Analysis of the gene expression profile of the atx1 mutant of Arabidopsis thaliana compared to the wild-type, using apices tissue of in in vitro plants and Affymetrix ATH1 chips.
ARABIDOPSIS TRITHORAX1 dynamically regulates FLOWERING LOCUS C activation via histone 3 lysine 4 trimethylation.
Age, Specimen part
View SamplesPlants respond to environmental stresses by altering transcription of genes involved in the response. The chromatin modifier ATX1 influences gene expression and factors that modulate ATX1 activity would affect indirectly the expression of ATX1-regulated genes. Here, we demonstrate that dehydration is such a factor indicating that ATX1 is involved in the plants response to drought. In addition, we show that a hitherto unknown Arabidopsis gene, At3g10550, encodes MYO1, a phosphoinositide 3-phosphatase related to the animal myotubularins. By a functional genomics approach, we show that ATX1 and MYO1 participate in overlapping drought-response pathways. The shared set of genes, representing the ultimate targets of an ATX1-MYO1 signaling mechanism responding to drought, provided insights into the relationship of the epigenetic factor and the lipid phosphatase from the other end of the response pathway.
The Arabidopsis chromatin modifier ATX1, the myotubularin-like AtMTM and the response to drought.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Dynamic changes in genome-wide histone H3 lysine 4 methylation patterns in response to dehydration stress in Arabidopsis thaliana.
Specimen part
View SamplesThese microarrays are part of a study where a comparison was made between the change in transcription and H3K4 mono-, di-, and tri-methylation levels (via ChIP-seq) in the Arabidopsis thaliana genome when plants are subjected to water deficit stress. Water deficit stress causes a large number of genes to change their transcript levels, which provided a large set of genes to examine for corresponding chromatine changes.
Dynamic changes in genome-wide histone H3 lysine 4 methylation patterns in response to dehydration stress in Arabidopsis thaliana.
No sample metadata fields
View SamplesWe report a transcriptome comparison of HEK293 cells modified at the DPYSL2 gene promoter dinucleotide repeat (chr8:26,435,510-26,435,534) by CRISPR/Cas9 to change from the common 11 repeats to the more rare 13 repeats Overall design: 11/11 repeat HEK 293 cells were modified by CRISPR/Cas 9. Cell were flow sorted by the co-transfected GFP and single cells were expanded. From those we selected 4 modified and 8 unmodified clones for RNA seq. RNA was extracted at 80% confluency
The DPYSL2 gene connects mTOR and schizophrenia.
Specimen part, Cell line, Subject
View SamplesAging at the cellular level is driven by changes in gene activity and epigenetic state that are only partially understood. We performed a comprehensive epigenomic analysis of the pancreatic ß cell, key player in glucose homeostasis and diabetes, in adolescent and very old mice. Globally, we observe a general methylation drift resulting in an overall more leveled methylome, suggesting that the maintenance of highly differential methylation patterns becomes compromised with advanced age. Importantly, we discover targeted changes in the methylation status of ß cell proliferation and function genes that go against the global methylation drift, are specific to ß cells, and correlate with repression of the proliferation program and activation of metabolic regulators. These targeted alterations frequently occur at distal cis-regulator elements, and are associated with specific chromatin marks and transcription factor occupancy in young ß cells. Strikingly, we find the insulin secretory response to glucose much improved in mature ß cells in mice, as predicted by the changes in methylome and transcriptome and in contrast to the decline in function observed in aged human ß cells. Thus, aging of terminally differentiated cells in mammals is not always coupled to functional decline. Overall design: RNA-seq was done on 3 biological replicas from old and three from young beta cells. each sample originated from a pool of 5-10 mic.e H3K27me3 ChIP-seq was done with two replicas for old mice (pool of 4-7 mice) and the rest of the ChIPseq (H3K4me1, H3K27ac and young H3K27me3) was sone with one sample (pool of few mice). BIS-seq was done on one sample from a pool of 10 young mice and one sample of a pool of old mice (18-22 months old)
Aging-Dependent Demethylation of Regulatory Elements Correlates with Chromatin State and Improved β Cell Function.
