Embryo exposure to heat shock and teratogen
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ABSTRACT:
PROVIDER: PRJNA87919 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Analysis of embryos exposed to either: [1] 40 uM 4-hydroperoxycyclophosphamide for 1 or 5 hours at 37°C [2] 43°C heat shock for 15 minutes followed by 1 or 5 hours at 37°C This SuperSeries is composed of the SubSeries listed below.
2004-02-24 | GSE905 | GEO
Project description:Analysis of embryos exposed to either: [1] 40 uM 4-hydroperoxycyclophosphamide for 1 or 5 hours at 37°C [2] 43°C heat shock for 15 minutes followed by 1 or 5 hours at 37°C This SuperSeries is composed of the following subset Series: GSE866: CP 1hr GSE869: HS 1hr GSE870: HS 5hr GSE888: CP 5hr
2004-02-23 | E-GEOD-905 | biostudies-arrayexpress
Project description:Ethanol is a well-known teratogen. While this teratogenic potential is well-characterized clinically, the mechanisms through which ethanol exposure results in developmental defects remain unclear. Here we use the zebrafish model to elucidate eye-specific mechanisms that may underlie ethanol-mediated microphthalmia (reduced eye size), using time-series microarray analysis of gene expression of eye tissues of embryos exposed to 1.5% ethanol vs. untreated embryos. We identified 62 genes differentially expressed in ethanol-treated as compared to control zebrafish eyes from all sampling times over the period of retinal neurogenesis (24-48 hours post-fertilization). Application of the EDGE (extraction of differential gene expression) algorithm identified over 3000 genes differentially expressed over developmental time in ethanol-treated embryo eyes as compared to untreated embryo eyes. These lists included several genes indicating a mis-regulated cellular stress response (heat shock response) due to ethanol exposure. Combined treatment with sub-threshold levels of ethanol and a morpholino (MO) targeting heat shock factor 1 (hsf-1) mRNA resulted in a microphthalmic phenotype, suggesting convergent molecular pathways. Manipulation of the heat shock response by thermal preconditioning partially prevented ethanol-mediated microphthalmia while maintaining Hsf-1 expression. Together these data are consistent with roles for reduced Hsf-1 in mediating microphthalmic effects of embryonic ethanol exposure in zebrafish.
2014-01-01 | GSE51427 | GEO
Project description:Ethanol is a well-known teratogen. While this teratogenic potential is well-characterized clinically, the mechanisms through which ethanol exposure results in developmental defects remain unclear. Here we use the zebrafish model to elucidate eye-specific mechanisms that may underlie ethanol-mediated microphthalmia (reduced eye size), using time-series microarray analysis of gene expression of eye tissues of embryos exposed to 1.5% ethanol vs. untreated embryos. We identified 62 genes differentially expressed in ethanol-treated as compared to control zebrafish eyes from all sampling times over the period of retinal neurogenesis (24-48 hours post-fertilization). Application of the EDGE (extraction of differential gene expression) algorithm identified over 3000 genes differentially expressed over developmental time in ethanol-treated embryo eyes as compared to untreated embryo eyes. These lists included several genes indicating a mis-regulated cellular stress response (heat shock response) due to ethanol exposure. Combined treatment with sub-threshold levels of ethanol and a morpholino (MO) targeting heat shock factor 1 (hsf-1) mRNA resulted in a microphthalmic phenotype, suggesting convergent molecular pathways. Manipulation of the heat shock response by thermal preconditioning partially prevented ethanol-mediated microphthalmia while maintaining Hsf-1 expression. Together these data are consistent with roles for reduced Hsf-1 in mediating microphthalmic effects of embryonic ethanol exposure in zebrafish. time series, 9 samples, no replicates
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Project description:The Heat Shock response (HSR) is a highly conserved transcriptional program induced by the exposure to a variety of environmental stressors. Following an insult, a small subset of genes, known as the Heat Shock genes, are rapidly induced by the Heat Shock Factors (HSFs) to maintain protein homeostasis and ensure cell survival. In this study, we demonstrate that the RNAPII interactor RPRD1B is required for proper transcription of heat shock induced genes and for survival to heat shock.
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Project description:The Heat Shock response (HSR) is a highly conserved transcriptional program induced by the exposure to a variety of environmental stressors. Following an insult, a small subset of genes, known as the Heat Shock genes, are rapidly induced by the Heat Shock Factors (HSFs) to maintain protein homeostasis and ensure cell survival. In this study, we demonstrate that the RNAPII interactor RPRD1B is required for proper transcription of heat shock induced genes and for survival to heat shock.
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Project description:ATAC-seq in human K562 erythroleukemia cells that were either unconditioned (s_uC and HSS_uC), preconditioned with a single heat shock exposure (s_pC), or preconditioned with multiple heat exposures (HSS_pC). After two day recovery from the preconditioning, during which the cells underwent two mitotic divisions, the cells were additionally subjected to a single heat shock to analyze heat-induced changes in chromatin accessibility in unconditioned versus preconditioned cells.
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Project description:The proteomics data revealed a comprehensive response mechanism of S. melonis TY exposure to heat shock.
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Project description:Whole-genome analysis of heat shock factor binding sites in Drosophila melanogaster. Heat shock factor IP DNA or Mock IP DNA from heat shocked Kc 167 cells compared to whole cell extract on Agilent 2x244k tiling arrays.
2011-01-05 | GSE19744 | GEO
Project description:The Heat Shock response (HSR) is a highly conserved transcriptional program induced by the exposure to a variety of environmental stressors. Following an insult, a small subset of genes, known as the Heat Shock genes, are rapidly induced by the Heat Shock Factors (HSFs) to maintain protein homeostasis and ensure cell survival. In parallel, a large portion of the genome becomes repressed. HS associated global gene repression is still largely poorly understood. In this study, we demonstrate that transcription downregulation during Heat shock is mainly achieved by premature transcription termination through the disruption of telescripting.
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