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accession-icon SRP115384
Regulation of posterior body and ectodermal morphogenesis in zebrafish by localized Yap1 and Wwtr1
  • organism-icon Danio rerio
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

The vertebrate embryo undergoes a series of dramatic morphological changes as the body extends to form the complete anterior-posterior axis during the somite-forming stages. The molecular mechanisms regulating these complex processes are still largely unknown. We show that the Hippo pathway transcriptional coactivators Yap1 and Wwtr1 are specifically localized to the ectoderm and notochord, and play a critical and unexpected role in posterior body extension by regulating the assembly of Fibronectin underneath the ectoderm and surrounding the notochord. We also find that Yap1/Wwtr1, also acting through Fibronectin, have an essential role in the ectodermal morphogenesis necessary to form the initial dorsal and ventral fins, a process that had been thought to involve bending of an epithelial sheet, but which we now show involves active cell migration. Our results reveal how the Hippo pathway transcriptional program, localized to two specific tissues, acts to control essential morphological events in the vertebrate embryo. Overall design: two biological replicates of tails of yap1/wwtr1 double homozygous mutants and siblings (24 each at 16-18 somite stage) were collected for RNAseq. Tails are tissues of the posterior end until the third newest somite (S-III).

Publication Title

Regulation of posterior body and epidermal morphogenesis in zebrafish by localized Yap1 and Wwtr1.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP068656
RNA sequencing of adult zebrafish spinal cord
  • organism-icon Danio rerio
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

The goal of this study is to determine gene expression changes in the adult zebrafish spinal cord at 2 weeks after complete transection. Overall design: 2 samples were analyzed in duplicates: sham injured spinal cord and transected spinal cord at 2 weeks post-injury

Publication Title

Injury-induced ctgfa directs glial bridging and spinal cord regeneration in zebrafish.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12039
Regulation of endothelial gene expression by miR-126 in human and zebrafish
  • organism-icon Danio rerio, Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Zebrafish Genome Array (zebrafish)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

miR-126 regulates angiogenic signaling and vascular integrity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12012
Regulation of zebrafish endothelial gene expression by miR-126
  • organism-icon Danio rerio
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Fish, JE, Santoro, MM, Morton, SU, Yu, S, Yeh, RF, Wythe, JD, Ivey, KI, Bruneau, BG, Stainier, DYR, and Srivastava, D. (2008). miR-126 Regulates Angiogenic Signaling and Vascular Integrity. Developmental Cell 15, 272-284.

Publication Title

miR-126 regulates angiogenic signaling and vascular integrity.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE12011
Regulation of human endothelial gene expression by miR-126
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish), Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Fish, JE, Santoro, MM, Morton, SU, Yu, S, Yeh, RF, Wythe, JD, Ivey, KI, Bruneau, BG, Stainier, DYR, and Srivastava, D. (2008). miR-126 Regulates Angiogenic Signaling and Vascular Integrity. Developmental Cell 15, 272-284.

Publication Title

miR-126 regulates angiogenic signaling and vascular integrity.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP119354
Atrial Molecular Asymmetry Precedes the Emergence of Cardiac Septation [RNA-seq]
  • organism-icon Danio rerio
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Comparison of the meis2b+ and the meis2b- halves of the atrium of the adult zebrafish atrium reveals the existence of two different transcriptional domains. These two domains analogous to that of the two atria in terrestrial vertebrates Overall design: To determine the expression profiles of the Tg(meis2b-reporter)-positive vs -negative atrial compartments, a total of 6 hearts of 3 mpf Tg(meis2b-reporter) zebrafish were micro-dissected. A total of 4 pools were made: the first two pools, each contained 3 Tg(meis2b-reporter)-positive atrial compartments, and the other two contained the Tg(meis2b-reporter)-negative halves.

Publication Title

Distinct myocardial lineages break atrial symmetry during cardiogenesis in zebrafish.

