run_metadata
17 rows where experiment.library_selection = "Oligo-dT", experiment.library_source = "TRANSCRIPTOMIC SINGLE CELL" and tissue_curation = "Whole Organism"
This data as json, CSV (advanced)
| Link | rowid ▼ | run.accession | experiment.accession | sample.accession | study.accession | bioproject | study.title | study.alias | study.type | study.abstract | study.attributes | study.PMIDs | sample.description | sample.title | sample.alias | sample.centername | sample.attributes | GEOsample.title | GEOsample.dataprocessing | GEOsample.source | GEOsample.treatmentprotocol | GEOsample.extractprotocol | GEOsample.growthprotocol | GEOsample.characteristics | GEOsample.accession | experiment.title | experiment.alias | experiment.library_name | experiment.design_description | experiment.library_construction_protocol | experiment.attributes | experiment.library_strategy | experiment.library_source | experiment.library_selection | experiment.library_layout | experiment.platform | experiment.instrument_model | experiment.spot_descriptor | experiment.study_ref | run.title | 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.r3_length | run.r4_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 | tech_variant | submission.bioprojectsource.country | earliest_date | devstage_curation | devstage_curation_coarse | tissue_curation | tissue_curation_coarse |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 26493 | 26493 | SRR26044865 | SRX21761777 | SRS18868295 | SRP459729 | PRJNA1015262 | Rtf1 dependent transcriptional pausing regulates cardiogenesis | PRJNA1015262 | Other | During heart development an evolutionarily conserved network of cardiac transcription factors collaborate to define the precise timing and location of cardiac progenitor specification. Accumulating evidence suggests that cardiac progenitor specification is subject to transcriptional control beyond the level of transcription initiation. The PAF1C component Rtf1 is a multifunctional transcription regulatory protein that modulates pausing and elongation of RNA Pol II as well as histone epigenetic modifications. By transient knockdown and CRISPR mutagenesis we found that Rtf1 is essential for cardiogenesis and that without xxx activity cardiac progenitors arrest in an immature state. This role in early cardiogenesis was evolutionarily conserved between fish and mammals. We also found that Rtf1's Plus3 domain which confers interaction with the pausing/elongation factor Spt5 was required for Rtf1's ability to support cardiac progenitor formation while other regions of the protein were dispensable. We examined the occupancy of RNA Pol II at cardiac genes in rtf1 morphants using ChIP seq and found that Pol II signals at the TSS of genes was reduced suggesting a reduction in transcriptional pausing. Intriguingly pharmacological or morpholino antisense reduction of pause release in rtf1 morphants and mutants restored the formation of cardiac cells and improved Pol II occupancy at the TSS of key cardiac genes. Our findings highlight the crucial role that transcriptional pausing plays in promoting normal levels of gene expression in a cardiac developmental context. | Rtf1MO single cell Multiome GEX 11 12 somite stage | strain:AB|age:11 12 somite stage|collection date:2021 03 10|geo loc name:USA:California Los Angeles|sex:n/a|tissue:whole embryo|morpholino:rtf1|assay:GEX|BioSampleModel:Model organism or animal | 10x single cell multiome analysis of 11 12 somite stage zebrafish embryos: single cell RNA seq | GEX MO | GEX MO | Chromium Next GEM Single Cell Multiome ATAC + Gene Expression Kit | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina NovaSeq 6000 | SRP459729 | MO-3GEX_S2_L002_R2_001.fastq.gz MO-3GEX_S2_L002_R1_001.fastq.gz MO-3GEX_S2_L002_I2_001.fastq.gz MO-3GEX_S2_L002_I1_001.fastq.gz MO-3GEX_S2_L001_R2_001.fastq.gz MO-3GEX_S2_L001_R1_001.fastq.gz MO-3GEX_S2_L001_I2_001.fastq.gz MO-3GEX_S2_L001_I1_001.fastq.gz | fastq fastq fastq fastq fastq fastq fastq fastq | 50770012872.0 | 367898644.0 | MO 3GEX S2 L001 I1 001.fastq.gz | 0:10 1:10 2:28 3:90 | A:10123747774;C:6493264924;G:7104700568;T:9387645989;N:1518705 | 10 | 10 | 28 | 90 | 10123747774 | 6493264924 | 7104700568 | 9387645989 | 1518705 | SRX21761777 | SRS18868295 | SRA1710715 | University of California, Los Angeles|Molecular, Cell, and Developmental Biology | University of California, Los Angeles | 1 | 0.87322 | 0.43479 | 0.76881 | 0.57534 | 90 | B | usable mapping rate | illumina | novaseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2023-09-12 | Segmentation | Embryo | Whole Organism | All anatomical structures | |||||||||||||||||||||||||
| 26494 | 26494 | SRR26044866 | SRX21761776 | SRS18868294 | SRP459729 | PRJNA1015262 | Rtf1 dependent transcriptional pausing regulates cardiogenesis | PRJNA1015262 | Other | During heart development an evolutionarily conserved network of cardiac transcription factors collaborate to define the precise timing and location of cardiac progenitor specification. Accumulating evidence suggests that cardiac progenitor specification is subject to transcriptional control beyond the level of transcription initiation. The PAF1C component Rtf1 is a multifunctional transcription regulatory protein that modulates pausing and elongation of RNA Pol II as well as histone epigenetic modifications. By transient knockdown and CRISPR mutagenesis we found that Rtf1 is essential for cardiogenesis and that without xxx activity cardiac progenitors arrest in an immature state. This role in early cardiogenesis was evolutionarily conserved between fish and mammals. We also found that Rtf1's Plus3 domain which confers interaction with the pausing/elongation factor Spt5 was required for Rtf1's ability to support cardiac progenitor formation while other regions of the protein were dispensable. We examined the occupancy of RNA Pol II at cardiac genes in rtf1 morphants using ChIP seq and found that Pol II signals at the TSS of genes was reduced suggesting a reduction in transcriptional pausing. Intriguingly pharmacological or morpholino antisense reduction of pause release in rtf1 morphants and mutants restored the formation of cardiac cells and improved Pol II occupancy at the TSS of key cardiac genes. Our findings highlight the crucial role that transcriptional pausing plays in promoting normal levels of gene expression in a cardiac developmental context. | Control single cell Multiome GEX 11 12 somite stage | strain:AB|age:11 12 somite stage|collection date:2021 03 10|geo loc name:USA:California Los Angeles|sex:n/a|tissue:whole