g. inSerratia), and is likely influenced by the immediate environment, MM-102 purchase i.e. whether it is replete or deficient in nutrients that can repair a metabolic imbalance.
To establish a cell-cell communication defect as the underlying cause of an altered phenotype relies on addition of purified signal molecule at an appropriate time and concentration to the cells in the environment under study. Addition of AI-2 or DPD to biofilm communities has revealed that some organisms require low levels (amounts undetectable in theV. harveyibioluminescent assay (0.08 nM DPD) effectively Cilengitide restored phenotypes for oral commensalsStreptococcus oralisandActinomyces reslundiiwhilst high levels did not ); and others require levels similar to those encounteredin vivoto complement altered
phenotypes exhibited byluxSmutants (e.g. inStaphylococcus epidermidis).In vivolevels of DPD are in the μM range (e.g. 1.95 μMV. harveyiand 0.26 μMStrept. mutans) Establishing a definitive role for disruption of the AMC in the maintenance of a phenotype may also be problematic. It cannot be predicted that the transcription of all the genes encoding AMC participating enzymes will alter upon interruption of the cycle, as biochemical pathways are often controlled by regulation of one or two key enzymes. Although SAM levels influence methioninede novosynthesis in enteric bacteria, AMC disruption may not result in major changes in gene expression as growth media contain all the methionine and SAM required by the CH5424802 cells. An initial step towards greater understanding of the consequences of AI-2 production andluxSinactivation would be to study
transcriptome changes under Etomidate conditions where it had been established that AI-2 is produced, and compare this to non-AI-2-containing conditions. Planktonic, exponentially growingC. jejunihas been shown to produce functional AI-2 capable of inducing bioluminescence in aV. harveyibioassay whereas culture supernatants from an isogenicluxSmutant strain had no effect on bioluminescence . TheC. jejuni luxSmutant was comparable to the wild type in its growth rate and its ability to resist oxidative stress and invade Caco-2 monolayers, however it showed significantly decreased motility in semisolid media leading to the suggestion that a quorum sensing role of AI-2 inC. jejunicould involve regulation of motility . In line with this, a null mutation ofluxSinC. jejunistrain 81116 reduced motility and transcription offlaA. Recently, the effect ofluxSmutation inC. jejunistrain 81-176 on global gene expression has been reported to be limited, with gene expression modulations focused primarily upon genes involved in motility and metabolism . With the aim of gaining further insight into the potential role of AI-2 as a quorum sensing molecule inC.