Environmental factors shape the phenotypes of multicellular organisms. The production of stomata—the epidermal pores required for gas exchange in plants—is highly plastic, and provides a powerful platform to address environmental influence on cell differentiation [1-3]. Rising temperatures are already impacting plant growth, a trend expected to worsen in the near future [4]. High temperature inhibits stomatal production but the underlying mechanism is not known [5]. Here, we show that elevated temperature suppresses the expression of SPEECHLESS (SPCH), the bHLH transcription factor that serves as the master regulator of stomatal lineage initiation [6,7]. Our genetic and expression analyses indicate that the suppression of SPCH and stomatal production is mediated by the bHLH transcription factor PHYTOCHROME-INTERACTING FACTOR 4 (PIF4), a core component of high temperature signaling [8]. Importantly, we demonstrate that upon exposure to high temperature, PIF4 accumulates in the stomatal precursors and binds to the promoter of SPCH. In addition, we find SPCH feeds back negatively to the PIF4 gene. We propose a model where the high temperature-activated PIF4 binds and represses SPCH expression to restrict stomatal production at high temperature. Our work identifies a molecular link connecting high temperature signaling and stomatal development, and reveals a direct mechanism by which production of a specific cell lineage can be controlled by a broadly-expressed environmental signaling factor. Overall design: Gene expression profiles following 12 hr Dex-induction of control and ML1p:SPCH1-4A-expressing Arabidopsis plants grown in liquid culture. Four replicates per line at 0 and 12 hr.
Direct Control of SPEECHLESS by PIF4 in the High-Temperature Response of Stomatal Development.
Age, Subject
View SamplesWe used the microarray data to analyse the host cell responses on mouse macrophages infected with the three Influenza A viruses
Systems-based approach to examine the cytokine responses in primary mouse lung macrophages infected with low pathogenic avian Influenza virus circulating in South East Asia.
Specimen part
View SamplesThe experiment was designed to generate a time series for epithelial model during development. Each time point had 3 replicates. The data set contained 5 time points over 10 days. They are day0, day3, day5,day7,day10.
Dynamic and physical clustering of gene expression during epidermal barrier formation in differentiating keratinocytes.
Age, Specimen part, Time
View SamplesWe report the identification of Rnase R resistent stable intronic sequence RNAs (sisRNAs) in Drosophila. Overall design: RNA was obtained from 0-2 hr embryos and subjected to deep sequencing. ---------------------------------------- Authors state "We screened by manual inspection on the genome browser after mapping the reads to the genome" and "We managed to obtain 6 candidates with this approach".
Maternally Inherited Stable Intronic Sequence RNA Triggers a Self-Reinforcing Feedback Loop during Development.
Subject
View SamplesThe conserved Mef2 transcription factor is a major regulator of gene expression and differentiation. Recent genomic studies have identified a large number of mef2-regulated target genes with distinct temporal expression profiles during Drosophila myogenesis. However, the question remains as to how a single transcription factor can control such diverse patterns of gene expression. The aim of this project was to investigate whether there are genes with different mef2-requirements for their expression during muscle differentiation in vivo during the development of Drosophila melanogaster.
mef2 activity levels differentially affect gene expression during Drosophila muscle development.
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Genome-wide mapping of DNA hydroxymethylation in osteoarthritic chondrocytes.
Specimen part
View SamplesExamination of the genome-wide distribution of 5hmC in osteoarthritic chondrocytes compared to normal chondrocytes in order to elucidate the effect on OA-specific gene expression.
Genome-wide mapping of DNA hydroxymethylation in osteoarthritic chondrocytes.
Specimen part
View SamplesThe Human T-cell Leukemia Virus (HTLV)-type-I non-structural protein p30 plays an important role in virus transmission and gene regulation. p30 has been documented to inhibit the export of certain viral mRNA transcripts from the nucleus to the cytoplasm. This nuclear retainment of RNA molecules essentially results in gene silencing, where protein products are not produced.
Genome wide analysis of human genes transcriptionally and post-transcriptionally regulated by the HTLV-I protein p30.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Preferential epigenetic programming of estrogen response after in utero xenoestrogen (bisphenol-A) exposure.
Age, Specimen part
View SamplesBisphenol-A (BPA) is an environmentally ubiquitous estrogen-like endocrine-disrupting compound. Exposure toBPAin utero hasbeen linked to female reproductive disorders, including endometrial hyperplasia and breast cancer. Estrogens are an etiological factor in many of these conditions. We sought to determine whether in utero exposure to BPA altered the global CpG methylation pattern of the uterine genome, subsequent gene expression, and estrogen response. Pregnant mice were exposed to an environmentally relevant dose of BPA or DMSO control. Uterine DNA and RNA were examined by using methylated DNA immunoprecipitation methylation microarray, expression microarray, and quantitative PCR. In utero BPA exposure altered the global CpG methylation profile of the uterine genome and subsequent gene expression. The effect on gene expression was not apparent until sexual maturation, which suggested that estrogen response was the primary alteration. Indeed, prenatal BPA exposure preferentially altered adult estrogen-responsive gene expression. Changes in estrogen response were accompanied by altered methylation that preferentially affected estrogen receptor-a (ERa)binding genes. The majority of genes that demonstrated both altered expression and ERa binding had decreased methylation. BPA selectively altered the normal developmental programming of estrogen-responsive genes via modification of the genes that bind ERa. Gene environment interactions driven by early life xenoestrogen exposure likely contributes to increased risk of estrogen related disease in adults.Jorgensen, E. M.,Alderman,M.H., III,Taylor, H. S. Preferential epigenetic programmingof estrogen response after in utero xenoestrogen (bisphenol-A) exposure.
Preferential epigenetic programming of estrogen response after in utero xenoestrogen (bisphenol-A) exposure.
Age, Specimen part
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