drl expression initiates during gastrulation and condenses as a band of cells at the prospective lateral embryo margin. In late epiboly, drl:EGFP is detectable as a band of scattered EGFP-fluorescent cells; after gastrulation, drl:EGFP-positive cells coalesce at the embryo margin that then in somitogenesis break down into the anterior and posterior lateral plate with subsequent cell migrations that form the posterior vascular/hematopoietic stripes and the anterior cardiovascular and myeloid precursors.
Chamber identity programs drive early functional partitioning of the heart.
Age, Specimen part
View SamplesWe report global RNA expression profiles from whole zebrafish hearts 24 hours after ventricle amputation. Zebrafish were exposed to atropine or water following surgery.
Nerves Regulate Cardiomyocyte Proliferation and Heart Regeneration.
Specimen part, Treatment
View SamplesIn order to identify genes dysregulated by the aberrant transcriptional activity of RUNX1-RUNX1T1, we used microarrays to determine the effect of this mutation on gene expression during myeloid and erythroid development of normal human progenitor cells.
Transcriptional dysregulation mediated by RUNX1-RUNX1T1 in normal human progenitor cells and in acute myeloid leukaemia.
Specimen part
View SamplesLymphoblast cells from a patient with Freidriech's Ataxia were incubated with pyrrole-imidazole polyamides targeted to the GAA triplet repeat in the intron 1. The polyamides were shown in cell culture to increase levels of endogenous frataxin mRNA. A normal sibling derived lymphoblast cell line was used as a control.
DNA sequence-specific polyamides alleviate transcription inhibition associated with long GAA.TTC repeats in Friedreich's ataxia.
No sample metadata fields
View SamplesHuman brain structure and size requires regulated division of neural stem cells (NSCs). NSCs undergo precise divisions to self-renew and to produce intermediate neural progenitors (INPs) and neurons. The factors that regulate NSC divisions remain poorly understood, as do mechanistic explanations of how aberrant NSC division causes reduced brain size, as seen in microcephaly. Here we demonstrate that Magoh, a component of the core exon junction complex (EJC) that binds spliced RNA, controls cerebral cortical size by regulating NSC division. Magoh haploinsufficiency causes microcephaly due to INP depletion, neuronal apoptosis, and improper mitotic spindle orientation. Defective mitosis underlies these phenotypes as depletion of EJC components disrupts mitotic spindle integrity, chromosome number and genomic stability. We show that an essential function of Magoh is to regulate expression of the human microcephaly protein, LIS1, and that Lis1 addition rescues neurogenesis defects caused by Magoh knockdown, thus providing a genetic explanation for the microcephaly. This study uncovers new requirements for the EJC in brain development, NSC maintenance, mitosis and chromosome stability, thus implicating this complex in the pathogenesis of microcephaly.
The exon junction complex component Magoh controls brain size by regulating neural stem cell division.
Specimen part
View SamplesIn this data set, we reported for the first time that huanglongbing disease (HLB) induces major changes in the expression of global genes in flavedo, vascular and juice vesicle tissues of citrus fruit.
Gene expression in Citrus sinensis fruit tissues harvested from huanglongbing-infected trees: comparison with girdled fruit.
Specimen part
View SamplesThe purpose of the present work was to examine gene expression patterns in a rat keratinocyte line exposed to a 56Fe ion beam
Gene expression and cell cycle arrest in a rat keratinocyte line exposed to 56Fe ions.
No sample metadata fields
View SamplesBackground: Friedreich ataxia, an autosomal recessive neurodegenerative and cardiac disease, is caused by abnormally low levels of frataxin, an essential mitochondrial protein. All Friedreich ataxia patients carry a GAA/TTC repeat expansion in the first intron of the frataxin gene, either in the homozygous state or in compound heterozygosity with other loss-of-function mutations. The GAA expansion inhibits frataxin expression through a heterochromatin-mediated repression mechanism. Histone modifications that are characteristic of silenced genes in heterochromatic regions occur at expanded alleles in cells from Friedreich ataxia patients, including increased trimethylation of histone H3 at lysine 9 and hypoacetylation of histones H3 and H4.
HDAC inhibitors correct frataxin deficiency in a Friedreich ataxia mouse model.
No sample metadata fields
View SamplesIntegration of the HIV-1 provirus in the host genome ensures a persistent supply of latently infected cells. This latent reservoir is recalcitrant to antiretroviral therapy (ART) making lifelong treatment the only option for patients. The “shock and kill” strategy aims to eradicate latent HIV by reactivating proviral gene expression followed by ART treatment. Gene specific transcriptional activation can be achieved using the RNA-guided CRISPR-Cas9 system comprising small guide RNAs (sgRNAs) with a nuclease deficient Cas9 mutant (dCas9) fused to the VP64 transactivation domain (dCas9-VP64). We engineered this system to target 23 sites within the LTR promoter of HIV-1 and identified a “hotspot” for activation. We studied the functionality of activating sgRNAs to transcriptionally modulate the latent proviral genome across multiple different in vitro latency cell models including several J-Lat, ACH2 J1.1 and the CEM T cell model comprising a single clonal population of integrated mCherry-IRES-Tat from a full-length HIV LTR (LChIT). While we observed variable responses of latent cell models to well-characterized chemical stimuli, we detected consistent efficient activation of latent virus mediated by activator sgRNAs. In addition, transcriptome analysis of chemically treated cells revealed massive non-specific gene dysregulation whereas by comparison, dCas9-VP64/sgRNAs induced specific activation of the integrated provirus. In conclusion, we show the potential for CRISPR-mediated gene activation systems to provide enhanced efficiency and specificity in a targeted latency reactivation strategy. This represents a promising approach to a “functional cure” of HIV/AIDS. Overall design: Three experimental conditions (sgRNA control, TNF treated and sgRNA against the LTR of HIV-1) were analyzed in triplicate using two sequencing lanes
Potent and Targeted Activation of Latent HIV-1 Using the CRISPR/dCas9 Activator Complex.
No sample metadata fields
View SamplesSingle cell RNAseq analysis of hair cells isolated from the mouse utricle at three postnatal time points Overall design: Utricular hair cells were isolated at P12 (49 cells) and P100 (23 cells) and then combined with a previously published single cell data set (samples from GSE71982) containing 35 utricular hair cells isolated at P1 (Burns et al., 2015) The previously published single cell P1 samples have been re-normalized. These samples are included in this series and all processed data are available in the file ute_normalized_data.txt, available at the foot of this record.
Characterization of spatial and temporal development of Type I and Type II hair cells in the mouse utricle using new cell-type-specific markers.
Specimen part, Subject
View Samples