Ontology highlight
ABSTRACT:
PROVIDER: PRJEB14821 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1538272_1.fastq.gz | Fastqsanger.gz | |||
| ERR1538272_2.fastq.gz | Fastqsanger.gz | |||
| ERR1538273_1.fastq.gz | Fastqsanger.gz | |||
| ERR1538273_2.fastq.gz | Fastqsanger.gz | |||
| ERR1538274_1.fastq.gz | Fastqsanger.gz |
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Project description:The processes of adaptation to environmental heat and aerobic exercise training improve efficiency in various body systems and bring about acclimatory homeostasis. In order to examine the global genomic responses of the soleus and heart following exposure of rats to these stressors, nylon cDNA Atlas Array was used. Male rats were exposed to one of the following stressors: heat acclimation, aerobic training (treadmill), and combined heat acclimation and aerobic training for short (2, 3 days) and long (1 mo) time period. The study comprised seven experimental groups: Controls-untreated. Heat acclimated groups (2dac, Acc)â exposure to environmental heat at 34C for 2 or 30 days. Exercise groups (3dex, Ex)â graduated training protocol under normothermic conditions for 3 and 30 days at 24C. Exercise training and heat acclimation â (3dexac, ExAc)- exposed to both environmental heat and aerobic exercise as above. The Series data tables appended below: 1) Heart - normalized log2 ratio of geomeans defined as treatment/control 2) Soleus - normalized log2 ratio of geomeans defined as treatment/control 21 samples, 3 pool each, of: 1)Â Control untreated rats 2)Â Long-term heat acclimated rats 3)Â Long-term aerobic-exercised trained rats. 4)Â Rats exposed to long-term heat acclimation and exercise training. 5)Â Short term heat acclimated rats. 6)Â Short term aerobic exercised trained rats 7)Â Rats exposed to short-term heat acclimation and exercise training.
2010-05-27 | E-GEOD-7799 | biostudies-arrayexpress
Project description:Biofilm formation is considered the most important factor involved in pathogenicity of Staphylococcus epidermidis.We investigated the role of two-component signal transduction system (TCS) srrAB, which was up-regulated under micro-aerobic condition, in the growth and biofilm formation of S. epidermidis.AsrrA-deficient mutant (∆srrA) derived from S. epidermidis1457 (SE1457), exhibited dramatic reduction in growth and biofilm formation underboth aerobic and micro-aerobic conditions, and more sensitive to several different types of antimicrobial agents, H2O2 and SDS. In New Zealand Rabbit model of S. epidermidis biofilm infection, ∆srrA hardly formed biofilm compared to that of SE1457. Phenotypic alteration was restored to the wide-type levelwhen srrAB were complemented into ∆srrA. Further study found that the initial adherence capacity and production of polysaccharide intercellular adhesion (PIA) in ∆srrA were decreased, while extracellular DNA (eDNA) was increased. Transcriptional Analysisby qRT-PCR demonstrated that expression level of icaRin ∆srrA was up-regulated compared to that of SE1457 under aerobic condition, while down-regulated under micro-aerobic condition;icaA and altE were down-regulated under both conditions. Expression of genes involved in respiratory metabolism, such as qoxB(quinol oxidase polypeptide II), ctaA(heme A synthase), and pfl(pyruvate formatelyase), etc. were down-regulated in ∆srrAunder both conditions. Electrophoretic mobility shift assay (EMSA) revealed that phosphorylated SrrA bound to the promoter regions of icaR, icaA, atlE, qoxB,ctaA, andpflB just like binding its own promoter region srr. Taken together, our results demonstrate that srrAB may provide a mechanistic link between respiratory metabolism, environmental signals, and regulation of biofilm formation in S. epidermidis.
