Small RNA-seq on MCF10A, HCT116 and HCT116p53-/- cell lines after induction of DNA damage (5 Gy Irradiation). Overall design: Small RNA-seq on MCF10A, HCT116 and HCT116p53-/- at 4 and 24 hours after induction of DNA damage (5 Gy Irradiation), done in duplicate with respective control (0 hour) using illumina Genome Analyzer IIx
p53 shapes genome-wide and cell type-specific changes in microRNA expression during the human DNA damage response.
Cell line, Treatment, Subject, Time
View SamplesMessenger (m)RNA export from the nucleus is essential for eukaryotic gene expression. Here, we identify a transcript-selective nuclear export mechanism affecting certain human transcripts, enriched for functions in genome duplication and repair, controlled by inositol polyphosphate multikinase (IPMK), an enzyme catalyzing inositol polyphosphate and phosphoinositide turnover. We studied transcripts encoding RAD51, a protein essential for DNA repair by homologous recombination (HR), to characterize the mechanism underlying IPMK-regulated mRNA export. IPMK depletion or catalytic inactivation selectively decreases the nuclear export of RAD51 mRNA, and RAD51 protein abundance, thereby impairing HR. Recognition of a sequence motif in the untranslated region of RAD51 transcripts by the mRNA export factor ALY requires IPMK. Phosphatidylinositol (3,4,5)-trisphosphate (PIP3), an IPMK product, restores ALY recognition in IPMK-depleted cell extracts, suggesting a mechanism underlying transcript selection. Our findings implicate IPMK in a transcript-selective mRNA export pathway controlled by phosphoinositide turnover that preserves genome integrity in humans.
Human inositol polyphosphate multikinase regulates transcript-selective nuclear mRNA export to preserve genome integrity.
Cell line
View SamplesStranded, single-end, polyA+, transcriptional profiles were created from ovaries of sterile and fertile sov heteroallelic mutants and Gal4 driven sov RNAi knockdowns. Overall design: 15 ovaries from 4-5 day old post-eclosion females grown in uncrowded conditions were dissected and pooled for each biological replicate for a total of three replicates per genotype. Total RNA was extracted from tissues and polyA RNA was isolated and used to prepare stranded RNAseq libraries. 50 bp single-end sequencing was performed and mapped to Drosophila melanogaster release 6.21 genome.
<i>Drosophila</i> Heterochromatin Stabilization Requires the Zinc-Finger Protein Small Ovary.
Sex, Subject
View SamplesLipid overload and adipocyte dysfunction are key to the development of insulin resistance and can be induced by a high-fat diet. CD1d-restricted invariant natural killer T (iNKT) cells have been proposed as mediators between lipid overload and insulin resistance, but recent studies found decreased iNKT cell numbers and marginal effects of iNKT cell depletion on insulin resistance under high-fat diet conditions. Here, we focused on the role of iNKT cells under normal conditions. We showed that iNKT celldeficient mice on a low-fat diet, considered a normal diet for mice, displayed a distinctive insulin resistance phenotype without overt adipose tissue inflammation. Insulin resistance was characterized by adipocyte dysfunction, including adipocyte hypertrophy, increased leptin, and decreased adiponectin levels. The lack of liver abnormalities in CD1d-null mice together with the enrichment of CD1d-restricted iNKT cells in both mouse and human adipose tissue indicated a specific role for adipose tissueresident iNKT cells in the development of insulin resistance. Strikingly, iNKT cell function was directly modulated by adipocytes, which acted as lipid antigen-presenting cells in a CD1d-mediated fashion. Based on these findings, we propose that, especially under low-fat diet conditions, adipose tissueresident iNKT cells maintain healthy adipose tissue through direct interplay with adipocytes and prevent insulin resistance.
Natural killer T cells in adipose tissue prevent insulin resistance.
Specimen part
View SamplesSingle cell RNA seq and bioinformatic analysis is used to characterize myeloid differentiation to uncover novel transcriptional networks and key drivers of hematoipoietic development Overall design: Single cell RNA seq of different hematopoietic populations integrated with Chip seq involving multiple markers
Single-cell analysis of mixed-lineage states leading to a binary cell fate choice.
No sample metadata fields
View SamplesSingle cell RNA seq and bioinformatic analysis is used to characterize myeloid differentiation to uncover novel transcriptional networks and key drivers of hematoipoietic development Overall design: Single cell RNA seq of different hematopoietic populations integrated with Chip seq involving multiple markers
Single-cell analysis of mixed-lineage states leading to a binary cell fate choice.
No sample metadata fields
View SamplesSingle cell RNA seq and bioinformatic analysis is used to characterize myeloid differentiation to uncover novel transcriptional networks and key drivers of hematoipoietic development Overall design: Single cell RNA seq of different hematopoietic populations integrated with Chip seq involving multiple markers
Single-cell analysis of mixed-lineage states leading to a binary cell fate choice.
No sample metadata fields
View SamplesSingle cell RNA seq and bioinformatic analysis is used to characterize myeloid differentiation to uncover novel transcriptional networks and key drivers of hematoipoietic development Overall design: Single cell RNA seq of different hematopoietic populations integrated with Chip seq involving multiple markers
Single-cell analysis of mixed-lineage states leading to a binary cell fate choice.
No sample metadata fields
View SamplesSingle cell RNA seq and bioinformatic analysis is used to characterize myeloid differentiation to uncover novel transcriptional networks and key drivers of hematoipoietic development Overall design: Single cell RNA seq of different hematopoietic populations integrated with Chip seq involving multiple markers
Single-cell analysis of mixed-lineage states leading to a binary cell fate choice.
No sample metadata fields
View SamplesSingle cell RNA seq and bioinformatic analysis is used to characterize myeloid differentiation to uncover novel transcriptional networks and key drivers of hematoipoietic development Overall design: Single cell RNA seq of different hematopoietic populations integrated with Chip seq involving multiple markers
Single-cell analysis of mixed-lineage states leading to a binary cell fate choice.
Specimen part, Cell line, Subject
View Samples