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GSE93047
Arabidopsis thaliana
6 Downloadable Samples
Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Sulfite reductase (SiR) plays an essential role in the assimilatory sulfur reduction pathway by catalyzing the reduction of sulfite to sulfide. The T-DNA insertion mutant line sir1-1 shows lower amounts of SiR transcript, protein and lower activity and is severely affected in growth. In this study we performed global transcriptome analysis to investigate the impact of the mutation in the shoot of 7-week-old plants.
Publication Title
Sulfur availability regulates plant growth via glucose-TOR signaling.
Sample Metadata Fields
Age
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Mouse embryonic fibroblasts deficient for p53 and expressing mutant RasV12 were infected with lentiviral constructs carrying short hairpin RNAs targeting ARF or a scrambled control. Four days post infection, cells were harvested for microarray analysis.
Publication Title
ARF and p53 coordinate tumor suppression of an oncogenic IFN-β-STAT1-ISG15 signaling axis.
Sample Metadata Fields
No sample metadata fields
View Samples- Drosophila melanogaster
- 12 Downloadable Samples
Illumina HiSeq 2000
Description
Purpose: Investigating the role of Drosophila G9a in oxidative stress responses. Methods: Flies were collected after eclosion and allowed to recover from CO2 exposure for 5 days prior to paraquat exposure. Paraquat (Methyl viologen dichloride hydrate 98 %; Sigma 856177) was mixed into the flyfood at 40 °C to a final concentration of 50 mM. For OS induction, 5-9 day old flies were transferred to paraquat containing food and incubated at 25 °C and 70 % humidity. At each time point, flies were flash frozen in liquid nitrogen followed by vortexing and filtering through a series of sieves to isolate heads from other body parts. 200 fly heads per sample were used for RNA extraction using QIAGEN lipid mini tissue kit. The TruSeq RNA Sample Preparation Kit v2 (Illumina) was used to prepare adapter ligated PCR fragments for sequencing. PCR was used to selectively enrich the fragments containing the adapters. The PCR fragments were validated using Agilent 2200 TapeStation. Single indexed samples were multiplexed and sequenced on an Illumina HiSeq 2000 sequencing system (Illumina) in single-end mode with a read length of 35 bp. Quality of sequenced reads was assessed with FastQC. The RNAseq experiments were conducted on two biological duplicates for each condition. Sequenced reads were aligned with Burrows-Wheeler algorithm (BWA) (Li & Durbin, 2010) to the Drosophila reference genome (BDGP.5, http://www.fruitfly.org/) and per gene read counts were generated with HTSeq count (Anders et al, 2015). 25–30 million reads with high quality alignment were obtained for each sample and used for differential expression analysis. DESeq (Anders & Huber, 2010) was used to obtain library size-normalized read counts and to calculate differential expression of genes in 4 pairwise comparisons: 0 h versus 6 h and 0 h versus 12 h after OS in both G9a mutants and controls (fold change =1.5, adjusted p-value= 0.05, Benjamini-Hochberg). Results: We found 2731 genes to be differential expressed in at least one of the four pairwise comparisons. The largest group of differentially expressed (DE) genes are highly augmented upon OS induction in the G9a mutant (41.7 % of all DE genes). The second largest group of DE genes (23.9 % of all DE genes) were more downregulated in G9a mutant in response to OS. Genes that are over-activated in G9a mutants are predominantly involved in OS response and OS mediated damage, whereas genes that are downregulated in G9a mutants are involved in energy metabolism. Conclusions: Our data suggest that G9a provides an epigenetic mechanism that safeguards an appropriate transcriptional response to OS and preserves immediately available energy, thereby acting as a critical regulatory hub between the transcriptional and physiological responses to oxidative stress. Overall design: fly-head mRNA libraries of 5-9 days old male G9aDD1 mutant and control during 0, 6 and 12 hours of paraquat oxidative stress exposure were sequenced in duplicate on Hi-seq 2000.
Publication Title
The histone methyltransferase G9a regulates tolerance to oxidative stress-induced energy consumption.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
In the present study, we investigated the importance of histone deacetylase 6 (HDAC6) for glucocorticoid receptor (GR) mediated effects on glucose metabolism, and its potential as a therapeutic target for the prevention of glucocorticoid (GC)-induced diabetes. Dexamethasone (dex)-induced hepatic glucose output and GR translocation were analysed in wildtype (wt) and HDAC6-deficient (HDAC6ko) mice. The effect of the specific HDAC6-inhibitor tubacin was analysed in-vitro. Wt and HDAC6ko mice were subjected to 3 weeks dex treatment before analysis of glucose and insulin tolerance. HDAC6ko mice showed impaired dex-induced hepatic GR translocation. Accordingly, dex induced expression of a large number of hepatic genes was significantly attenuated in mice lacking HDAC6 and by tubacin in-vitro. Glucose output of primary hepatocytes from HDAC6ko mice was diminished. A significant improvement of dex-induced whole-body glucose intolerance as well as insulin resistance in HDAC6ko mice compared to wt littermates was observed. The present study demonstrates that HDAC6 is an essential regulator of hepatic GC stimulated gluconeogenesis and impairment of whole body glucose metabolism through modification of GR nuclear translocation. Selective pharmacological inhibition of HDAC6 may provide a future therapeutic option against the pro-diabetogenic actions of GCs.
Publication Title
Histone deacetylase 6 (HDAC6) is an essential modifier of glucocorticoid-induced hepatic gluconeogenesis.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples