Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1241139 | ENA |
REPOSITORIES: ENA
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Project description:Competition among nitrate reducing bacteria (NRB) and sulfate reducing bacteria (SRB) for resources in anoxic environments is generally thought to be governed largely by thermodynamics. It is now recognized that intermediates of nitrogen and sulfur cycling (e.g., hydrogen sulfide, nitrite, etc.) can also directly impact NRB and SRB activities in freshwater, wastewater and sediment, and therefore may play important roles in competitive interactions. Here, using Intrasporangium calvum C5 as a model NRB, we performed comparative transcriptomic and metabolomic analyses to demonstrate that the reduced sulfur compounds cysteine and sulfide differentially inhibit respiratory growth on nitrate, and that inhibition by each can be selectively relieved by a specific carbon source. These findings provide mechanistic insights into the interplay and stratification of NRBs and SRBs in diverse environments.
2020-10-01 | GSE158822 | GEO
Project description:Hydrogen sulfide (H2S), a metabolic endproduct of sulfate-reducing bacteria in the large intestine, represents a genotoxic insult to the colonic epithelium, which may also be linked with chronic disorders such as ulcerative colitis and colorectal cancer. The present study defined the early (30 minutes) and late (4 hours) response of non-transformed human intestinal epithelial cells (FHs 74 Int) to sulfide. We measured the genotoxicity of Na2S using the single cell gel electrophoresis (comet) assay. Changes in gene expression were analyzed after exposure to a genotoxic–but not cytotoxic–concentration of sulfide (500 μM Na2S) using pathway specific quantitative RT-PCR gene arrays
2008-10-10 | GSE11688 | GEO
Project description:Hydrogen sulfide (H2S), a metabolic endproduct of sulfate-reducing bacteria in the large intestine, represents a genotoxic insult to the colonic epithelium, which may also be linked with chronic disorders such as ulcerative colitis and colorectal cancer. The present study defined the early (30 minutes) and late (4 hours) response of non-transformed human intestinal epithelial cells (FHs 74 Int) to sulfide. We measured the genotoxicity of Na2S using the single cell gel electrophoresis (comet) assay. Changes in gene expression were analyzed after exposure to a genotoxic–but not cytotoxic–concentration of sulfide (500 μM Na2S) using pathway specific quantitative RT-PCR gene arrays.
2008-10-10 | GSE11678 | GEO
Project description:Species-specific qPCR for sulfide-oxidizing bacteria
| PRJEB30777 | ENA
Project description:As one of the most important environmental factors, heat stress (HS) has been found to affect various biological activities of organisms such as growth, signal transmission, primary metabolism and secondary metabolism. Ganoderma lucidum has become a potential model system for evaluating how environmental factors regulate the secondary metabolism of basidiomycetes. Previous research showed that HS can induce the biosynthesis of ganoderic acids (GAs). In this study, we found the existence of hydrogen sulfide in Ganoderma lucidum; moreover, HS increased GAs biosynthesis and could affect the hydrogen sulfide content. We found that sodium hydrosulfide (NaHS), an exogenous donor of hydrogen sulfide, could revert the increased GAs biosynthesis elicited by HS. This result indicated that an increased content of hydrogen sulfide, within limits, was associated with HS-induced GAs biosynthesis. Our results further showed that the GAs content was increased in CBS-silenced strains and could be reverted to WT strain levels by the addition of NaHS. Transcriptomic analyses indicated that that H2S can affect various intracellular signal pathways and physiological processes in G. lucidum. Further studies showed that H2S could affect the intracellular calcium concentration and thus regulate the biosynthesis of GAs. This study demonstrated that hydrogen sulfide is involved in the regulation of secondary metabolic processes induced by heat stress in filamentous fungi.
2021-10-12 | GSE121270 | GEO
Project description:Interventions: Case series:nill;The control group:nill
Primary outcome(s): Hydrogen sulfide;Pathological diagnosis
Study Design: Case-Control study
| 2671665 | ecrin-mdr-crc
Project description:Hydrogen sulfide producing bacteria enrichments Raw sequence reads
| PRJNA1147460 | ENA
Project description:The aim of this experiment was to determine how exposure of Hydrogen sulfide impacts gene expression in Mycobacterium tuberculosis. RNA was isolated from actively growing mycobacterial cells (0.6-0.8 OD600) using Trizol according to established protocols (27). Briefly, cells were exposed to 25 µM GYY4137 for 1 hr under carefully controlled conditions (n=3/group) and RNA isolated. Unexposed cells received spent GYY4137 (without any capacity to produce Hydrogen sulfide).
2020-01-04 | E-MTAB-7421 | biostudies-arrayexpress
Project description:Hypertension is a major risk factor for chronic kidney disease (CKD) and renal inflammation is an integral part in this pathology. Hydrogen sulfide (H2S) has been shown to mitigate renal damage through reduction in blood pressure and reactive oxygen species; however, the exact mechanisms are not clear. While several studies have underlined the role of epigenetics in renal inflammation and dysfunction, the mechanisms through which epigenetic regulators play role in hypertension are not well defined. We used microarrays to detail the global programme of gene expression underlying hypertension in the kidney and how hydrogen sulfide supplementation alleviates these effects.
2016-12-23 | GSE92857 | GEO
Project description:The production of endogenous hydrogen sulfide (H2S) has been shown to confer antibiotic tolerance in all bacteria studied to date. Therefore, this mediator has been speculated to be a universal defense mechanism against antibiotics in bacteria. This is assuming that all bacteria produce endogenous H2S. In this study, we established that the pathogenic bacteria Acinetobacter baumannii does not produce endogenous H2S, giving us the opportunity to test the effect of exogenous H2S on antibiotic tolerance in a bacterium that does not produce it. By using a H2S-releasing compound to modulate the sulfide content in A. baumannii, we demonstrated that instead of conferring antibiotic tolerance, exogenous H2S sensitized A. baumannii to multiple antibiotic classes, and was able to revert acquired resistance to gentamicin. Exogenous H2S triggered a perturbation of redox and energy homeostasis that translated into hypersensitivity to antibiotic killing. We propose that H2S could be used as an antibiotic-potentiator and resistance-reversion agent in bacteria that do not produce it.
2021-06-08 | PXD020384 | Pride