Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.5.1.47 (cysteine synthase)
 625 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasmids of the H incompatibility complex confer protection against all known channel-forming colicins (PacB character) and resistance to potassium tellurite (Te(r)) to Escherichia coli strains. A DNA clone (2.2 kbp) from plasmid Mip233 (IncHI3) expressing PacB-Te(r) phenotypes was studied. DNA sequence analysis revealed a high degree of homology with the enzyme O-acetylserine sulfhydrylase. Size of the PacB-Te(r) transcript was estimated as 1200 bases. A single polypeptide was found on SDS-polyacrylamide gel with a molecular mass estimated of 34 kDa. The effect of channel-forming colicins and tellurite was analyzed at physiological and transcriptional levels. Results suggest that the pacB gene product could be a reductase-like enzyme. It is also suggested that presence of the PacB character among H plasmid confers selective advantage on cells sharing an ecological niche.
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PMID:On the mechanism of resistance to channel-forming colicins (PacB) and tellurite, encoded by plasmid Mip233 (IncHI3). 1106 4

The gram-positive human pathogen Staphylococcus aureus is often isolated with media containing potassium tellurite, to which it has a higher level of resistance than Escherichia coli. The S. aureus cysM gene was isolated in a screen for genes that would increase the level of tellurite resistance of E. coli DH5alpha. The protein encoded by S. aureus cysM is sequentially and functionally homologous to the O-acetylserine (thiol)-lyase B family of cysteine synthase proteins. An S. aureus cysM knockout mutant grows poorly in cysteine-limiting conditions, and analysis of the thiol content in cell extracts showed that the cysM mutant produced significantly less cysteine than wild-type S. aureus SH1000. S. aureus SH1000 cannot use sulfate, sulfite, or sulfonates as the source of sulfur in cysteine biosynthesis, which is explained by the absence of genes required for the uptake and reduction of these compounds in the S. aureus genome. S. aureus SH1000, however, can utilize thiosulfate, sulfide, or glutathione as the sole source of sulfur. Mutation of cysM caused increased sensitivity of S. aureus to tellurite, hydrogen peroxide, acid, and diamide and also significantly reduced the ability of S. aureus to recover from starvation in amino acid- or phosphate-limiting conditions, indicating a role for cysteine in the S. aureus stress response and survival mechanisms.
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PMID:Role of a cysteine synthase in Staphylococcus aureus. 1499 87

Environmental toxicants influence development, behavior, and ultimately survival. The nematode Caenorhabditis elegans has proven to be an exceptionally powerful model for toxicological studies. Here, we develop novel technologies to describe the effects of cyanide toxicity with high spatiotemporal resolution. Importantly, we use these methods to examine the genetic underpinnings of cyanide resistance. Caenorhabditis elegans that lack the EGL-9 oxygen sensing enzyme have been shown to be resistant to hydrogen cyanide (HCN) gas produced by the pathogen Pseudomonas aeruginosa PAO1. We demonstrate that the cyanide resistance exhibited by egl-9 mutants is completely dependent on the HIF-1 hypoxia-inducible factor and is mediated by the cysl-2 cysteine synthase, which likely functions in metabolic pathways that inactivate cyanide. Further, the expression of cysl-2 correlates with the degree of cyanide resistance exhibited in each genetic background. We find that each mutant exhibits similar relative resistance to HCN gas on plates or to aqueous potassium cyanide in microfluidic chambers. The design of the microfluidic devices, in combination with real-time imaging, addresses a series of challenges presented by mutant phenotypes and by the chemical nature of the toxicant. The microfluidic assay produces a set of behavioral parameters with increased resolution that describe cyanide toxicity and resistance in C. elegans, and this is particularly useful in analyzing subtle phenotypes. These multiparameter analyses of C. elegans behavior hold great potential as a means to monitor the effects of toxicants or chemical interventions in real time and to study the biological networks that underpin toxicant resistance.
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PMID:Multiparameter behavioral analyses provide insights to mechanisms of cyanide resistance in Caenorhabditis elegans. 2380