Similar Datasets
Project description:Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage.
2009-05-26 | GSE14913 | GEO
Project description:Transcriptional profiling of early C. elegans embryos comparing control (N2) embryos with mes-2 mutant embryos at different developmental stages: 2E (24-40 cells), 4E (50-90 cells) and 8E stage (100-200 cells). Goal was to determine the effects of mes-2 loss on global gene expression as embryos transit from a developmentally plastic state (2E stage) to the onset of differentiation (8E stage). Our microarray data showed that early-expressed genes remain active, differentiation genes fail to reach wild-type levels in mes-2 mutant embryos at the 8E stage. Two-condition experiment, wild type vs. mes-2 embryos. Biological replicates: 3 control replicates, 3 mes-2 replicates for each stage.
2010-05-18 | E-GEOD-14913 | biostudies-arrayexpress
Project description:Using staged embryos, we find many more genes with poised RNA polymerase than had been observed previously in C. elegans embryos, suggesting that early embryos accumulate poised PolII, and that poising is dynamic. Embryos were staged at the 8E and Bean stages of development prior to ChIP-seq
2015-07-01 | E-GEOD-68280 | biostudies-arrayexpress
Project description:Both genetic and environmental factors are implicated in Type 1 Diabetes (T1D). Since environmental factors can trigger epigenetic changes, we hypothesized that variations in histone posttranslational modifications (PTMs) at the promoter/enhancer regions of T1D susceptible genes may be associated with T1D. We therefore evaluated histone PTM variations at known T1D susceptible genes in blood cells from T1D patients versus healthy non-diabetic controls, and explored their connections to T1D. We used the chromatin-immunoprecipitation-linked-to-microarray approach to profile key histone PTMs, including H3-lysine-4 trimethylation (H3K4me3), H3K27me3, H3K9me3, H3K9 acetylation (H3K9Ac) and H4K16Ac at genes within the T1D susceptible loci in lymphocytes, and H3K4me3, H3K9me2, H3K9Ac and H4K16Ac at the IDDM1 region in monocytes of T1D patients and healthy controls separately. We screened for potential variations in histone PTMs using computational methods to compare datasets from T1D and controls. Interestingly, we observed marked variations in H3K9Ac levels at the upstream regions of HLA-DRB1 and HLA-DQB1 within the IDDM1 locus in T1D monocytes relative to controls. Additional experiments with THP-1 monocytes demonstrated increased expression of HLA-DRB1 and HLA-DQB1 in response to interferon- and TNF-treatment that were accompanied by changes in H3K9Ac at the same promoter regions as that seen in the patient monocytes. These results suggest that the H3K9Ac status of HLA-DRB1 and HLA-DQB1, two genes highly associated with T1D, may be relevant to their regulation and transcriptional response towards external stimuli. Thus, the promoter/enhancer architecture and chromatin status of key susceptible loci could be important determinants in their functional association to T1D susceptibility.
2012-06-01 | GSE36397 | GEO
Project description:Both genetic and environmental factors are implicated in Type 1 Diabetes (T1D). Since environmental factors can trigger epigenetic changes, we hypothesized that variations in histone posttranslational modifications (PTMs) at the promoter/enhancer regions of T1D susceptible genes may be associated with T1D. We therefore evaluated histone PTM variations at known T1D susceptible genes in blood cells from T1D patients versus healthy non-diabetic controls, and explored their connections to T1D. We used the chromatin-immunoprecipitation-linked-to-microarray approach to profile key histone PTMs, including H3-lysine-4 trimethylation (H3K4me3), H3K27me3, H3K9me3, H3K9 acetylation (H3K9Ac) and H4K16Ac at genes within the T1D susceptible loci in lymphocytes, and H3K4me3, H3K9me2, H3K9Ac and H4K16Ac at the IDDM1 region in monocytes of T1D patients and healthy controls separately. We screened for potential variations in histone PTMs using computational methods to compare datasets from T1D and controls. Interestingly, we observed marked variations in H3K9Ac levels at the upstream regions of HLA-DRB1 and HLA-DQB1 within the IDDM1 locus in T1D monocytes relative to controls. Additional experiments with THP-1 monocytes demonstrated increased expression of HLA-DRB1 and HLA-DQB1 in response to interferon- and TNF-treatment that were accompanied by changes in H3K9Ac at the same promoter regions as that seen in the patient monocytes. These results suggest that the H3K9Ac status of HLA-DRB1 and HLA-DQB1, two genes highly associated with T1D, may be relevant to their regulation and transcriptional response towards external stimuli. Thus, the promoter/enhancer architecture and chromatin status of key susceptible loci could be important determinants in their functional association to T1D susceptibility.
2012-06-01 | GSE36402 | GEO