No sample metadata fields
View SamplesType-2 innate lymphoid cells (ILC2s) promote anti-helminth responses and contribute to allergies. Though Bcl11b has been previously considered a T-lineage identity transcription factor (TF) that restrains the innate-cell genetic programs, we report here that Bcl11b is highly expressed in mature ILC2s and acts upstream of the key ILC2 TFs Gfi1, Gata-3, and of IL-33 receptor IL1rl1 (T1ST2). Additionally, Bcl11b-/- ILC2s de-repressed Ror?t, Ahr and IL-23 receptor, normally expressed in type-3 ILCs (ILC3s). Consequently, Bcl11b-/- ILC2s lost ILC2 functions and gained ILC3 functions, expanding in response to the protease allergen papain, however producing IL-17 and IL-22, and not IL-5 and IL-13, causing lung neutrophilia rather than eosinophilia, and diminished mucus production. Our results broaden Bcl11b's role from a T-cell only TF, and establishes that Bcl11b sustains mature ILC2 genetic and functional programs and lineage fidelity through positive regulation of essential ILC2 TFs and negative regulation of pivotal ILC3 TFs. Overall design: RNA-seq analysis on sorted ILC2s from the mLNs of Bcl11bF/F Cre-ERT2 and wildtype mice at steady state following tamoxifen mediated deletion of Bcl11b
Transcription Factor Bcl11b Controls Identity and Function of Mature Type 2 Innate Lymphoid Cells.
No sample metadata fields
View SamplesNeuropathic pain is a complex chronic condition, characterized by a wide range of sensory, cognitive, and affective symptoms. Indeed, a large percentage of neuropathic pain patients are also afflicted with depression and anxiety disorders -- a pattern that is reliably replicated in animal models. Mounting evidence from clinical and preclinical studies indicates that chronic pain corresponds with adaptations in several brain networks involved in mood, motivation, and reward. Chronic stress is also a major determinant for depression. However, whether chronic pain and chronic stress affect similar mechanisms, and whether chronic pain can affect gene expression patterns known to be involved in depression, remains poorly understood. We employed the spared nerve injury model (SNI) of neuropathic pain in adult C57BL\6 mice and performed next-generation RNA-sequencing in order to monitor changes in gene expression in three brain regions known to be implicated in the pathophysiology of depression and in the modulation of pain: the nucleus accumbens (NAc), the medial prefrontal cortex (mPFC), and the periaqueductal grey (PAG). We observed mostly unique transcriptome profiles across the three brain regions but found common intracellular signal transduction pathways and biological functions were affected. A large amount of genes showing SNI-induced altered expression have been implicated in depression, anxiety, or chronic pain. In addition, we identified genes that are similarly regulated in a murine model of depression: chronic unpredictable stress. Our study provides the first unbiased characterization of neuropathic pain-induced long-term gene expression changes in three distinct brain regions, and presents evidence that neuropathic pain affects the expression of several genes that are also regulated by chronic stress. Overall design: RNA-seq samples were generated from 3 brain regions (nucleus accumbens, medial prefrontal cortex, and periaqueductal grey) of adult male mice, 2.5 months after sham or spared nerve injury to the sciatic nerve.
Neuropathic pain promotes adaptive changes in gene expression in brain networks involved in stress and depression.
Sex, Specimen part, Treatment, Subject
View SamplesThe sensory epithelium of cochleas and vestibules of mice were compared. The two tissues are quite similar in structure, but have distinct roles in hearing and balance. By comparing their gene expression, we hoped to identify key regulators of differentiation. Overall design: Cochlear and vestibular sensory epithelium was dissected from 20 inner ears of 10 P0 C57Bl/6J mice, generating 2.4 and 1.5 µg of total RNA, respectively. 450 ng RNA from each sample was used to create libraries with the TruSeq Stranded mRNA Sample Prep Kit (Illumina), followed by high-throughput sequencing at 100 bp paired end (PE) at the Technion Genome Center, Haifa, Israel. Six samples were generated, 3 cochlear and 3 vestibular, for sequencing in triplicate.
Computational analysis of mRNA expression profiling in the inner ear reveals candidate transcription factors associated with proliferation, differentiation, and deafness.
Sex, Specimen part, Cell line, Subject
View SamplesThe interaction between a pathogen and a host is a highly dynamic process in which both agents activate complex programs. Here, we introduce a single-cell RNA-Seq method (scDual-Seq) that simultaneously captures both host and pathogen transcriptomes and use it to study the process of infection of individual mouse macrophages with the intracellular pathogen Salmonella typhimurium. Among the infected macrophages, we found three subpopulations and we show evidence for a linear progression through these subpopulations, supporting a model in which these three states correspond to consecutive stages of infection. Overall design: 96 single cells in 4 time point of infection (0,2.5,4,8 hours after infection)
scDual-Seq: mapping the gene regulatory program of Salmonella infection by host and pathogen single-cell RNA-sequencing.
Cell line, Subject, Time
View Samples