embryo|morpholino:uninjected|assay:GEX|BioSampleModel:Model organism or animal | 10x single cell multiome analysis of 11 12 somite stage zebrafish embryos: single cell RNA seq | GEX WT | GEX WT | Chromium Next GEM Single Cell Multiome ATAC + Gene Expression Kit | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina NovaSeq 6000 | SRP459729 | WT-3GEX_S1_L001_I1_001.fastq.gz WT-3GEX_S1_L001_I2_001.fastq.gz WT-3GEX_S1_L001_R1_001.fastq.gz WT-3GEX_S1_L001_R2_001.fastq.gz WT-3GEX_S1_L002_I1_001.fastq.gz WT-3GEX_S1_L002_I2_001.fastq.gz WT-3GEX_S1_L002_R1_001.fastq.gz WT-3GEX_S1_L002_R2_001.fastq.gz | fastq fastq fastq fastq fastq fastq fastq fastq | 54878873586.0 | 397672997.0 | WT 3GEX S1 L001 I1 001.fastq.gz | 0:10 1:10 2:28 3:90 | A:10837179080;C:7155333415;G:7765967855;T:10030437304;N:1652076 | 10 | 10 | 28 | 90 | 10837179080 | 7155333415 | 7765967855 | 10030437304 | 1652076 | SRX21761776 | SRS18868294 | SRA1710715 | University of California, Los Angeles|Molecular, Cell, and Developmental Biology | University of California, Los Angeles | 1 | 0.89445 | 0.37406 | 0.75481 | 0.57841 | 90 | B | usable mapping rate | illumina | novaseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2023-09-12 | Segmentation | Embryo | Whole Organism | All anatomical structures | |||||||||||||||||||||||||
| 26495 | 26495 | SRR26044766 | SRX21761676 | SRS18868295 | SRP459729 | PRJNA1015262 | Rtf1 dependent transcriptional pausing regulates cardiogenesis | PRJNA1015262 | Other | During heart development an evolutionarily conserved network of cardiac transcription factors collaborate to define the precise timing and location of cardiac progenitor specification. Accumulating evidence suggests that cardiac progenitor specification is subject to transcriptional control beyond the level of transcription initiation. The PAF1C component Rtf1 is a multifunctional transcription regulatory protein that modulates pausing and elongation of RNA Pol II as well as histone epigenetic modifications. By transient knockdown and CRISPR mutagenesis we found that Rtf1 is essential for cardiogenesis and that without xxx activity cardiac progenitors arrest in an immature state. This role in early cardiogenesis was evolutionarily conserved between fish and mammals. We also found that Rtf1's Plus3 domain which confers interaction with the pausing/elongation factor Spt5 was required for Rtf1's ability to support cardiac progenitor formation while other regions of the protein were dispensable. We examined the occupancy of RNA Pol II at cardiac genes in rtf1 morphants using ChIP seq and found that Pol II signals at the TSS of genes was reduced suggesting a reduction in transcriptional pausing. Intriguingly pharmacological or morpholino antisense reduction of pause release in rtf1 morphants and mutants restored the formation of cardiac cells and improved Pol II occupancy at the TSS of key cardiac genes. Our findings highlight the crucial role that transcriptional pausing plays in promoting normal levels of gene expression in a cardiac developmental context. | Rtf1MO single cell Multiome GEX 11 12 somite stage | strain:AB|age:11 12 somite stage|collection date:2021 03 10|geo loc name:USA:California Los Angeles|sex:n/a|tissue:whole embryo|morpholino:rtf1|assay:GEX|BioSampleModel:Model organism or animal | 10x single cell multiome analysis of 11 12 somite stage zebrafish embryos: single cell RNA seq | GEX MO | GEX MO | Chromium Next GEM Single Cell Multiome ATAC + Gene Expression Kit | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina NovaSeq 6000 | SRP459729 | MO_3GEX_S2_L004_R2_001.fastq.gz MO_3GEX_S2_L004_R1_001.fastq.gz MO_3GEX_S2_L004_I2_001.fastq.gz MO_3GEX_S2_L004_I1_001.fastq.gz MO_3GEX_S2_L003_R2_001.fastq.gz MO_3GEX_S2_L003_R1_001.fastq.gz MO_3GEX_S2_L003_I2_001.fastq.gz MO_3GEX_S2_L003_I1_001.fastq.gz | fastq fastq fastq fastq fastq fastq fastq fastq | 2914080840.0 | 13245822.0 | MO 3GEX S2 L003 I1 001.fastq.gz | 0:10 1:10 2:100 3:100 | A:726829083;C:402485666;G:452882760;T:1066890018;N:76873 | 10 | 10 | 100 | 100 | 726829083 | 402485666 | 452882760 | 1066890018 | 76873 | SRX21761676 | SRS18868295 | SRA1710703 | University of California, Los Angeles|Molecular, Cell, and Developmental Biology | University of California, Los Angeles | 2 | 0.22802 | 0.87048 | 0.10701 | 0.42845 | 0.95595 | 0.77015 | 0.60757 | 0.57362 | 100 | 100 | T | B | mate1 technical by mapping diff | illumina | novaseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2023-09-12 | Segmentation | Embryo | Whole Organism | All anatomical structures | |||||||||||||||||||
| 26496 | 26496 | SRR26044767 | SRX21761675 | SRS18868294 | SRP459729 | PRJNA1015262 | Rtf1 dependent transcriptional pausing regulates cardiogenesis | PRJNA1015262 | Other | During heart development an evolutionarily conserved network of cardiac transcription factors collaborate to define the precise timing and location of cardiac progenitor specification. Accumulating evidence suggests that cardiac progenitor specification is subject to transcriptional control beyond the level of transcription initiation. The PAF1C component Rtf1 is a multifunctional transcription regulatory protein that modulates pausing and elongation of RNA Pol II as well as histone epigenetic modifications. By transient knockdown and CRISPR mutagenesis we found that Rtf1 is essential for cardiogenesis and that without xxx activity cardiac progenitors arrest in an immature state. This role in early cardiogenesis was evolutionarily conserved between fish and mammals. We also found that Rtf1's Plus3 domain which confers interaction with the pausing/elongation factor Spt5 was required for Rtf1's ability to support cardiac progenitor formation while other regions of the protein were dispensable. We examined the occupancy of RNA Pol II at cardiac genes in rtf1 morphants using ChIP seq and found that Pol II signals at the TSS of genes was reduced suggesting a reduction in transcriptional pausing. Intriguingly pharmacological or morpholino antisense reduction of pause release in rtf1 morphants and mutants restored the formation of cardiac cells and improved Pol II occupancy at the TSS of key cardiac genes. Our findings highlight the crucial role that transcriptional pausing plays in promoting normal levels of gene expression in a cardiac developmental context. | Control single cell Multiome GEX 11 12 somite stage | strain:AB|age:11 12 somite stage|collection date:2021 03 10|geo loc name:USA:California Los Angeles|sex:n/a|tissue:whole embryo|morpholino:uninjected|assay:GEX|BioSampleModel:Model organism or animal | 10x single cell multiome analysis of 11 12 somite stage zebrafish embryos: single cell RNA seq | GEX WT | GEX WT | Chromium Next GEM Single Cell Multiome ATAC + Gene Expression Kit | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina NovaSeq 6000 | SRP459729 | WT_3GEX_S1_L004_R2_001.fastq.gz WT_3GEX_S1_L004_R1_001.fastq.gz WT_3GEX_S1_L004_I2_001.fastq.gz WT_3GEX_S1_L004_I1_001.fastq.gz WT_3GEX_S1_L003_R2_001.fastq.gz WT_3GEX_S1_L003_R1_001.fastq.gz WT_3GEX_S1_L003_I2_001.fastq.gz WT_3GEX_S1_L003_I1_001.fastq.gz | fastq fastq fastq fastq fastq fastq fastq fastq | 4986906540.0 | 22667757.0 | WT 3GEX S1 L003 I1 001.fastq.gz | 0:10 1:10 2:100 3:100 | A:1227427708;C:695004251;G:785531191;T:1825414315;N:173935 | 10 | 10 | 100 | 100 | 1227427708 | 695004251 | 785531191 | 1825414315 | 173935 | SRX21761675 | SRS18868294 | SRA1710703 | University of California, Los Angeles|Molecular, Cell, and Developmental Biology | University of California, Los Angeles | 2 | 0.21872 | 0.89321 | 0.09696 | 0.36976 | 0.9558 | 0.75639 | 0.62213 | 0.46544 | 100 | 100 | T | B | mate1 technical by mapping diff | illumina | novaseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2023-09-12 | Segmentation | Embryo | Whole Organism | All anatomical structures | |||||||||||||||||||
| 26497 | 26497 | SRR26044613 | SRX21761588 | SRS18868295 | SRP459729 | PRJNA1015262 | Rtf1 dependent transcriptional pausing regulates cardiogenesis | PRJNA1015262 | Other | During heart development an evolutionarily conserved network of cardiac transcription factors collaborate to define the precise timing and location of cardiac progenitor specification. Accumulating evidence suggests that cardiac progenitor specification is subject to transcriptional control beyond the level of transcription initiation. The PAF1C component Rtf1 is a multifunctional transcription regulatory protein that modulates pausing and elongation of RNA Pol II as well as histone epigenetic modifications. By transient knockdown and CRISPR mutagenesis we found that Rtf1 is essential for cardiogenesis and that without xxx activity cardiac progenitors arrest in an immature state. This role in early cardiogenesis was evolutionarily conserved between fish and mammals. We also found that Rtf1's Plus3 domain which confers interaction with the pausing/elongation factor Spt5 was required for Rtf1's ability to support cardiac progenitor formation while other regions of the protein were dispensable. We examined the occupancy of RNA Pol II at cardiac genes in rtf1 morphants using ChIP seq and found that Pol II signals at the TSS of genes was reduced suggesting a reduction in transcriptional pausing. Intriguingly pharmacological or morpholino antisense reduction of pause release in rtf1 morphants and mutants restored the formation of cardiac cells and improved Pol II occupancy at the TSS of key cardiac genes. Our findings highlight the crucial role that transcriptional pausing plays in promoting normal levels of gene expression in a cardiac developmental context. | Rtf1MO single cell Multiome GEX 11 12 somite stage | strain:AB|age:11 12 somite stage|collection date:2021 03 10|geo loc name:USA:California Los Angeles|sex:n/a|tissue:whole embryo|morpholino:rtf1|assay:GEX|BioSampleModel:Model organism or animal | 10x single cell multiome analysis of 11 12 somite stage zebrafish embryos: single cell RNA seq | GEX MO | GEX MO | Chromium Next GEM Single Cell Multiome ATAC + Gene Expression Kit | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina NovaSeq 6000 | SRP459729 | MO_3GEX_S2_L002_R2_001.fastq.gz MO_3GEX_S2_L002_R1_001.fastq.gz MO_3GEX_S2_L002_I2_001.fastq.gz MO_3GEX_S2_L002_I1_001.fastq.gz MO_3GEX_S2_L001_R2_001.fastq.gz MO_3GEX_S2_L001_R1_001.fastq.gz MO_3GEX_S2_L001_I2_001.fastq.gz MO_3GEX_S2_L001_I1_001.fastq.gz | fastq fastq fastq fastq fastq fastq fastq fastq | 21527638854.0 | 155997383.0 | MO 3GEX S2 L001 I1 001.fastq.gz | 0:10 1:10 2:28 3:90 | A:4285470476;C:2755587559;G:3034249420;T:3964137056;N:319959 | 10 | 10 | 28 | 90 | 4285470476 | 2755587559 | 3034249420 | 3964137056 | 319959 | SRX21761588 | SRS18868295 | SRA1710658 | University of California, Los Angeles|Molecular, Cell, and Developmental Biology | University of California, Los Angeles | 1 | 0.87277 | 0.43202 | 0.7725 | 0.56861 | 90 | B | usable mapping rate | illumina | novaseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2023-09-12 | Segmentation | Embryo | Whole Organism | All anatomical structures | |||||||||||||||||||||||||
| 26498 | 26498 | SRR26044614 | SRX21761587 | SRS18868294 | SRP459729 | PRJNA1015262 | Rtf1 dependent transcriptional pausing regulates cardiogenesis | PRJNA1015262 | Other | During heart development an evolutionarily conserved network of cardiac transcription factors collaborate to define the precise timing and location of cardiac progenitor specification. Accumulating evidence suggests that cardiac progenitor specification is subject to transcriptional control beyond the level of transcription initiation. The PAF1C component Rtf1 is a multifunctional transcription regulatory protein that modulates pausing and elongation of RNA Pol II as well as histone epigenetic modifications. By transient knockdown and CRISPR mutagenesis we found that Rtf1 is essential for cardiogenesis and that without xxx activity cardiac progenitors arrest in an immature state. This role in early cardiogenesis was evolutionarily conserved between fish and mammals. We also found that Rtf1's Plus3 domain which confers interaction with the pausing/elongation factor Spt5 was required for Rtf1's ability to support cardiac progenitor formation while other regions of the protein were dispensable. We examined the occupancy of RNA Pol II at cardiac genes in rtf1 morphants using ChIP seq and found that Pol II signals at the TSS of genes was reduced suggesting a reduction in transcriptional pausing. Intriguingly pharmacological or morpholino antisense reduction of pause release in rtf1 morphants and mutants restored the formation of cardiac cells and improved Pol II occupancy at the TSS of key cardiac genes. Our findings highlight the crucial role that transcriptional pausing plays in promoting normal levels of gene expression in a cardiac developmental context. | Control single cell Multiome GEX 11 12 somite stage | strain:AB|age:11 12 somite stage|collection date:2021 03 10|geo loc name:USA:California Los Angeles|sex:n/a|tissue:whole embryo|morpholino:uninjected|assay:GEX|BioSampleModel:Model organism or animal | 10x single cell multiome analysis of 11 12 somite stage zebrafish embryos: