Ontology highlight
ABSTRACT:
PROVIDER: PRJNA943105 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We are studying the tree P. euphratica growing in its natural habitat in the Negev desert in Israel. We have used leaf RNA samples from trees growing from four different areas in the desert valley Ein Avdat with contrasting growth conditions, with the primary factor being how much water the trees have access to. Area A trees grow close to a stream. Area B trees are further away from the stream. Area C trees are growing on a slope with no water. Parking place trees grow at a parking place (1km from Area A, B and C) where there is a water irrigation system, and these trees are regularly watered once a week. The control sample in each hybridization is always RNA isolated from a pool of 5 trees from the parking place. The hybridizations are comparing the following: Area A -- parking place Area B -- parking place Area C -- parking place Each hybridization is done with a dye swap and three different biological repeats for a total of 18 hybridizations.
2004-11-30 | E-MEXP-182 | biostudies-arrayexpress
Project description:L-Arginine (L-Arg) is the substrate for both inducible nitric oxide synthase and arginase, which are upregulated in human IBD and in mouse colitis models. We have found that L-Arg supplementation enhances wound restitution in vitro, and improves the clinical parameters of weight loss, survival, and colon weight/length, in dextran sulfate sodium (DSS) induced murine colitis. Our aim was to further identify the potential mechanisms underlying the clinical benefit of L-Arg supplementation. 12 Total samples were analyzed, 3 samples from each of 4 groups. We generated the following pairwise comparisons: Ctrl vs Ctrl + L-Arg; Ctrl vs DSS; DSS vs DSS + L-Arg; Ctrl + L-Arg vs DSS, Ctrl + L-Arg vs DSS + L-Arg. Genes with a p-value < 0.01 and a fold-change ≥2 were selected. To identify genes that were altered in response to L-Arg, we performed the following multiple sample comparisons using a p-value < 0.01 and a fold-change ≥2: Ctrl vs DSS vs DSS + L-Arg
2012-06-26 | E-GEOD-34874 | biostudies-arrayexpress
Project description:During limb development, Hoxd genes are transcribed in two waves: Early on, when the arm and forearm are specified and subsequently, when digits form. While the latter phase is controlled by enhancers centromeric to the HoxD cluster, we show here that the early phase requires enhancers located in the opposite telomeric gene desert. The transition between the two types of regulations involves a functional switch between two distinct topological domains, as reflected by a subset of genes mapping centrally into the cluster, which initially interact with the telomeric domain and subsequently shift to establish new contacts on the opposite side. This transition between two regulatory landscapes generates an intermediate area of low Hox dose developing into the wrist, the transition between our arms and our hands. This intriguing correspondence between genomic and morphological boundaries illustrates the mechanism underlying collinear Hox gene regulation in our developing appendages. Chromatin ImmoPrecipitation on chip (Tiling array): Distribution of H3K4me3 and H3K27me3 in early limb buds at E9.5, E10.5 and proximal late limbs E12.5. Distribution of H3K27me3 in del(8-13) and del(8-13)/del(attP-TpSB3) E10.5 limb buds. Distribution of H3K27me3 in WT and homozygote del(Nsi-Atf2) (Montavon et al., 2011) forelimb autopods.
2013-06-07 | E-GEOD-45454 | biostudies-arrayexpress
Project description:This study reveals that the millions of satellite II (HSATII) sequences in the human genome can bind and impact distribution of epigenetic regulators, and that this goes awry in cancer. In many cancers master epigenetic factors form two-types of cancer-specific nuclear bodies, caused by locus-specific deregulation of HSATII DNA and RNA, respectively. DNA demethylation at the 1q12 mega-satellite, common in cancer, causes PRC1 aggregation into prominent Cancer-Associated Polycomb (CAP) bodies. These loci remain silent, whereas HSATII loci in regions low in PRC1 become de-repressed, reflecting imbalanced distribution of UbH2A on these and other PcG-regulated loci. Large nuclear foci of HSATII RNA form and sequester copious MeCP2 into Cancer-Associated Satellite Transcript (CAST) bodies. Hence, HSATII DNA and RNA have an exceptional capacity to “sponge” epigenetic factors into abnormal nuclear bodies in cancer. Results support a new concept that demethylation of “junk” repeats can trigger further epigenetic compromise by compartmentalizing regulatory factors within nuclear structure.
2017-03-29 | GSE94973 | GEO