Sample Metadata Fields

Age, Specimen part, Cell line, Subject

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accession-icon SRP140689
Loss of the Mia40a oxidoreductase leads to hepato-pancreatic insufficiency in the zebrafish
  • organism-icon Danio rerio
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Development and function of tissues and organs are powered by the activity of mitochondria. In humans, inherited genetic mutations that lead to progressive mitochondrial pathology often manifest during infancy and can lead to death, reflecting the indispensable nature of mitochondrial function and biogenesis. Here, we describe a zebrafish mutant for the gene mia40a, the life-essential homologue of the evolutionarily conserved Mia40 oxidoreductase which drives the biogenesis of cysteine-rich mitochondrial proteins. We report that mia40a mutant animals undergo progressive cellular respiration defects and develop enlarged mitochondria in skeletal muscles before their ultimate at the larval stage. We generated a rich transcriptomic and proteomic resource that allowed us to identify abnormalities in the development of endodermal organs, in particular the liver and pancreas. We identify the acinar cells of the exocrine pancreas to be severely affected by mutations in the MIA pathway. Our data contribute to a better understanding of the molecular, cellular and organismal effects of mitochondrial deficiency, important for the accurate diagnosis and future treatment strategies of these diseases. Overall design: Embryos obtained from an in-cross of heterozygous mia40awaw1/+ siblings were genotyped at 3 dpf. Pools of five mia40+/+ or mia40waw1/waw1 larvae, derived from the same clutch, were collected at indicated time-points for RNA extraction and transcriptomic profiling. Larvae used in 8 dpf experiments were subjected to external feeding from 5dpf before being collected for the analysis at 8dpf.

Publication Title

Loss of the Mia40a oxidoreductase leads to hepato-pancreatic insufficiency in zebrafish.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE26191
Chromatin Remodeling Complex Dosage Modulates Transcription Factor Function in Heart Development
  • organism-icon Mus musculus
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Dominant mutations in cardiac transcription factor genes cause human inherited congenital heart defects (CHDs), but their molecular basis is not understood. Transcription factors and Brg1/Brm-associated factor (BAF) chromatin remodeling complex interactions suggest potential mechanisms, but the role of BAF complexes in cardiogenesis is not known. Here we show that dosage of Brg1 is critical for mouse and zebrafish cardiogenesis. Disrupting the balance between Brg1 and disease-causing cardiac transcription factors, including Tbx5, Tbx20, and Nkx2-5, causes severe cardiac anomalies, revealing an essential allelic balance between Brg1 and these cardiac transcription factor genes. This suggests that relative levels of transcription factors and BAF complexes are important for heart development, which is supported by reduced occupancy of Brg1 at cardiac genes in Tbx5 haploinsufficient hearts. Our results reveal complex dosage-sensitive interdependence between transcription factors and BAF complexes, providing a potential mechanism underlying transcription factor haploinsufficiency, with implications for multigenic inheritance of CHDs.

Publication Title

Chromatin remodelling complex dosage modulates transcription factor function in heart development.

Sample Metadata Fields

Specimen part

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accession-icon GSE146110
The role of lncRNA Lassie in endothelial cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

The vascular endothelium forms a physical barrier between blood and the surrounding tissue. Its constant exposure to haemodynamic shear stress controls endothelial barrier function which is of major importance for vascular homeostasis. The role of long non-coding RNAs (lncRNAs) in this process remains elusive. Here we identify the shear stress-induced lncRNA LASSIE (linc00520) as a stabilizer of adherens junctions (AJs) in endothelial cells (ECs), that is indispensable for normal endothelial barrier function and shear stress sensing. Silencing of LASSIE in ECs resulted in impaired cell survival, loss of cell-cell contacts and failure to align in the direction of flow. RNA affinity purification followed by mass spectrometry identified several junction proteins associated with LASSIE, including the endothelial adhesion protein PECAM-1 and intermediate filament (IF) protein nestin. Proteomic analysis of VE-cadherin-associated proteins showed that LASSIE silencing reduces VE-cadherin interaction with nestin and microtubule (MT)-associated cytoskeletal proteins. We confirmed that LASSIE silencing results in a decreased connection between VE-Cadherin and the cytoskeleton, resulting in loss of barrier function and shear stress sensing. Together, this study identifies the shear stress-induced lncRNA LASSIE as a critical link between AJs and the IF cytoskeleton, which is indispensable for normal EC junction stabilization and shear stress sensing.

Publication Title

Long non-coding RNA LASSIE regulates shear stress sensing and endothelial barrier function.

Sample Metadata Fields

Specimen part

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accession-icon SRP068242
Differential gene expression m39 vs. siblings
  • organism-icon Danio rerio
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

RNAseq analysis of cloche m39 mutant zebrafish embryos and wild type siblings at 90% epiboly - tailbud stage Overall design: In order to isolate the cloche gene, RNAseq was performed on a deletion allele of the zebrafish cloche mutant. RNA was extracted from individual embryos at a stage the cloche gene was predicted to be expressed based on previous literature. RNA from the respective genoptypes was then pooled and subjected to RNAseq analysis.

Publication Title

Cloche is a bHLH-PAS transcription factor that drives haemato-vascular specification.

Sample Metadata Fields

No sample metadata fields

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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