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Mus musculus
24 Downloadable Samples
Illumina HiSeq 2500
Description
For most multigenic disorders, clinical manifestation (penetrance) and presentation (expressivity) are likely to be an outcome of genetic interaction between multiple susceptibility genes. Here, using gene knockouts in mice we evaluated genetic interaction between loss of Ret and loss of Sema3d, two Hirschsprung disease (HSCR) susceptibility genes. We intercrossed Ret and Sema3d double null heterozygotes to generate mice with the nine possible genotypes and assessed survival by counting various genotypes, myenteric plexus development by acetylcholinesterase (AchE) staining and embryonic day 12.5 (E12.5) gut transcriptome by RNA-sequencing. Survival rates of Ret wildtype, null heterozygote and null homozygote mice at E12.5, birth and weaning were not influenced by the genotypes at Sema3d locus and vice-versa. Loss of myenteric plexus was observed only in all Ret null homozygotes, irrespective of the genotypes at Sema3d locus, and Sema3d null heterozygote and homozygote mice had normal gut innervation. As compared to wildtype mice gut gene expression, loss of Ret in null homozygotes led to differential expression of ~300 genes, whereas loss of Sema3d in null homozygotes had no major consequence and there was no evidence supporting major interaction between the two genes influencing gut transcriptome. Overall, given the null alleles and phenotypic assays used, we did not find evidence for genetic interaction between Ret and Sema3d affecting survival, myenteric plexus formation or gut transcriptome. Overall design: poly-A RNA-seq in embryonic day 12.5 mouse gut from 3 wildtype males, 3 wildtype females, 3 Ret null homozyogote males, 3 Ret null homozyogote females, 3 Sema3d null homozyogote males, 3 Sema3d null homozyogote females, 3 Ret-Sema3d double null homozyogote males, 3 Ret-Sema3d double null homozyogote females
Publication Title
Testing the Ret and Sema3d genetic interaction in mouse enteric nervous system development.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- NextSeq 500
Description
The adipocytes functions as a central organ in the regulation of metabolic homeostasis. Factors which contribute to the adipocyte differentiation and function would be the promising targets to combat the obesity and associated metabolic disorders. The activating transcription factor 7 (ATF7), a stress-responsive chromatin regulator, has recently been shown to be involved in the energy metabolism; however, the underlying mechanisms are still unknown. Here, we show that ATF7 is required for adipocyte differentiation and it interacts with histone dimethyltransferase G9a in adipocyte to repress the interferon-stimulated genes (ISGs) expression, which suppresses adipogenesis. Ablation of ATF7 promotes the beige biogenesis and browning of inguinal white adipose tissue (iWAT). ATF7 binds to the transcription regulatory regions of Ucp1 gene, and silences it by maintaining the histone H3K9 dimethylation level. These results establish the multifunction of ATF7 in adipocyte and provide molecular insights into the epigenetic control of development and function of adipose tissues. Overall design: Beige adipocytes derived from WT and ATF7 KO inguinal WAT preadipocytes with rosiglitazone treatment, in duplicate; white adipocytes derived from WT and ATF7 KO inguinal WAT preadipocytes without rosiglitazone treatment, in duplicate; beige adipocytes derived from control and ATF7 overexpressing C3H10t1/2 with rosiglitazone treatment, in duplicate, using NextSeq500 Illumina.
Publication Title
The Transcription Factor ATF7 Controls Adipocyte Differentiation and Thermogenic Gene Programming.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Escherichia coli
- 12 Downloadable Samples
Affymetrix E. coli Genome 2.0 Array (ecoli2)
Description
As part of our studies on the biological functions of polyamines we have used a mutant of Escherichia coli that lacks all the genes for polyamine biosynthesis for a global transcription analysis on the effect of added polyamines. The most striking early response to polyamine addition is the increased expression of the genes for the glutamate dependent acid resistance system (GDAR) that is essential for the survival of bacteria when passing through the acid environment of the stomach. Not only were the two genes for glutamate decarboxylases (gadA and gadB) and the gene for glutamate --aminobutyrate antiporter (gadC) induced by polyamine addition, but also the various genes involved in the regulation of this system were induced. We confirmed the importance of polyamines for the induction of the GDAR system by direct measurement of glutamate decarboxylase activity and acid-survival. Effects of deletions of the regulatory genes in the GDAR system and on the effects of overproduction of two of these genes were also studied. Strikingly, overproductions of the alternate sigma factor rpoS and of the regulatory gene gadE resulted in very high levels of glutamate decarboxylase and almost complete protection against acid stress even in the absence of any polyamines. Thus, these data show that a major function of polyamines in E. coli is protection against acid stress by increasing the synthesis of glutamate decarboxylase, presumably by increasing the levels of the rpoS and gadE regulators.
Publication Title
Polyamines are critical for the induction of the glutamate decarboxylase-dependent acid resistance system in Escherichia coli.
Sample Metadata Fields
Treatment
View Samples
GSE99859- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Assisted reproductive technologies, including in vitro fertilization (IVF), are now frequently used, and increasing evidence indicates that IVF causes gene expression changes in children and adolescents that increase the risk of metabolic diseases. Although such gene expression changes are thought to be due to IVF-induced epigenetic changes, the mechanism remains elusive.