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Project description:Zymomonas mobilis is an aerotolerant anaerobe and prolific ethanologen with attractive characteristics for industrial biofuel production. Here, we examine the effect of oxygen exposure on metabolism and gene expression in Z. mobilis by combining targeted metabolomics, mRNA sequencing, and shotgun proteomics. We found that exposure to oxygen profoundly influenced metabolism, inducing both transient metabolic bottlenecks and long-term metabolic remodeling. In particular, oxygen induced a severe but temporary metabolic bottleneck in the methyl erythritol 4-phosphate pathway for isoprenoid biosynthesis, likely caused by oxidative damage to the iron-sulfur co-factors of the final two enzymes of the pathway. This bottleneck was resolved with minimal changes in expression level of enzymes in the pathway but pronounced upregulation of enzymes related to iron-sulfur cluster maintenance and biogenesis (i.e. flavodoxin reductase and the suf operon). We also detected prominent changes in glucose utilization under aerobic conditions. Specifically, we observed increased gluconate production following exposure to oxygen, accounting for 18% of glucose uptake after 24 hours of aerobic growth. Our results suggest that under aerobic conditions, electrons from the oxidation of glucose to gluconate are delivered to the electron transport chain to minimize oxidative damage by reducing reactive oxygen species such as H2O2. This model is supported by the simultaneous upregulation of three membrane-bound dehydrogenases, cytochrome c peroxidase, and a cytochrome bd terminal oxidase.
2019-01-18 | PXD011545 | Pride
Project description:Biofilm formation is considered the most important factor involved in pathogenicity of Staphylococcus epidermidis.We investigated the role of two-component signal transduction system (TCS) srrAB, which was up-regulated under micro-aerobic condition, in the growth and biofilm formation of S. epidermidis.AsrrA-deficient mutant (M-bM-^HM-^FsrrA) derived from S. epidermidis1457 (SE1457), exhibited dramatic reduction in growth and biofilm formation underboth aerobic and micro-aerobic conditions, and more sensitive to several different types of antimicrobial agents, H2O2 and SDS. In New Zealand Rabbit model of S. epidermidis biofilm infection, M-bM-^HM-^FsrrA hardly formed biofilm compared to that of SE1457. Phenotypic alteration was restored to the wide-type levelwhen srrAB were complemented into M-bM-^HM-^FsrrA. Further study found that the initial adherence capacity and production of polysaccharide intercellular adhesion (PIA) in M-bM-^HM-^FsrrA were decreased, while extracellular DNA (eDNA) was increased. Transcriptional Analysisby qRT-PCR demonstrated that expression level of icaRin M-bM-^HM-^FsrrA was up-regulated compared to that of SE1457 under aerobic condition, while down-regulated under micro-aerobic condition;icaA and altE were down-regulated under both conditions. Expression of genes involved in respiratory metabolism, such as qoxB(quinol oxidase polypeptide II), ctaA(heme A synthase), and pfl(pyruvate formatelyase), etc. were down-regulated in M-bM-^HM-^FsrrAunder both conditions. Electrophoretic mobility shift assay (EMSA) revealed that phosphorylated SrrA bound to the promoter regions of icaR, icaA, atlE, qoxB,ctaA, andpflB just like binding its own promoter region srr. Taken together, our results demonstrate that srrAB may provide a mechanistic link between respiratory metabolism, environmental signals, and regulation of biofilm formation in S. epidermidis. Microarrays covering different S. epidermidis genomes were used to assess the impact of the two component system srrAB on growth and biofilm formation, by comparing WT with srrA mutant transcriptomes
2014-11-21 | E-GEOD-47101 | biostudies-arrayexpress
Project description:To gain further insights into the molecular basis of the effects of oxygen on biofilm formation by S. mutans (Ahn and Burne, 2007), we used DNA microarrays to analyze gene expression profiles of cells cultured under aerobic or anaerobic conditions. Keywords: Oxygen, Biofilm, Caries, Microarray
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Project description:S. aureus biofilms are associated with the organism's ability to cause disease. Biofilm associated bacteria must cope with the host's innate immune system. We used commercially available Affymetrix S. aureus GeneChips to compare the gene expression properties of 4 and 6 day established biofilms following short (1 hr)- and long (24 hr)- term exposure to macrophages and neutrophils.
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