single cell RNA seq | GEX WT | GEX WT | Chromium Next GEM Single Cell Multiome ATAC + Gene Expression Kit | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina NovaSeq 6000 | SRP459729 | WT_3GEX_S1_L001_I1_001.fastq.gz WT_3GEX_S1_L001_I2_001.fastq.gz WT_3GEX_S1_L001_R1_001.fastq.gz WT_3GEX_S1_L001_R2_001.fastq.gz WT_3GEX_S1_L002_I1_001.fastq.gz WT_3GEX_S1_L002_I2_001.fastq.gz WT_3GEX_S1_L002_R1_001.fastq.gz WT_3GEX_S1_L002_R2_001.fastq.gz | fastq fastq fastq fastq fastq fastq fastq fastq | 24359922978.0 | 176521181.0 | WT 3GEX S1 L001 I1 001.fastq.gz | 0:10 1:10 2:28 3:90 | A:4802729436;C:3179460152;G:3468651943;T:4435697892;N:366867 | 10 | 10 | 28 | 90 | 4802729436 | 3179460152 | 3468651943 | 4435697892 | 366867 | SRX21761587 | SRS18868294 | SRA1710658 | University of California, Los Angeles|Molecular, Cell, and Developmental Biology | University of California, Los Angeles | 1 | 0.89475 | 0.37342 | 0.75668 | 0.45872 | 90 | B | usable mapping rate | illumina | novaseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2023-09-12 | Segmentation | Embryo | Whole Organism | All anatomical structures | |||||||||||||||||||||||||
| 31963 | 31963 | SRR28832522 | SRX24395271 | SRS21150709 | SRP504662 | PRJNA1105232 | Loss of alpha Ba crystallin but not alpha A crystallin increases age related cataract in the zebrafish lens | PRJNA1105232 | Other | The vertebrate eye lens is an unusual organ in that most of its cells lack nuclei and the ability to replace aging protein. The small heat shock protein alpha crystallins evolved to become key components of this lens possibly because of their ability to prevent aggregation of aging protein that would otherwise lead to lens opacity. Most vertebrates express two alpha crystallins alpha A and alpha B crystallin and mutations in each are linked to human cataract. In a mouse knockout model only the loss of alpha A crystallin led to early stage lens cataract. We have used the zebrafish as a model system to investigate the role of alpha crystallins during lens development. Interestingly while zebrafish express one lens specific alpha A crystallin gene cryaa they express two alpha B crystallin genes with one evolving lens specificity cryaba and the other retaining the broad expression of its mammalian ortholog cryabb. In this study we used individual mutant zebrafish lines for all three alpha crystallin genes to determine the impact of their loss on age related cataract. Surprisingly unlike mouse knockout models we found that the loss of the alpha Ba crystallin gene cryaba led to an increase in lens opacity compared to cryaa null fish at 24 month of age. Loss of alpha A crystallin did not increase the prevalence of cataract. We also used single cell RNA Seq and RT qPCR data to show a shift in the lens expression of zebrafish alpha crystallins between 5 dpf and 10 dpf dpf with 5 dpf and 6 dpf lenses expressing cryaa almost exclusively and expression of cryaba and cryabb becoming more prominent post 10 dpf. These data show that cryaa is the primary alpha crystallin during early lens development while the protective role for cryaba becomes more important during lens aging. This study is the first to quantify cataract prevalence in wild type zebrafish showing that lens opacities develop in approximately 25% of fish by 18 month of age. None of the three alpha crystallin mutants showed a compensatory increase in t… | 7b | strain:ABC|dev stage:7 dpf|collection date:2020 10|geo loc name:USA: Oregon|sex:N/A|tissue:whole larvae|treatment:replicate B|BioSampleModel:Model organism or animal | scRNA seq of whole zebrafish larvae | 7b | 7b | 10X Chromium | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina HiSeq 4000 | SRP504662 | 7b_concatenated_R1.fastq.gz 7b_concatenated_R2.fastq.gz | fastq fastq | 67688938179.0 | 524720451.0 | 7b concatenated R1.fastq.gz | 0:28 1:101 | A:18993507272;C:15386021146;G:15634918803;T:17652028346;N:22462612 | 28 | 101 | 18993507272 | 15386021146 | 15634918803 | 17652028346 | 22462612 | SRX24395271 | SRS21150709 | SRA1854140 | University of Oregon|Institute of Neuroscience | University of Oregon | T | B | sc-like readlen | illumina | hiseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2024-04-29 | Larval | Larval | Whole Organism | All anatomical structures | ||||||||||||||||||||||||||||||||
| 31964 | 31964 | SRR28832523 | SRX24395270 | SRS21150708 | SRP504662 | PRJNA1105232 | Loss of alpha Ba crystallin but not alpha A crystallin increases age related cataract in the zebrafish lens | PRJNA1105232 | Other | The vertebrate eye lens is an unusual organ in that most of its cells lack nuclei and the ability to replace aging protein. The small heat shock protein alpha crystallins evolved to become key components of this lens possibly because of their ability to prevent aggregation of aging protein that would otherwise lead to lens opacity. Most vertebrates express two alpha crystallins alpha A and alpha B crystallin and mutations in each are linked to human cataract. In a mouse knockout model only the loss of alpha A crystallin led to early stage lens cataract. We have used the zebrafish as a model system to investigate the role of alpha crystallins during lens development. Interestingly while zebrafish express one lens specific alpha A crystallin gene cryaa they express two alpha B crystallin genes with one evolving lens specificity cryaba and the other retaining the broad expression of its mammalian ortholog cryabb. In this study we used individual mutant zebrafish lines for all three alpha crystallin genes to determine the impact of their loss on age related cataract. Surprisingly unlike mouse knockout models we found that the loss of the alpha Ba crystallin gene cryaba led to an increase in lens opacity compared to cryaa null fish at 24 month of age. Loss of alpha A crystallin did not increase the prevalence of cataract. We also used single cell RNA Seq and RT qPCR data to show a shift in the lens expression of zebrafish alpha crystallins between 5 dpf and 10 dpf dpf with 5 dpf and 6 dpf lenses expressing cryaa almost exclusively and expression of cryaba and cryabb becoming more prominent post 10 dpf. These data show that cryaa is the primary alpha crystallin during early lens development while the protective role for cryaba becomes more important during lens aging. This study is the first to quantify cataract prevalence in wild type zebrafish showing that lens opacities develop in approximately 25% of fish by 18 month of age. None of the three alpha crystallin mutants showed a compensatory increase in t… | 7a | strain:ABC|dev stage:7 dpf|collection date:2020 10|geo loc name:USA: Oregon|sex:N/A|tissue:whole larvae|treatment:replicate A|BioSampleModel:Model organism or animal | scRNA seq of whole zebrafish larvae | 7a | 7a | 10X Chromium | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina HiSeq 4000 | SRP504662 | 7a_concatenated_R1.fastq.gz 7a_concatenated_R2.fastq.gz | fastq fastq | 79101784254.0 | 613192126.0 | 7a concatenated R1.fastq.gz | 0:28 1:101 | A:22179167002;C:18012103520;G:18280647088;T:20603509593;N:26357051 | 28 | 101 | 22179167002 | 18012103520 | 18280647088 | 20603509593 | 26357051 | SRX24395270 | SRS21150708 | SRA1854140 | University of Oregon|Institute of Neuroscience | University of Oregon | T | B | sc-like readlen | illumina | hiseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2024-04-29 | Larval | Larval | Whole Organism | All anatomical structures | ||||||||||||||||||||||||||||||||
