Gene expression analysis of Photobacterium profundum DB110 and TW30 toxR mutant strain at 0.1 MPa and 28 MPa
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ABSTRACT:
ORGANISM(S): Photobacterium profundum
PROVIDER: GSE38259 | GEO | 2012/12/22
SECONDARY ACCESSION(S): PRJNA167564
REPOSITORIES: GEO
Similar Datasets
Project description:Here we report the massively parallel cDNA sequencing (RNA-seq) analysis performed using high throughput sequencing of wild type (DB110) and toxR (TW30) mutant strains of the deep-sea bacterium Photobacterium profundum. ToxR is a transmembrane DNA-binding protein first discovered in Vibrio cholerae and able to regulate numerous genes involved in virulence. In P. profundum the abundance and activity of the same protein is influenced by hydrostatic pressure and is able to regulate genes in a pressure-dependent manner. To better characterize the ToxR regulon, we have compared the genes differentially expressed in response to pressure changes with those whose expression is altered between wild type and toxR mutant strains. Four samples were analyzed: DB110 strain grown at 0.1 MPa, DB110 strain grown at 28 MPa, TW30 strain grown at 0.1 MPa, TW30 strain grown at 28 MPa. Two independent coltures (replicates) were grown for each sample, RNA was extracted from each replicate and RNAs from the two replicates were pooled together to reduce biological variability. No replicates were included in experimental design.
2012-12-22 | E-GEOD-38259 | biostudies-arrayexpress
Project description:Hydrostatic pressure is one of the physical factors affecting cellular physiology. Hydrostatic pressure of a few hundred MPa decreases the viability of yeast cells, and pressure of a few tens MPa decreases the growth rate. To understand the effect of hydrostatic pressure, we employed yeast, Saccharomyces cerevisiae, DNA microarrays and analyzed genome-wide mRNA expression profiles under hydrostatic pressures. In this experiment, we selected a hydrostatic pressure of 30 MPa at 25 degrees C because yeast cells are able to grow with this condition. Keywords: stress response
2007-11-01 | GSE9403 | GEO
Project description:Hydrostatic pressure is one of the physical factors affecting cellular physiology. Hydrostatic pressure of a few hundred MPa decreases the viability of yeast cells, and pressure of a few tens MPa decreases the growth rate. To understand the effect of hydrostatic pressure, we employed yeast, Saccharomyces cerevisiae, DNA microarrays and analyzed genome-wide mRNA expression profiles under hydrostatic pressures. In this experiment, we selected a hydrostatic pressure of 40 MPa at 25 degrees C because the condition is not lethal for yeast cells but the growth was suppressed. Keywords: stress response
2007-11-01 | GSE9406 | GEO
Project description:Piezophysiology of genome wide gene expression levels in the yeast Saccharomyces cerevisiae: Hydrostatic pressure is one of the physical factors affecting cellular physiology. Hydrostatic pressure of a few hundred MPa decreases the viability of yeast cells, and pressure of a few tens MPa decreases the growth rate. To understand the effect of hydrostatic pressure, we employed yeast DNA microarrays and analyzed genome-wide gene-expression levels after the pressure treatment with 180 MPa (immediate) at 4 degrees C and recovery incubation for 1 h and 40 MPa (16 h) at 4 degrees C and recovery incubation for 1 h. The transcription of genes involved in energy metabolism, cell defense, and protein metabolism was significantly induced by the pressure treatment. Genome-wide expression profiles suggested that high pressure caused damage to cellular organelles, since the induced gene products were localized in the membrane structure and/or cellular organelles. Hierarchical clustering analysis suggested that the damage caused by the pressure was similar to that caused by detergents, oils, and freezing/thawing. We also estimated the contribution of induced genes to barotolerance using some strains that have the deletion in the corresponding genes. Keywords: stress response
2007-11-01 | GSE9407 | GEO
Project description:Hydrostatic pressure is one of the main mechanical stimuli cartilage cells are submitted to during joint loading. If moderate hydrostatic pressure is known to be beneficial to cartilage differentiation, excessive pressure, on the other hand, induces changes in cartilage similar to those observed in osteoarthritic cartilage. Therefore, the purpose of the experiment is to identify new target genes of high hydrostatic pressure in chondrocyte precursor cells.
2017-12-02 | E-MTAB-5326 | biostudies-arrayexpress
Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxR’s genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. cholerae’s major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites.
2016-03-23 | GSE72473 | GEO
Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxR’s genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. cholerae’s major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites.
2016-03-23 | GSE72472 | GEO
Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxR’s genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. cholerae’s major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites.
2016-03-23 | GSE72471 | GEO
Project description:P. profundum SS9 strain cells were grown at two different pressure conditions 0.1 MPa and at 28 MPa. RNA extracted from the two different cultures was labelled with Cy5 and Cy3 and competitively hybridized on the same slide.
2005-07-28 | E-MEXP-210 | biostudies-arrayexpress
Project description:The transcriptional factor ToxR initiates a virulence regulatory cascade required for V. cholerae to express critical host colonization factors and cause disease. Genome-wide expression studies suggest that ToxR regulates many genes important for V. cholerae pathogenesis, yet our knowledge of the direct regulon controlled by ToxR is limited to just four genes. Here, we determine ToxRâs genome-wide DNA-binding profile and show that ToxR is a global regulator of both progenitor genome-encoded genes and horizontally acquired islands encoding the majority of V. choleraeâs major virulence factors. Our results suggest that ToxR has gained regulatory control over important acquired elements that not only drive V. cholerae pathogenesis but that also define the major transitions of V. cholerae pandemic lineages. We demonstrate that ToxR shares nearly half its regulon with the histone-like nucleoid structuring protein H-NS, and antagonizes H-NS for control of critical colonization functions. This regulatory interaction is the major role of ToxR in V. cholerae colonization since deletion of H-NS abrogates the need of ToxR in V. cholerae host colonization. By comparing the genome-wide binding profiles of ToxR and other critical virulence regulators, we show that despite similar predicted DNA binding requirements, ToxR is unique in its global control of progenitor-encoded and acquired genes. Our results suggest that, like H-NS, factors in addition to linear DNA sequence drive selection of ToxR binding sites. We used ChIP-seq to identify ToxR binding sites across the genome to determine the direct regulon of ToxR
2016-03-23 | E-GEOD-72473 | biostudies-arrayexpress