Project description:To gain a better understanding of the transcription factors that regulate central carbon metabolism in Rhodobacter sphaeroides ChIP-seq was used to determine the genome-wide binding locations of 2 transcription factors: CceR (RSP_1663) and AkgR (RSP_0981) both predicted to be involved in the regulation of of central carbon and energy metabolism. Genome-wide protein-DNA interaction analysis of 2 transcription factors predicted to be involved in regulation of central carbon metabolism CceR and AkgR
Project description:By integrating sequence information from closely related bacteria with a compendium of high-throughput gene expression datasets, a large-scale transcriptional regulatory networks was constructed for Rhodobacter sphaeroides. Predictions from this network were validated in part using genome-wide analysis for 3 transcription factors (PpsR, RSP_0489 and RSP_3341). Genome-wide protein-DNA interaction analysis of 3 transcription factors predicted to be involved in photosynthesis (PpsR), carbon metabolism (RSP_0489) and iron homeostasis (RSP_3341) were used to validate predictions from a large-scale reconstruction of R. sphaeroides transcriptional regulatory network.
Project description:To gain a deeper understanding of the transcription factors that regulate photosynthesis in Rhodobacter sphaeroides ChIP-seq was used to determine the genome-wide binding locations of 4 transcription factors (FnrL, PrrA, CrpK and RSP_2888) known or predicted to be involved in the regulation of photosynthesis. Genome-wide protein-DNA interaction analysis of 4 transcription factors known or predicted to be involved in the regulation of photosynthesis in Rhodobacter sphaeroides, using ChIP-seq and complementary assays.
Project description:This SuperSeries is composed of the following subset Series: GSE39711: RpoHI and RpoHII regulons in Rhodobacter sphaeroides 2.4.1 from chromatin immuno-precipitation GSE39712: RpoHI and RpoHII regulons in Rhodobacter sphaeroides 2.4.1 from gene expression profiling Refer to individual Series
Project description:To gain a better understanding of the transcription factors that regulate central carbon metabolism in Rhodobacter sphaeroides global gene expression analysis was used to determine genes under the regulatory influence of 2 transcription factors: CcmR (RSP_1663) and AkgR (RSP_0981) both predicted to be involved in the regulation of central carbon and energy metabolism. Microarray analysis conducted for deletion strains of 2 transcription factors known or predicted to be involved in the regulation of central carbon metabolism in Rhodobacter sphaeroides using the R. sphaeroides Affymetrix gene chip. These deletion mutant expression profiles were compared to that of wild type cells to determine differentially expressed genes regulated by these transcription factors.
Project description:We report that ancestral zinc-finger-domain transcriptional regulators, previously reported to control virulence/symbiosis, implement a cell cycle (SM-bM-^FM-^RG1) transcriptional switch. To unravel how this G1-phase transcriptional program is reinstated during a primitive cell cycle, we first defined G1-specific promoters in the model bacterium Caulobacter crescentus by comparative ChIP-Seq analysis. We then exploited one such promoter as genetic proxy, to identify two conserved developmental regulator paralogs, MucR1/2, that constitute a quadripartite and homeostatic regulatory module directing the switch from SM-bM-^FM-^RG1-phase transcription. Surprisingly, MucR orthologs that regulate virulence and symbiosis gene transcription in Brucella, Agrobacterium or Sinorhizobium support the G1 transcriptional switch in Caulobacter. Pan-genomic ChIP-Seq analyses in Sinorhizobium and Caulobacter show that this module targets orthologous genes. Thus, this ancestral bacterial lineage from which eukaryotic organelles descended may coordinate virulence/symbiosis with other cell cycle functions using a primordial transcription factor fold that is now primarily found in the eukaryotic domain of life. Examination of 5 transcripton factor binding in two different species