| 31965 | 31965 | SRR28832524 | SRX24395269 | SRS21150710 | SRP504662 | PRJNA1105232 | Loss of alpha Ba crystallin but not alpha A crystallin increases age related cataract in the zebrafish lens | PRJNA1105232 | Other | The vertebrate eye lens is an unusual organ in that most of its cells lack nuclei and the ability to replace aging protein. The small heat shock protein alpha crystallins evolved to become key components of this lens possibly because of their ability to prevent aggregation of aging protein that would otherwise lead to lens opacity. Most vertebrates express two alpha crystallins alpha A and alpha B crystallin and mutations in each are linked to human cataract. In a mouse knockout model only the loss of alpha A crystallin led to early stage lens cataract. We have used the zebrafish as a model system to investigate the role of alpha crystallins during lens development. Interestingly while zebrafish express one lens specific alpha A crystallin gene cryaa they express two alpha B crystallin genes with one evolving lens specificity cryaba and the other retaining the broad expression of its mammalian ortholog cryabb. In this study we used individual mutant zebrafish lines for all three alpha crystallin genes to determine the impact of their loss on age related cataract. Surprisingly unlike mouse knockout models we found that the loss of the alpha Ba crystallin gene cryaba led to an increase in lens opacity compared to cryaa null fish at 24 month of age. Loss of alpha A crystallin did not increase the prevalence of cataract. We also used single cell RNA Seq and RT qPCR data to show a shift in the lens expression of zebrafish alpha crystallins between 5 dpf and 10 dpf dpf with 5 dpf and 6 dpf lenses expressing cryaa almost exclusively and expression of cryaba and cryabb becoming more prominent post 10 dpf. These data show that cryaa is the primary alpha crystallin during early lens development while the protective role for cryaba becomes more important during lens aging. This study is the first to quantify cataract prevalence in wild type zebrafish showing that lens opacities develop in approximately 25% of fish by 18 month of age. None of the three alpha crystallin mutants showed a compensatory increase in t… | 6b | strain:ABC|dev stage:6 dpf|collection date:2020 10|geo loc name:USA: Oregon|sex:N/A|tissue:whole larvae|treatment:replicate B|BioSampleModel:Model organism or animal | scRNA seq of whole zebrafish larvae | 6b | 6b | 10X Chromium | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina HiSeq 4000 | SRP504662 | 6b_concatenated_R1.fastq.gz 6b_concatenated_R2.fastq.gz | fastq fastq | 69567742683.0 | 539284827.0 | 6b concatenated R1.fastq.gz | 0:28 1:101 | A:19762887143;C:15877063714;G:15450633995;T:18460750107;N:16407724 | 28 | 101 | 19762887143 | 15877063714 | 15450633995 | 18460750107 | 16407724 | SRX24395269 | SRS21150710 | SRA1854140 | University of Oregon|Institute of Neuroscience | University of Oregon | T | B | sc-like readlen | illumina | hiseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2024-04-29 | Larval | Larval | Whole Organism | All anatomical structures | ||||||||||||||||||||||||||||||||
| 31966 | 31966 | SRR28832525 | SRX24395268 | SRS21150711 | SRP504662 | PRJNA1105232 | Loss of alpha Ba crystallin but not alpha A crystallin increases age related cataract in the zebrafish lens | PRJNA1105232 | Other | The vertebrate eye lens is an unusual organ in that most of its cells lack nuclei and the ability to replace aging protein. The small heat shock protein alpha crystallins evolved to become key components of this lens possibly because of their ability to prevent aggregation of aging protein that would otherwise lead to lens opacity. Most vertebrates express two alpha crystallins alpha A and alpha B crystallin and mutations in each are linked to human cataract. In a mouse knockout model only the loss of alpha A crystallin led to early stage lens cataract. We have used the zebrafish as a model system to investigate the role of alpha crystallins during lens development. Interestingly while zebrafish express one lens specific alpha A crystallin gene cryaa they express two alpha B crystallin genes with one evolving lens specificity cryaba and the other retaining the broad expression of its mammalian ortholog cryabb. In this study we used individual mutant zebrafish lines for all three alpha crystallin genes to determine the impact of their loss on age related cataract. Surprisingly unlike mouse knockout models we found that the loss of the alpha Ba crystallin gene cryaba led to an increase in lens opacity compared to cryaa null fish at 24 month of age. Loss of alpha A crystallin did not increase the prevalence of cataract. We also used single cell RNA Seq and RT qPCR data to show a shift in the lens expression of zebrafish alpha crystallins between 5 dpf and 10 dpf dpf with 5 dpf and 6 dpf lenses expressing cryaa almost exclusively and expression of cryaba and cryabb becoming more prominent post 10 dpf. These data show that cryaa is the primary alpha crystallin during early lens development while the protective role for cryaba becomes more important during lens aging. This study is the first to quantify cataract prevalence in wild type zebrafish showing that lens opacities develop in approximately 25% of fish by 18 month of age. None of the three alpha crystallin mutants showed a compensatory increase in t… | 6a | strain:ABC|dev stage:6 dpf|collection date:2020 10|geo loc name:USA: Oregon|sex:N/A|tissue:whole larvae|treatment:replicate A|BioSampleModel:Model organism or animal | scRNA seq of whole zebrafish larvae | 6a | 6a | 10X Chromium | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina HiSeq 4000 | SRP504662 | 6a_concatenated_R1.fastq.gz 6a_concatenated_R2.fastq.gz | fastq fastq | 69092868528.0 | 535603632.0 | 6a concatenated R1.fastq.gz | SRX24395268 | SRS21150711 | SRA1854140 | University of Oregon|Institute of Neuroscience | University of Oregon | T | B | sc-like readlen | illumina | hiseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2024-04-29 | Larval | Larval | Whole Organism | All anatomical structures | |||||||||||||||||||||||||||||||||||||||||
