User:Eflemi2/Prokaryotic Diversity sandbox
Interspecies Quorum Sensing Quorum sensing is a way bacteria in a community can determine how many of their own and other species are in an area. Bacteria secrete these molecules, which increase in proportion to cell number. Once the molecule hits a certain concentration it triggers the transcription of certain genes such as virulence factors. It has been discovered that bacteria can not only interact via quorum sensing with members of their own species but that there is a kind of universal molecule that allows them to gather information about other species as well (1). This universal molecule is called auto-inducer 2 or AI-2 (1).
AI-2 was first discovered in the light producing system of the bacteria Vibrio harveyi. The pathway that induces Vibrio harveyi luminescence is controlled by two parallel pathways (2). The first pathway uses a typical AI-1 homoserine lactone signaling molecule. However the bacteria were also found to recognize a second auto inducer AI-2 (4). Interestingly scientist also found that V. harveyi luminescence could be induced by 75 other bacterial species AI-2 molecules (7). This discovery lead to the proposal of AI-2 as a universal form of communication between bacteria species. In addition to information about cell densities AI-2 can provide information on the growth phase and prosperity of cells in a population. It has a greater ability to store information than other quorum sensing molecules because its production is tied to cell growth. The production of AI-2 peaks in late log phase for many bacteria (1). The structure of AI-2 was discovered recently to be a fused 2-member ring with boron bridging the gap between the diesters (Chen 2002).
The enzyme LuxS is responsible for AI-2 synthesis (7). The gene encoding for LuxS has been detected in 35 of the 89 bacterial genomes sequenced and in all of the bacteria the gene had little variation (2). In every bacterium found so far that produces the AI-2 signaling molecule the LuxS gene was also found. There are three enzymes that make DPD (4,5-dihydroxy 2,3 pentanedione) which is the substrate LuxS uses to make AI-2 (7). The pathway for synthesizing AI-2 was found to be identical in V. harveyi, E coli, Salmonella typhimurium, V. cholerea, and Enterococcus faecalis providing further evidence that this molecule may be a universal signal among bacteria (6). Shigella flexneri use AI-2 to mediate virulence.
The major virulence factor in Shigella is the plasmid vir B. The AI-2 signaling pathway was shown to be responsible for the observed peak of vir B (1). Although it was determined that AI-2 is not crucial for virulence that it does increase the expression of the plasmid. AI-2 also regulates the virulence of Enteroinvasive and Enterohemoragic E.coli (2). It is likely the high concentrations of AI-2 produced by normal gut flora effect the production of AI-2 in Shigella and its subsequent virulence (1).
AI-2 is required for the biofilm formation in P. ginivalis and S. gordonii. S. gordonii is a major cause of dental plaque and its adherence is essential for many other pathogenic bacteria to also adhere to teeth. P. ginivalis causes periodontal disease. If both the bacteria do not posses a functional copy of the LuxS gene they cannot form a bioflim However if either one of the bacteria do have the LuxS gene they can form bioflims suggesting again this molecule is used for communication between unrelated species (2).
Other bacterial uses for AI-2 Clostridium perferinges- regulates toxin production (2) P. luminescence- controls the timing of antibiotics (2) V. cholerea- used in the pathogenic cascade (3)
Since the LuxS enzyme is not present in Eukaryotes it is a good potential target for antibiotics. Also AI-2 signaling seems to control many virulence factors in bacteria so blocking this signal could lead to knew ways to control bacterial infections such as cholera (3). Since the AI-2 molecule seems to be involved in the virulence cascade if we could block the uptake of AI-2 then we could potentially stop the virulence cascade.
1.[1] 2.[2] 3.[3] 4.[4] 5.[5] 7. 6.[6]
- ^ Willam A. Day (2001). American Society for Microbiology. 69 (1).
{{cite journal}}: Missing or empty|title=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Bassler, Bonnie (2003). "LuxS quorum sensing more than just a numbers game". Current Opinion in Microbiology. 10 (6): 191–197.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Whitehead, Barnard, Slater, Simpson (2001). Quorum Sensing in Gram Negative Bacteria. Department of Biochemistry University of Cambridge.
{{cite book}}: CS1 maint: multiple names: authors list (link) - ^ Xu, Lin (5). "Role of the luxs Quorum-Sensing in Bioflim formation and virulence of Stapholococcus epidermis". American Society for Microbiology. 74 (1): 488–496.
{{cite journal}}: Check date values in:|date=and|year=/|date=mismatch (help); Unknown parameter|coauthors=ignored (|author=suggested) (help); Unknown parameter|month=ignored (help) - ^ Schauder (2001). "The LuxS familyy of bacterial autoinducers". Molecular Microbiology.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Miller (2004). "Salmonella recongnizes a distinct quorum sensing mechanism". Molecular Cell. 15 (5): 677–687. doi:10.1016/j.molcel.2004.07.020. PMID 15350213.
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