Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

ChIP-chip of Spo14 and Mvp1

ABSTRACT: Genome-wide localization of two new RNA pol II interacting proteins. We use C-LYTAG to map binding sites of Spo14 and Mvp1 along the S. cerevisiae genome. Two biological replicates of each experiment were done. Keywords: ChIp-chip Two independent biological replicates of each IP. We used three macroarrays: V5R2-L1-20, V5R2-L1-21 and V5R2-L1-22 that were hybridized with Whole Cell Extract (WCE) and then with two biological samples of immunoprecipitated (IP) Mvp1 (V5R2-L1-20 and V5R2-L1-21) and Spo14 (V5R2-L1-20 and V5R2-L1-22)

ORGANISM(S): Saccharomyces cerevisiae

SUBMITTER: Jose Perez-Ortin

PROVIDER: E-GEOD-16905 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

The conserved foot domain of RNA pol II associates with proteins involved in transcriptional initiation and/or early elongation.

García-López M Carmen MC Pelechano Vicent V Mirón-García M Carmen MC Garrido-Godino Ana I AI García Alicia A Calvo Olga O Werner Michel M Pérez-Ortín José E JE Navarro Francisco F

Genetics 20110927 4

RNA polymerase (pol) II establishes many protein-protein interactions with transcriptional regulators to coordinate different steps of transcription. Although some of these interactions have been well described, little is known about the existence of RNA pol II regions involved in contact with transcriptional regulators. We hypothesize that conserved regions on the surface of RNA pol II contact transcriptional regulators. We identified such an RNA pol II conserved region that includes the majori ...[more]

PMID: 21954159

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Project description:Insulin resistance is a heterogeneous disorder caused by a range of genetic and environmental factors, and we hypothesise that its aetiology varies considerably between individuals. This heterogeneity provides significant challenges to the development of effective therapeutic regimes for long-term management of type 2 diabetes. We describe a novel strategy, using large-scale gene expression profiling, to develop a gene expression signature (GES) that reflects the overall state of insulin resistance in cells and patients. The GES was developed from 3T3-L1 adipocytes that were made M-bM-^@M-^\insulin resistantM-bM-^@M-^] by treatment with tumour necrosis factor (TNF-alpha and then reversed with aspirin and troglitazone (M-bM-^@M-^\re-sensitizedM-bM-^@M-^]). The GES consisted of 5 genes whose expression levels best discriminated between the insulin resistant and insulin re-sensitized states. We then used this GES to screen a compound library for agents that affected the GES genes in 3T3-L1 adipocytes in a way that most closely resembled the changes seen when insulin resistance was successfully reversed using aspirin and troglitazone. This screen identified both known and new insulin sensitising compounds including non-steroidal anti-inflammatory agents, beta-adrenergic antagonists, beta-lactams and sodium channel blockers. We tested the biological relevance of this GES in participants in the San Antonio Family Heart Study (n = 1,240) and showed that patients with the lowest GES scores were more insulin resistant (according to HOMA_IR and fasting plasma insulin levels, P < 0.001). These findings show that GES technology can be used for both discovery of insulin sensitising compounds and characterisation of patients into subtypes of insulin resistance according to GES scores, opening the possibility of developing a personalised medicine approach to type 2 diabetes. Three-condition experiment, Vehicle, TNF and TNF+ASA+TGZ with biological replicates: 22 Vehicle, 21 TNF and 21 TNF+ASA+TGZ , independently grown and harvested. One replicate per array.

Project description:The PhoPR two-component system is essential for virulence in Mycobacterium tuberculosis where it controls expression of approximately 2% of the genes, including those for the ESX-1 secretion apparatus, a major virulence determinant. Mutations in phoP lead to compromised production of pathogen-specific cell wall components and attenuation both ex vivo and in vivo. Using antibodies against the native protein in ChIP-seq experiments (chromatin immunoprecipitation followed by high-throughput sequencing) we demonstrated that PhoP binds to at least 35 loci on the M. tuberculosis genome. The PhoP regulon comprises several transcriptional regulators as well as genes for polyketide synthases and PE/PPE proteins. Integration of ChIP-seq results with high-resolution transcriptomic analysis (RNA-seq) revealed that PhoP controls 30 genes directly, whilst regulatory cascades are responsible for signal amplification and downstream effects. The most prominent site of PhoP regulation was located in the intergenic region between rv2395 and PE_PGRS41, where the mcr7 gene codes for a small non-coding RNA (ncRNA). Northern blot experiments confirmed the absence of Mcr7 in the M. tuberculosis phoP mutant as well as low-level expression of the ncRNA in M. tuberculosis complex members other than M. tuberculosis. By means of genetic and proteomic analyses we demonstrated that Mcr7 modulates translation of the tatC mRNA thereby impacting the activity of the Twin Arginine Translocation (Tat) protein secretion apparatus. As a result, secretion of the immunodominant Ag85 complex and the beta-lactamase BlaC is affected, among others. Mcr7, the first ncRNA of M. tuberculosis whose function has been established, therefore represents a missing link between the PhoPR two-component system and the downstream functions necessary for successful infection of the host. ChiP-Seq: M. tuberculosis H37Rv (GC1237) cultures grown in vitro to exponential phase. Two wild type samples plus one isogenic phoP mutant as control

Dataset Information

ChIP-chip of Spo14 and Mvp1

Publications

The conserved foot domain of RNA pol II associates with proteins involved in transcriptional initiation and/or early elongation.

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