| 31967 | 31967 | SRR28832526 | SRX24395267 | SRS21150707 | SRP504662 | PRJNA1105232 | Loss of alpha Ba crystallin but not alpha A crystallin increases age related cataract in the zebrafish lens | PRJNA1105232 | Other | The vertebrate eye lens is an unusual organ in that most of its cells lack nuclei and the ability to replace aging protein. The small heat shock protein alpha crystallins evolved to become key components of this lens possibly because of their ability to prevent aggregation of aging protein that would otherwise lead to lens opacity. Most vertebrates express two alpha crystallins alpha A and alpha B crystallin and mutations in each are linked to human cataract. In a mouse knockout model only the loss of alpha A crystallin led to early stage lens cataract. We have used the zebrafish as a model system to investigate the role of alpha crystallins during lens development. Interestingly while zebrafish express one lens specific alpha A crystallin gene cryaa they express two alpha B crystallin genes with one evolving lens specificity cryaba and the other retaining the broad expression of its mammalian ortholog cryabb. In this study we used individual mutant zebrafish lines for all three alpha crystallin genes to determine the impact of their loss on age related cataract. Surprisingly unlike mouse knockout models we found that the loss of the alpha Ba crystallin gene cryaba led to an increase in lens opacity compared to cryaa null fish at 24 month of age. Loss of alpha A crystallin did not increase the prevalence of cataract. We also used single cell RNA Seq and RT qPCR data to show a shift in the lens expression of zebrafish alpha crystallins between 5 dpf and 10 dpf dpf with 5 dpf and 6 dpf lenses expressing cryaa almost exclusively and expression of cryaba and cryabb becoming more prominent post 10 dpf. These data show that cryaa is the primary alpha crystallin during early lens development while the protective role for cryaba becomes more important during lens aging. This study is the first to quantify cataract prevalence in wild type zebrafish showing that lens opacities develop in approximately 25% of fish by 18 month of age. None of the three alpha crystallin mutants showed a compensatory increase in t… | 5c | strain:ABC|dev stage:5 dpf|collection date:2020 10|geo loc name:USA: Oregon|sex:N/A|tissue:whole larvae|treatment:replicate C|BioSampleModel:Model organism or animal | scRNA seq of whole zebrafish larvae | 5c | 5c | 10X Chromium | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina HiSeq 4000 | SRP504662 | 5c_concatenated_R1.fastq.gz 5c_concatenated_R2.fastq.gz | fastq fastq | 42738149952.0 | 331303488.0 | 5c concatenated R1.fastq.gz | 0:28 1:101 | A:12472930469;C:9646780605;G:9513754487;T:11098062350;N:6622041 | 28 | 101 | 12472930469 | 9646780605 | 9513754487 | 11098062350 | 6622041 | SRX24395267 | SRS21150707 | SRA1854140 | University of Oregon|Institute of Neuroscience | University of Oregon | T | B | sc-like readlen | illumina | hiseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2024-04-29 | Larval | Larval | Whole Organism | All anatomical structures | ||||||||||||||||||||||||||||||||
| 31968 | 31968 | SRR28832527 | SRX24395266 | SRS21150706 | SRP504662 | PRJNA1105232 | Loss of alpha Ba crystallin but not alpha A crystallin increases age related cataract in the zebrafish lens | PRJNA1105232 | Other | The vertebrate eye lens is an unusual organ in that most of its cells lack nuclei and the ability to replace aging protein. The small heat shock protein alpha crystallins evolved to become key components of this lens possibly because of their ability to prevent aggregation of aging protein that would otherwise lead to lens opacity. Most vertebrates express two alpha crystallins alpha A and alpha B crystallin and mutations in each are linked to human cataract. In a mouse knockout model only the loss of alpha A crystallin led to early stage lens cataract. We have used the zebrafish as a model system to investigate the role of alpha crystallins during lens development. Interestingly while zebrafish express one lens specific alpha A crystallin gene cryaa they express two alpha B crystallin genes with one evolving lens specificity cryaba and the other retaining the broad expression of its mammalian ortholog cryabb. In this study we used individual mutant zebrafish lines for all three alpha crystallin genes to determine the impact of their loss on age related cataract. Surprisingly unlike mouse knockout models we found that the loss of the alpha Ba crystallin gene cryaba led to an increase in lens opacity compared to cryaa null fish at 24 month of age. Loss of alpha A crystallin did not increase the prevalence of cataract. We also used single cell RNA Seq and RT qPCR data to show a shift in the lens expression of zebrafish alpha crystallins between 5 dpf and 10 dpf dpf with 5 dpf and 6 dpf lenses expressing cryaa almost exclusively and expression of cryaba and cryabb becoming more prominent post 10 dpf. These data show that cryaa is the primary alpha crystallin during early lens development while the protective role for cryaba becomes more important during lens aging. This study is the first to quantify cataract prevalence in wild type zebrafish showing that lens opacities develop in approximately 25% of fish by 18 month of age. None of the three alpha crystallin mutants showed a compensatory increase in t… | 4b | strain:ABC|dev stage:4 dpf|collection date:2020 10|geo loc name:USA: Oregon|sex:N/A|tissue:whole larvae|treatment:replicate B|BioSampleModel:Model organism or animal | scRNA seq of whole zebrafish larvae | 4b | 4b | 10X Chromium | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina HiSeq 4000 | SRP504662 | 4b_concatenated_R1.fastq.gz 4b_concatenated_R2.fastq.gz | fastq fastq | 71168549994.0 | 551694186.0 | 4b concatenated R1.fastq.gz | 0:28 1:101 | A:19966236558;C:16224236063;G:16033442126;T:18882486499;N:62148748 | 28 | 101 | 19966236558 | 16224236063 | 16033442126 | 18882486499 | 62148748 | SRX24395266 | SRS21150706 | SRA1854140 | University of Oregon|Institute of Neuroscience | University of Oregon | T | B | sc-like readlen | illumina | hiseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2024-04-29 | Larval | Larval | Whole Organism | All anatomical structures | ||||||||||||||||||||||||||||||||
