in patients these data indicate a metabolic vulnerability in melanoma that depends on the lipid droplet organelle. Overall design: Expression profiling by high throughput sequencing of zebrafish melanoma	pubmed:37268606	sgNT 1 bulk RNAseq	GSM6062265	source name:Skin\|tissue:Skin\|cell type:melanoma\|genotype:WT	sgNT 1 bulk RNAseq	Sequencing reads underwent quality control with FASTQC 0.11.9 trimming with TRIMMOMATIC 14.0.1 and aligned using Salmon 1.4.0 to the danio rerio GRCz11. Data analysis was conducted in R version 4.0.5. Differential expression and normalized counts were calculated using DESeq2 1.30.1 using default parameters. Normalized counts derived from DESeq2 processing. Data was processed using R version 4.0.5 and Seurat version 4.0.2. Cells with fewer than 200 unique genes and mitochondrial genes above 30% were filtered. Expression data was normalized using SCTransform with principal component analysis and UMAP dimensionality reduction performed at default parameters. Clustering was performed using the Seurat function FindClusters with resolution of 0.4. Cluster annotation for zebrafish cell type specific marker genes as done previously using FindAllMarkers. Assembly: GRCz11	Skin	Zebrafish tumors were dissected and sorted for tdTomato+ cells using the BD FACSAria cell sorter. Library construction followed the SMARTer Universal Low Input RNA Kit for Sequencing Takara according to manufacturer's instructions.	tissue:Skin\|cell type:melanoma\|genotype:WT	GSM6062265	GSM6062265: sgNT 1 bulk RNAseq; Danio rerio; RNA Seq	GSM6062265 r1	GSM6062265	1	Zebrafish tumors were dissected and sorted for tdTomato+ cells using the BD FACSAria cell sorter. Library construction followed the SMARTer Universal Low Input RNA Kit for Sequencing Takara according to manufacturer's instructions.	RNA-Seq	TRANSCRIPTOMIC	cDNA	PAIRED	ILLUMINA	Illumina NovaSeq 6000	SRP371883	loader:fastq load.py	NT_1_R1.fastq.gz NT_1_R2.fastq.gz	fastq fastq	4065801864.0	20127732.0	GSM6062265 r1	0:101 1:101	A:1126164942;C:831186106;G:895618283;T:1212785857;N:46676	101	101	1126164942	831186106	895618283	1212785857	46676	SRX14979860	SRS12729751	SRA1408865	Richard M. White, Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center	Richard M. White, Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center	2	0.92125	0.86236	0.09794	0.08896	0.73148	0.7457	0.52439	0.51074	101	101	B	B	biological fallback assumption	illumina	novaseq_era	full_length	cdna_unspecified	smarter	sc_generic	bulk	bulk	United States	2022-04-23	Undetermined	Undetermined	Skin	Surface Structure

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CREATE TABLE run_metadata("run.accession" VARCHAR, "experiment.accession" VARCHAR, "sample.accession" VARCHAR, "study.accession" VARCHAR, bioproject VARCHAR, "study.title" VARCHAR, "study.alias" VARCHAR, "study.type" VARCHAR, "study.abstract" VARCHAR, "study.attributes" VARCHAR, "study.PMIDs" VARCHAR, "sample.description" VARCHAR, "sample.title" VARCHAR, "sample.alias" VARCHAR, "sample.centername" VARCHAR, "sample.attributes" VARCHAR, "GEOsample.title" VARCHAR, "GEOsample.dataprocessing" VARCHAR, "GEOsample.source" VARCHAR, "GEOsample.treatmentprotocol" VARCHAR, "GEOsample.extractprotocol" VARCHAR, "GEOsample.growthprotocol" VARCHAR, "GEOsample.characteristics" VARCHAR, "GEOsample.accession" VARCHAR, "experiment.title" VARCHAR, "experiment.alias" VARCHAR, "experiment.library_name" VARCHAR, "experiment.design_description" VARCHAR, "experiment.library_construction_protocol" VARCHAR, "experiment.attributes" VARCHAR, "experiment.library_strategy" VARCHAR, "experiment.library_source" VARCHAR, "experiment.library_selection" VARCHAR, "experiment.library_layout" VARCHAR, "experiment.platform" VARCHAR, "experiment.instrument_model" VARCHAR, "experiment.spot_descriptor" VARCHAR, "experiment.study_ref" VARCHAR, "run.title" VARCHAR, "run.attributes" VARCHAR, "run.filename" VARCHAR, "run.semantic_name" VARCHAR, "run.total_bases" DOUBLE, "run.total_spots" DOUBLE, "run.alias" VARCHAR, "run.read_lengths" VARCHAR, "run.base_counts" VARCHAR, "run.r1_length" BIGINT, "run.r2_length" BIGINT, "run.r3_length" BIGINT, "run.r4_length" BIGINT, "run.Acount" BIGINT, "run.Ccount" BIGINT, "run.Gcount" BIGINT, "run.Tcount" BIGINT, "run.Ncount" BIGINT, "run.experiment" VARCHAR, "run.pool_member" VARCHAR, "submission.accession" VARCHAR, "submission.srasource" VARCHAR, "submission.bioprojectsource" VARCHAR, "seqdetective.n_mates" BIGINT, "seqdetective.mapping_rate.mate1" DOUBLE, "seqdetective.mapping_rate.mate2" DOUBLE, "seqdetective.nofeature_rate.mate1" DOUBLE, "seqdetective.nofeature_rate.mate2" DOUBLE, "seqdetective.sparsity.mate1" DOUBLE, "seqdetective.sparsity.mate2" DOUBLE, "seqdetective.pos_strand_rate.mate1" DOUBLE, "seqdetective.pos_strand_rate.mate2" DOUBLE, "seqdetective.readlen.mate1" BIGINT, "seqdetective.readlen.mate2" BIGINT, "seqdetective.judgement.mate1" VARCHAR, "seqdetective.judgement.mate2" VARCHAR, "seqdetective.judgement.reason" VARCHAR, platform_family VARCHAR, instrument_generation VARCHAR, read_bias VARCHAR, selection_class VARCHAR, prep_kit VARCHAR, sc_or_bulk VARCHAR, tech_class VARCHAR, technology VARCHAR, tech_variant VARCHAR, "submission.bioprojectsource.country" VARCHAR, earliest_date DATE, devstage_curation VARCHAR, devstage_curation_coarse VARCHAR, tissue_curation VARCHAR, tissue_curation_coarse VARCHAR);;
CREATE INDEX idx_run_bioproject ON run_metadata(bioproject);;
CREATE INDEX idx_run_run_accession ON run_metadata("run.accession");;