Project description:The epithelial to mesenchymal transition (EMT) has been well recognized for many decades as an essential early step in the progression of primary tumors towards metastases. Widespread epigenetic reprogramming of DNA and histone modifications tightly regulates gene expression and cellular activity during carcinogenesis, and epigenetic therapy has been developed to design efficient strategies for cancer treatment. As the first oral agent approved for the clinical treatment of cancer, sorafenib has significant inhibitory effects on tumor growth and EMT. However, a detailed understanding of the underlying epigenetic mechanism remains elusive. In this manuscript, we performed a ChIP-Seq assay to evaluate the activity of sorafenib on the genome-wide profiling of histone modifications. We demonstrate that sorafenib largely reverses the changes in histone modifications that occur during EMT in A549 alveolar epithelial cells. Sorafenib also significantly reduces the coordinated epigenetic switching of critical EMT-associated genes in accordance with their expression levels. Furthermore, we show that sorafenib potentiates histone acetylation by regulating the expression levels of histone-modifying enzymes. Collectively, these findings provide the first evidence that sorafenib inhibits the EMT process through an epigenetic mechanism, which holds enormous promise for identifying novel epigenetic candidate diagnostic markers and drug targets for the treatment of human malignancies. To further explore the underlying epigenetic mechanisms of EMT regulation by sorafenib, we chose conventional markers of active euchromatin such as H3K9ac and H3K4me3, and contrasted their architecture with the repressive structures associated with H3K27me3 and H3K9me3. The profiling of these four selected histone modifications was performed using ChIP-seq on control, TGF-M-NM-21-treated and sorafenib-treated cells. We further performed pair-wise comparisons among the three treatment conditions to assess the changes in the histone modifications within specific genomic regions during EMT.
Project description:A small number of transcription factors, including Oct-3/4 and Sox2, constitute the transcriptional network that maintains pluripotency in embryonic stem (ES) cells. Previous reports suggested that some of these factors form a complex that binds the Oct-Sox element, a composite sequence consisting of closely juxtaposed Oct-3/4-binding and Sox2-binding sites. However, little is known regarding the components of the complex. In this study, we show that Sall4, a member of the Spalt-like family of proteins, directly interacts with Sox2 and Oct-3/4. Sall4 in combination with Sox2 or Oct-3/4 simultaneously occupies the Oct-Sox elements in mouse ES cells. Sall4 knockdown led to differentiation of ES cells. Overexpression of Sall4 in ES cells increased reporter activities in a luciferase assay when the Pou5f1- or Nanog-derived Oct-Sox element was included in the reporter. Microarray analyses revealed that Sall4 and Sox2 bound to the same genes in ES cells significantly more frequently than expected from random coincidence. These factors appeared to bind the promoter regions of a subset of the Sall4- and Sox2-double-positive genes in precisely similar distribution patterns along the promoter regions, suggesting that Sall4 and Sox2 associate with such Sall4/Sox2-overlapping genes as a complex. Importantly, gene ontology analyses indicated that the Sall4/Sox2-overlapping gene set is enriched for genes involved in maintaining pluripotency. Sall4/Sox2/Oct-3/4-triple-positive genes identified by referring to a previous study identifying Oct-3/4-bound genes in ES cells were further enriched for pluripotency genes than Sall4/Sox2-double-positive genes. These results demonstrate that Sall4 contributes to the transcriptional network operating in pluripotent cells, together with Oct-3/4 and Sox2. ChIP-on-chip experiments using anti-Sall4 or anti-Sox2 antibody were performed.
Project description:Rhodobacter sphaeroides is the best studied photosynthetic bacterium, yet much remains unknown about its transcriptional regulatory processes on a genome-scale. We developed a work-flow for genome-scale reconstruction of transcriptional regulatory networks and applied it to sequence and gene expression data sets available for R. sphaeroides. To assess the predictive performance of our reconstructed model, we generated global transcript level and/or protein-DNA interaction data for 3 transcription factors (PpsR, RSP_0489 and RSP_3341). This dataset contains global transcript level analyses for RSP_0489 and RSP_3341 deletion strains, as well as matching wild type controls. Microarray analysis conducted for deletion strains of 2 previously uncharacterized transcription factors predicted to be involved in the regulation of carbon metabolism and iron homeostasis in R. sphaeroides using the R. sphaeroides Affymetrix gene chip. These deletion mutant expression profiles were compared to that of wild type cells to determine differentially expressed genes regulated by these transcription factors.