4.4.1.21: S-ribosylhomocysteine lyase
This is an abbreviated version!
For detailed information about S-ribosylhomocysteine lyase, go to the full flat file.
Word Map on EC 4.4.1.21
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4.4.1.21
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quorum
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quorum-sensing
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interspecies
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harveyi
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thioether
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4,5-dihydroxy-2,3-pentanedione
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nucleosidase
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luxs-dependent
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furanone
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medicine
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analysis
- 4.4.1.21
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quorum
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quorum-sensing
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interspecies
- harveyi
- thioether
- 4,5-dihydroxy-2,3-pentanedione
- nucleosidase
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luxs-dependent
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furanone
- medicine
- analysis
Reaction
Synonyms
AI-2 synthase, autoinducer-2 synthase, BsLuxS, EC 3.13.1.2, EC 3.2.1.148, EC 3.3.1.3, EcLuxS, lsrR, Lux S, LuxS, LuxS protein, S-ribosyl homocysteinase, S-ribosylhomocysteinase, S-ribosylhomocysteine lyase, S-ribosylhomocysteinelyase, VhLuxS
ECTree
4.4.1.21 S-ribosylhomocysteine lyaseAdvanced search results
results (
results (Engineering
Engineering on EC 4.4.1.21 - S-ribosylhomocysteine lyase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
C84A
C84D
C82A
inactive, mutation decreases autoinducer AI-2 production and biofilm formation
C82S
43fold decrease in activity, mutation decreases autoinducer AI-2 production and biofilm formation
F80M
7fold decrease in activity, mutation decreases autoinducer AI-2 production and biofilm formation
F80M/H87Y
42fold decrease in activity, mutation decreases autoinducer AI-2 production and biofilm formation
H87Y
37fold decrease in activity, mutation decreases autoinducer AI-2 production and biofilm formation
additional information
C84A
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site-directed mutagenesis, catalytically inactive mutant, the mutant contains a Co2+ ion, in the wild-type the substrate's cyclic ribosyl moiety is positioned adjacent to the Zn2+ ion, while in the mutant the noncyclic ribosyl is ligated to the Co2+ via its C2-O carbonyl oxygen
C84D
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site-directed mutagenesis, the mutant shows reduced activity compared to the wild-type enzyme
additional information
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a luxS deletion mutant shows obvious growth deficiency when cultured in the serum-free medium and biofilm formation is significantly enhanced, in a mouse infection model, the 50% lethal dose of the mutant strain is increased up to 96fold, and the ability to colonize in different mouse tissues is significantly decreased
additional information
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a luxS deletion mutant shows obvious growth deficiency when cultured in the serum-free medium and biofilm formation is significantly enhanced, in a mouse infection model, the 50% lethal dose of the mutant strain is increased up to 96fold, and the ability to colonize in different mouse tissues is significantly decreased
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additional information
the luxS isogenic mutant, prepared by marker exchange mutagenesis, shows an alteration in the dynamics and architecture of the biofilm formation, a decrease in the motility of the bacterium, and an enhanced virulence in the septicemic mouse model
additional information
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the luxS isogenic mutant, prepared by marker exchange mutagenesis, shows an alteration in the dynamics and architecture of the biofilm formation, a decrease in the motility of the bacterium, and an enhanced virulence in the septicemic mouse model
additional information
the DELTA luxS mutant abolishes AI-2 production and is more sensitive to hydrogen peroxide and cumene hydroperoxide than the wild type enzyme
additional information
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the DELTA luxS mutant abolishes AI-2 production and is more sensitive to hydrogen peroxide and cumene hydroperoxide than the wild type enzyme
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additional information
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inactivation of the luxS gene impairs motility, extracellular polysaccharide production, and tolerance for hydrogen peroxide, and reduces virulence on pear leaves
additional information
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inactivation of the luxS gene impairs motility, extracellular polysaccharide production, and tolerance for hydrogen peroxide, and reduces virulence on pear leaves
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additional information
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the luxS knockout mutant CMPG5412 shows drastically reduced persistence in mice which is related to less survival in simulated gastric juice, indicating that LuxS metabolism is crucial for the gastric stress resistance, the suppressor mutations in the luxS knockout mutant CMPG5413 compensates for the metabolic defects of the luxS mutation and restores the resistance to gastric juice but causes a defect in adherence, biofilm formation, and exopolysaccharide production
additional information
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the luxS knockout mutant CMPG5412 shows drastically reduced persistence in mice which is related to less survival in simulated gastric juice, indicating that LuxS metabolism is crucial for the gastric stress resistance, the suppressor mutations in the luxS knockout mutant CMPG5413 compensates for the metabolic defects of the luxS mutation and restores the resistance to gastric juice but causes a defect in adherence, biofilm formation, and exopolysaccharide production
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additional information
generation of a knockout mutant by insertional mutation of the luxS gene, transcriptomic and metabolomic changes of wild-type and mutant strains, overview
additional information
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generation of a knockout mutant by insertional mutation of the luxS gene, transcriptomic and metabolomic changes of wild-type and mutant strains, overview
additional information
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generation of a knockout mutant by insertional mutation of the luxS gene, transcriptomic and metabolomic changes of wild-type and mutant strains, overview
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additional information
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deletion of luxS alters biofilm formations in static and flow-through conditions, a luxS mutation does not cause a large difference in global gene expression
additional information
Shewanella oneidensis MR-1 / ATCC 700550
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deletion of luxS alters biofilm formations in static and flow-through conditions, a luxS mutation does not cause a large difference in global gene expression
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additional information
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disruption of luxS affects hyaluronidase and intermedilysin gene expressions and leads to 5fold decrease in haemolytic activity of the mutant
additional information
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a luxS null mutant, constructed by allelic exchange via the replacement of an erythromycin resistance determinant to the gene, is able to accelerate biofilm formation on a polystyrene surface during the mid-exponential growth phase
additional information
generation of a luxS null mutant of 05ZYH33 strain is obtained by homologous recombination
additional information
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generation of a luxS null mutant of 05ZYH33 strain is obtained by homologous recombination
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additional information
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inactive luxS leads to decreased virulence in Vibrio alginolyticus
additional information
the luxS mutants MYJS and MYJM exhibit a lower growth rate and defective flagellar biosynthesis, show a significant decrease in protease production and an increase in both extracellular polysaccharide production and biofilm development
additional information
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inactive luxS leads to decreased virulence in Vibrio alginolyticus
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