The HIF (hypoxia-inducible factor) transcription factor is the master regulator of the metazoan response to chronic hypoxia. In addition to promoting adaptations to low oxygen, HIF drives cytoprotective mechanisms in response to stresses and modulates neural circuit function. How most HIF targets act in the control of the diverse aspects of HIF-regulated biology remains unknown. We discovered that a HIF target, the C. elegans gene cyp-36A1, is required for numerous HIF-dependent processes, including modulation of gene expression, stress resistance, and behavior. cyp-36A1 encodes a cytochrome P450 enzyme that we show controls expression of more than a third of HIF-induced genes. CYP-36A1 acts cell non-autonomously by regulating the activity of the nuclear hormone receptor NHR-46, suggesting that CYP-36A1 functions as a biosynthetic enzyme for a hormone ligand of this receptor. We propose that regulation of HIF effectors through activation of cytochrome P450 enzyme/nuclear receptor signaling pathways could similarly occur in humans. Overall design: RNA-seq experiment characterizing C. elegans strains mutant for one or more member of the egl-9/hif-1/cyp-36A1 signaling pathway. Experiment was performed with two biological replicates per strain. N2 was used as the wild-type control.
Hypoxia-inducible factor cell non-autonomously regulates <i>C. elegans</i> stress responses and behavior via a nuclear receptor.
Specimen part, Subject
View SamplesWe profiled how animals RNA expression changes in response to osmotic stress, how lin-45 mutants have an altered response to osmotic stress, and how maternal preconditioning at 300 mM NaCl modifies progeny response to 500 mM NaCl Overall design: Examination of total RNAseq at 50 mM NaCl, 500 mM NaCl, and 500 mM NaCl from maternally preconditioned animals
Insulin-like signalling to the maternal germline controls progeny response to osmotic stress.
Subject, Time
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Chromosome-biased binding and gene regulation by the Caenorhabditis elegans DRM complex.
Specimen part
View SamplesDRM is a conserved transcription factor complex that includes E2F/DP and pRB family proteins and plays important roles in development and cancer. Here we perform microarray expression profiling analysis of lin-54, a DNA-binding member of the DRM complex. To identify genes regulated by LIN-54 in soma and germline, we analyzed wild-type and lin-54 mutant C. elegans embryos and isolated germlines. We chose embryos because they consist primarily of somatic cells, at a developmental stage with both active cell divisions and dynamic developmental gene expression programs. Since lin-54 null animals are sterile, embryos were obtained from a strain carrying the partial loss-of-function allele lin-54(n2990). Germlines were dissected from lin-54(n3423) null adults that lack detectable transcript and protein. The results revealed conserved roles for DRM in regulating genes involved in cell division, development, and reproduction. We find LIN-54 promotes expression of reproduction genes in the germline, but prevents ectopic activation of germline-specific genes in embryonic soma. Strikingly, genomics and cytological analyses show that DRM binding, a DRM binding motif, and LIN-54-regulated genes are all autosome-enriched. One paradoxical exception occurs the germline, where DRM binds autosomes but genes down-regulated in DRM mutants are enriched on X chromosomes.
Chromosome-biased binding and gene regulation by the Caenorhabditis elegans DRM complex.
Specimen part
View SamplesThe goal of this experiment was to determine gene expression changes during influenza A virus infection as the result of expression influenza virus inducible miRNAs in A549 cells.
Small RNA profiling of influenza A virus-infected cells identifies miR-449b as a regulator of histone deacetylase 1 and interferon beta.
Cell line
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Gene expression profiling of skin and blood in hidradenitis suppurativa.
Specimen part, Disease, Disease stage, Subject
View SamplesTo acquire a better understanding of the molecular pathogenesis of HS, we performed mRNA microarray studies to compare gene expression in lesional skin to healthy skin of HS patients.
Gene expression profiling of skin and blood in hidradenitis suppurativa.
Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Altering TET dioxygenase levels within physiological range affects DNA methylation dynamics of HEK293 cells.
Specimen part, Cell line, Treatment
View SamplesTo acquire a better understanding of the molecular pathogenesis of hidradenitis suppurativa (HS), we performed mRNA microarray studies to compare whole blood gene expression of HS patients to that of healthy normal subjects.
Gene expression profiling of skin and blood in hidradenitis suppurativa.
Specimen part, Disease, Disease stage, Subject
View SamplesOur study in zebrafish is the first to use an animal model to understand the biology of the developmental disorder Roberts Syndrome (RBS). RBS is caused by mutations in the ESCO2 gene.
A zebrafish model of Roberts syndrome reveals that Esco2 depletion interferes with development by disrupting the cell cycle.
Age, Specimen part
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