Project description:The effect of sulfide stress on Desulfovibrio vulgaris Hildenborough (DvH) gene expression was determined by comparing the gene expression profiles of DvH under conditions in which sulfide was allowed to accumulate (high sulfide, average concentration 10 mM) against DvH cells grown under conditions in which sulfide was removed by continuous gassing (low sulfide, average concentration 1 mM). High sulfide significantly decreased the instantaneous growth rate constant and final cell density of the culture indicating a decreased bioenergetic fitness. Changes in gene expression caused by exposure to high sulfide were determined using full-genome DvH microarrays. The transcription of ribosomal protein-encoding genes was decreased, in agreement with the lower growth rate of DvH under high sulfide conditions. Interestingly, expression of the gene for DsrD, located downstream of the genes for dissimilatory sulfite reductase (DsrAB) was also strongly down-regulated. In contrast, the expression of many genes involved in iron accumulation, stress response and proteolysis, and chemotaxis were increased. This indicates that high sulfide represents a significant stress condition, in which the bioavailability of metals like iron may be lowered and in which proteins (e.g. metalloenzymes) may need to be refolded, or proteolytically degraded. Overall this leads to a reduced growth rate and less efficient biomass production with available resources. For each condition 2 unique biological samples were hybridized to 4 arrays that each contained duplicate spots. Genomic DNA was used as universal reference.
Project description:The effect of sulfide stress on Desulfovibrio vulgaris Hildenborough (DvH) gene expression was determined by comparing the gene expression profiles of DvH under conditions in which sulfide was allowed to accumulate (high sulfide, average concentration 10 mM) against DvH cells grown under conditions in which sulfide was removed by continuous gassing (low sulfide, average concentration 1 mM). High sulfide significantly decreased the instantaneous growth rate constant and final cell density of the culture indicating a decreased bioenergetic fitness. Changes in gene expression caused by exposure to high sulfide were determined using full-genome DvH microarrays. The transcription of ribosomal protein-encoding genes was decreased, in agreement with the lower growth rate of DvH under high sulfide conditions. Interestingly, expression of the gene for DsrD, located downstream of the genes for dissimilatory sulfite reductase (DsrAB) was also strongly down-regulated. In contrast, the expression of many genes involved in iron accumulation, stress response and proteolysis, and chemotaxis were increased. This indicates that high sulfide represents a significant stress condition, in which the bioavailability of metals like iron may be lowered and in which proteins (e.g. metalloenzymes) may need to be refolded, or proteolytically degraded. Overall this leads to a reduced growth rate and less efficient biomass production with available resources.
Project description:Stress response of Methylococcus capsulatus str.Bath toward hydrogen sulfide (H2S) was investigated via physiological study and transcriptomic profiling. M. capsulatus (Bath) can grow and tolerate up to 0.75%vol H2S in headspace. Vast change in pH suggests biological relevant sulfide oxidation. Dozens of H2S-sensitive genes were identified from comparison of cell transcriptome in different H2S concentrations. Mc sulfide quinone reductase (SQR) and persulfide dioxygenase were found to be active during sulfide detoxification. Moreover, xoxF, a novel lanthanide(Ln)-dependent methanol dehydrogenase (MDH) was overexpressed in H2S while mxaF, a calcium-dependent MDH, was down-regulated, and such MDH switch phenomenon is also well known to be induced by addition of lanthanide via an as-yet-unknown mechanism. Activities in quorum sensing and RND efflux pump also suggest their role in sulfide detoxification, and might provide insight on the xoxF/mxaF switch mechanism.
Project description:Acinetobacter baumannii is an opportunistic nosocomial pathogen that is the causative agent of several serious infections in humans. Here, we investigate the response of A. baumannii toward sodium sulfide (Na2S), known to be associated with some biofilms at oxic/anoxic interfaces, as a model for how this major human pathogen manages sulfide homeostasis. These results reveal that A. baumannii encodes two persulfide‑sensing transcriptional regulators, a primary sigma54‑dependent transcriptional activator (FisR), and a secondary system controlled by the persulfide‑sensing repressor biofilm growth‑associated repressor (BigR) both of which regulate operons encoding for sulfide detoxification or transportation. In addition, sulfide induces an alternative cytochrome bd oxidase which is refractory to inhibition by H2S and represses importers of alternate sulfur sources. Lastly, our results suggest additional genes regulated by BigR beyond sulfide detoxification including genes associated with assembly of type 1 chaperone-usher pilus.
2020-06-15 | GSE148264 | GEO
Project description:Studies of simultaneous partial nitrification endogenous denitrification and phosphorus removal process
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.
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).