Publication Title
The transcription factor ATF7 mediates <i>in vitro</i> fertilization-induced gene expression changes in mouse liver.
Sample Metadata Fields
Specimen part
View Samples- Escherichia coli
- 6 Downloadable Samples
- Affymetrix E. coli Genome 2.0 Array (ecoli2)
Description
Glutathionylspermdine synthetase/amidase (Gss) and the encoding gene (gss) have only been described in two widely separated species; namely Escherichia coli and several members of the Kinetoplastida phyla. In the present paper we have studied the species distribution more extensively. It is striking that all of the 75 Enterobacteria species that has been sequenced contain sequences with very high degree of homology to the E. coli Gss protein. Although homologous sequences are also present in various other bacteria, in contrast to Enterobacteria they are not present in all species of a given phyla. As previously reported homologous sequences were found in all five species of Kinetoplastids tested (including Trypansosma cruzi), but it is striking that comparable sequences are not found in a variety of invertebrate and vertebrate species, Archea and plants. Studies in E. coli show that the highest accumulation of glutathionylspermidine is found in stationary phase cultures where most of the intracellular spermidine is converted to glutathionylspermidine. However, even in log phase cells there is some formation of glutathionylspermidine, and isotope exchange experiments show that there is a rapid exchange between glutathionylspermidine and intracellular spermidine. We have not been able to define a specific physiologic function for glutathionylspermidine, but microarray studies comparing gss+ and -gss strains of E. coli show that a large number of genes are either upregulated or downregulated by the loss of the gss gene.
Publication Title
Escherichia coli glutathionylspermidine synthetase/amidase: phylogeny and effect on regulation of gene expression.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 3 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
In order to evaluate the identification of genes and pathways, the global gene expression profiles were assessed in response to GO and rGO on Human hepatoma (HepG2) cells. We performed whole genome DNA microarray experiments using HepG2 cells exposed to GO and rGO for 24h.
Publication Title
A systems toxicology approach to the surface functionality control of graphene-cell interactions.
Sample Metadata Fields
Cell line, Treatment
View Samples- Escherichia coli
- 24 Downloadable Samples
- Affymetrix E. coli Genome 2.0 Array (ecoli2)
Description
To study the physiological roles of polyamines, we have carried out a global microarray analysis on the effect of adding polyamines to an Escherichia coli mutant that lacks polyamines because of deletions in the genes in the polyamine biosynthetic pathway. Previously, we have reported that the earliest response to the polyamine addition is the increased expression of the genes for the glutamate dependent acid resistance system (GDAR). We also presented preliminary evidence for the involvement of rpoS and gadE regulators. In the current study further confirmation of the regulatory roles of rpoS and gadE is shown by a comparison of genome-wide expression profiling data from a series of microarrays comparing the genes induced by polyamine addition to polyamine-free rpoS+/gadE+ cells with genes induced by polyamine addition to polyamine-free rpoS and gadE cells. The results indicate that most of the genes in the E. coli GDAR system that are induced by polyamines require rpoS and gadE. Our data also show that, gadE is the main regulator of GDAR and other acid-fitness-island genes. Both polyamines and rpoS are necessary for the expression of gadE genes from the three promoters of gadE (P1, P2 and P3). The most important effect of polyamine addition is the very rapid post-transcriptional increase in the level of RpoS sigma factor. Our current hypothesis is that polyamines increase the level of RpoS protein, and that this increased RpoS level is responsible for the stimulation of gadE expression, which in turn induces the GDAR system in E. coli.
Publication Title
Polyamines Stimulate the Level of the σ38 Subunit (RpoS) of Escherichia coli RNA Polymerase, Resulting in the Induction of the Glutamate Decarboxylase-dependent Acid Response System via the gadE Regulon.
Sample Metadata Fields
Treatment
View Samples- Arabidopsis thaliana
- 8 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Three bZIP transcription factors (TFs), namely GBF1, HY5, and HYH, form heterodimers with each other and regulate photomorphogenesis in an interdependent manner. GBF1 acts as both a positive and negative regulator of photomorphogenesis, whereas HY5 and HYH mainly act as positive regulators of photomorphogenesis. To study the effect of HY5 and HYH on GBF1-mediated genome-wide expression, transcript profiling was performed in the gbf1 single mutant and gbf1hy5 and gbf1hyh double mutants. Our study revealed that GBF1 mainly acts antagonistic to HY5 and HYH for genome-wide expression.
Publication Title
Genome-wide DNA binding of GBF1 is modulated by its heterodimerizing protein partners, HY5 and HYH.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
Total mRNA seq was perfomed on widtype and Ret null mouse embryonic gut at 2 stages of devlopment- E11.5 and E12.5 Overall design: Total RNA from 3 replicates each of wildtype and Ret null emryonic gut was converted to cDNA and run on HiSeq 2000 (75 bp paired end)
Publication Title
Enhancer Variants Synergistically Drive Dysfunction of a Gene Regulatory Network In Hirschsprung Disease.
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Combinatorial recruitment of CREB, C/EBPβ and c-Jun determines activation of promoters upon keratinocyte differentiation.
Sample Metadata Fields
Specimen part, Treatment
View Samples