| 31969 | 31969 | SRR28832528 | SRX24395265 | SRS21150705 | SRP504662 | PRJNA1105232 | Loss of alpha Ba crystallin but not alpha A crystallin increases age related cataract in the zebrafish lens | PRJNA1105232 | Other | The vertebrate eye lens is an unusual organ in that most of its cells lack nuclei and the ability to replace aging protein. The small heat shock protein alpha crystallins evolved to become key components of this lens possibly because of their ability to prevent aggregation of aging protein that would otherwise lead to lens opacity. Most vertebrates express two alpha crystallins alpha A and alpha B crystallin and mutations in each are linked to human cataract. In a mouse knockout model only the loss of alpha A crystallin led to early stage lens cataract. We have used the zebrafish as a model system to investigate the role of alpha crystallins during lens development. Interestingly while zebrafish express one lens specific alpha A crystallin gene cryaa they express two alpha B crystallin genes with one evolving lens specificity cryaba and the other retaining the broad expression of its mammalian ortholog cryabb. In this study we used individual mutant zebrafish lines for all three alpha crystallin genes to determine the impact of their loss on age related cataract. Surprisingly unlike mouse knockout models we found that the loss of the alpha Ba crystallin gene cryaba led to an increase in lens opacity compared to cryaa null fish at 24 month of age. Loss of alpha A crystallin did not increase the prevalence of cataract. We also used single cell RNA Seq and RT qPCR data to show a shift in the lens expression of zebrafish alpha crystallins between 5 dpf and 10 dpf dpf with 5 dpf and 6 dpf lenses expressing cryaa almost exclusively and expression of cryaba and cryabb becoming more prominent post 10 dpf. These data show that cryaa is the primary alpha crystallin during early lens development while the protective role for cryaba becomes more important during lens aging. This study is the first to quantify cataract prevalence in wild type zebrafish showing that lens opacities develop in approximately 25% of fish by 18 month of age. None of the three alpha crystallin mutants showed a compensatory increase in t… | 4a | strain:ABC|dev stage:4 dpf|collection date:2020 10|geo loc name:USA: Oregon|sex:N/A|tissue:whole larvae|treatment:replicate A|BioSampleModel:Model organism or animal | scRNA seq of whole zebrafish larvae | 4a | 4a | 10X Chromium | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina HiSeq 4000 | SRP504662 | 4a_concatenated_R1.fastq.gz 4a_concatenated_R2.fastq.gz | fastq fastq | 68732228646.0 | 532807974.0 | 4a concatenated R1.fastq.gz | 0:28 1:101 | A:19390338294;C:15653316754;G:15467157018;T:18205511068;N:15905512 | 28 | 101 | 19390338294 | 15653316754 | 15467157018 | 18205511068 | 15905512 | SRX24395265 | SRS21150705 | SRA1854140 | University of Oregon|Institute of Neuroscience | University of Oregon | T | B | sc-like readlen | illumina | hiseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2024-04-29 | Larval | Larval | Whole Organism | All anatomical structures | ||||||||||||||||||||||||||||||||
| 31970 | 31970 | SRR28832529 | SRX24395264 | SRS21150704 | SRP504662 | PRJNA1105232 | Loss of alpha Ba crystallin but not alpha A crystallin increases age related cataract in the zebrafish lens | PRJNA1105232 | Other | The vertebrate eye lens is an unusual organ in that most of its cells lack nuclei and the ability to replace aging protein. The small heat shock protein alpha crystallins evolved to become key components of this lens possibly because of their ability to prevent aggregation of aging protein that would otherwise lead to lens opacity. Most vertebrates express two alpha crystallins alpha A and alpha B crystallin and mutations in each are linked to human cataract. In a mouse knockout model only the loss of alpha A crystallin led to early stage lens cataract. We have used the zebrafish as a model system to investigate the role of alpha crystallins during lens development. Interestingly while zebrafish express one lens specific alpha A crystallin gene cryaa they express two alpha B crystallin genes with one evolving lens specificity cryaba and the other retaining the broad expression of its mammalian ortholog cryabb. In this study we used individual mutant zebrafish lines for all three alpha crystallin genes to determine the impact of their loss on age related cataract. Surprisingly unlike mouse knockout models we found that the loss of the alpha Ba crystallin gene cryaba led to an increase in lens opacity compared to cryaa null fish at 24 month of age. Loss of alpha A crystallin did not increase the prevalence of cataract. We also used single cell RNA Seq and RT qPCR data to show a shift in the lens expression of zebrafish alpha crystallins between 5 dpf and 10 dpf dpf with 5 dpf and 6 dpf lenses expressing cryaa almost exclusively and expression of cryaba and cryabb becoming more prominent post 10 dpf. These data show that cryaa is the primary alpha crystallin during early lens development while the protective role for cryaba becomes more important during lens aging. This study is the first to quantify cataract prevalence in wild type zebrafish showing that lens opacities develop in approximately 25% of fish by 18 month of age. None of the three alpha crystallin mutants showed a compensatory increase in t… | 3b | strain:ABC|dev stage:3 dpf|collection date:2020 10|geo loc name:USA: Oregon|sex:N/A|tissue:whole larvae|treatment:replicate B|BioSampleModel:Model organism or animal | scRNA seq of whole zebrafish larvae | 3b | 3b | 10X Chromium | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina HiSeq 4000 | SRP504662 | 3b_concatenated_R1.fastq.gz 3b_concatenated_R2.fastq.gz | fastq fastq | 64966771536.0 | 503618384.0 | 3b concatenated R1.fastq.gz | 0:28 1:101 | A:18187699043;C:14602482735;G:14672400468;T:17481975446;N:22213844 | 28 | 101 | 18187699043 | 14602482735 | 14672400468 | 17481975446 | 22213844 | SRX24395264 | SRS21150704 | SRA1854140 | University of Oregon|Institute of Neuroscience | University of Oregon | T | B | sc-like readlen | illumina | hiseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2024-04-29 | Larval | Larval | Whole Organism | All anatomical structures | ||||||||||||||||||||||||||||||||
| 31971 | 31971 | SRR28832530 | SRX24395263 | SRS21150703 | SRP504662 | PRJNA1105232 | Loss of alpha Ba crystallin but not alpha A crystallin increases age related cataract in the zebrafish lens | PRJNA1105232 | Other | The vertebrate eye lens is an unusual organ in that most of its cells lack nuclei and the ability to replace aging protein. The small heat shock protein alpha crystallins evolved to become key components of this lens possibly because of their ability to prevent aggregation of aging protein that would otherwise lead to lens opacity. Most vertebrates express two alpha crystallins alpha A and alpha B crystallin and mutations in each are linked to human cataract. In a mouse knockout model only the loss of alpha A crystallin led to early stage lens cataract. We have used the zebrafish as a model system to investigate the role of alpha crystallins during lens development. Interestingly while zebrafish express one lens specific alpha A crystallin gene cryaa they express two alpha B crystallin genes with one evolving lens specificity cryaba and the other retaining the broad expression of its mammalian ortholog cryabb. In this study we used individual mutant zebrafish lines for all three alpha crystallin genes to determine the impact of their loss on age related cataract. Surprisingly unlike mouse knockout models we found that the loss of the alpha Ba crystallin gene cryaba led to an increase in lens opacity compared to cryaa null fish at 24 month of age. Loss of alpha A crystallin did not increase the prevalence of cataract. We also used single cell RNA Seq and RT qPCR data to show a shift in the lens expression of zebrafish alpha crystallins between 5 dpf and 10 dpf dpf with 5 dpf and 6 dpf lenses expressing cryaa almost exclusively and expression of cryaba and cryabb becoming more prominent post 10 dpf. These data show that cryaa is the primary alpha crystallin during early lens development while the protective role for cryaba becomes more important during lens aging. This study is the first to quantify cataract prevalence in wild type zebrafish showing that lens opacities develop in approximately 25% of fish by 18 month of age. None of the three alpha crystallin mutants showed a compensatory increase in t… | 3a | strain:ABC|dev stage:3 dpf|collection date:2020 10|geo loc name:USA: Oregon|sex:N/A|tissue:whole larvae|treatment:replicate A|BioSampleModel:Model organism or animal | scRNA seq of whole zebrafish larvae | 3a | 3a | 10X Chromium | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | Illumina HiSeq 4000 | SRP504662 | 3a_concatenated_R1.fastq.gz 3a_concatenated_R2.fastq.gz | fastq fastq | 68966162664.0 | 534621416.0 | 3a concatenated R1.fastq.gz | 0:28 1:101 | A:19232364475;C:15520559864;G:15732756322;T:18456921265;N:23560738 | 28 | 101 | 19232364475 | 15520559864 | 15732756322 | 18456921265 | 23560738 | SRX24395263 | SRS21150703 | SRA1854140 | University of Oregon|Institute of Neuroscience | University of Oregon | T | B | sc-like readlen | illumina | hiseq_era | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | United States | 2024-04-29 | Larval | Larval | Whole Organism | All anatomical structures | ||||||||||||||||||||||||||||||||
| 60657 | 60657 | SRR15046102 | SRX11356738 | SRS9403587 | SRP278034 | PRJNA657343 | Satb2 acts as a gatekeeper for gene regulatory transitions during early embryonic development | PRJNA657343 | Other | Comprehensive integration of transcriptome genome wide occupancy and chromatin accessibility profiles in satb2 loss of function and gain of function systems to discover novel and evolutionary conserved molecular interplays between Satb2 and the genetic drivers of neurogenesis and neural crest development program. | scRNAseq | scRNAseq Satb2 MUT 14som | scRNAseq Satb2 MUT 14som | strain:Satb2 Mutant|age:14 somite|dev stage:14 somite|sex:not applicable|tissue:whole embryo|replicate:replicate = Biological replicate1|BioSampleModel:Model organism or animal | Satb2 mutants single cell RNAseq | Satb2 MUT 14ss scRNAseq | Satb2 MUT 14ss scRNAseq | according 10X three primemRNA seq V3.2 protocol | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | NextSeq 550 | SRP278034 | loader:fastq load.py | 23142978710.0 | 177123922.0 | scRNAseq Satb2 MUT 14som I1.fastq.gz | 0:8 1:30 2:92.66 | A:4753575949;C:3375880000;G:3751151628;T:4500225651;N:31436446 | 8 | 30 | 92 | 4753575949 | 3375880000 | 3751151628 | 4500225651 | 31436446 | SRX11356738 | SRS9403587 | SRA1254741 | IISER-PUNE|biology | IISER-PUNE | 1 | 0.80351 | 0.14479 | 0.79695 | 0.55274 | 101 | B | usable mapping rate | illumina | nextseq | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | India | 2021-07-13 | Segmentation | Embryo | Whole Organism | All anatomical structures | |||||||||||||||||||||||||
| 60658 | 60658 | SRR15046103 | SRX11356737 | SRS9403586 | SRP278034 | PRJNA657343 | Satb2 acts as a gatekeeper for gene regulatory transitions during early embryonic development | PRJNA657343 | Other | Comprehensive integration of transcriptome genome wide occupancy and chromatin accessibility profiles in satb2 loss of function and gain of function systems to discover novel and evolutionary conserved molecular interplays between Satb2 and the genetic drivers of neurogenesis and neural crest development program. | scRNAseq | scRNAseq WT 14som | scRNAseq WT 14som | strain:Wild type sibling|age:14 somite|dev stage:14 somite|sex:not applicable|tissue:whole embryo|replicate:replicate = Biological replicate1|BioSampleModel:Model organism or animal | Satb2 siblings single cell RNAseq | WT sibs 14ss scRNAseq | WT sibs 14ss scRNAseq | according 10X three primemRNA seq V3.2 protocol | RNA-Seq | TRANSCRIPTOMIC SINGLE CELL | Oligo-dT | PAIRED | ILLUMINA | NextSeq 550 | SRP278034 | loader:fastq load.py|options: mixedDeflines maxErrorCount=0 | 27847103625.0 | 200338875.0 | scRNAseq WT 14som I1.fastq.gz | 0:8 1:30 2:101 | A:5948912529;C:4138132473;G:4588280753;T:5527087357;N:31813263 | 8 | 30 | 101 | 5948912529 | 4138132473 | 4588280753 | 5527087357 | 31813263 | SRX11356737 | SRS9403586 | SRA1254741 | IISER-PUNE|biology | IISER-PUNE | 1 | 0.92298 | 0.15133 | 0.78906 | 0.54933 | 101 | B | usable mapping rate | illumina | nextseq | unknown | poly_a | unknown | sc | single_cell_droplet | 10x | India | 2021-07-13 | Segmentation | Embryo | Whole Organism | All anatomical structures |
Advanced export
JSON shape: default, array, newline-delimited
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");;