Every cell, a prokaryote or eukaryote has to sense its environment and adjust accordingly. In addition the cell should also be able to communicate with other cells. Quorum sensing is a system of stimulus and response correlated to population density. This is used as a chemical language by bacteria and fungus to talk.
Photo of Bonnie Bassler who works on Quorum Sensing
For her talks on quorum sensing use the following links
1. MTS53- Bonnie Bassler, the Bacterial wiretrap
The readers are advised to take a look into the talks which would give you the background information needed to read on (Am lazy enough, to not review it and post it here. Anyways the link is there).
So here’s the deal. Each bacterium decides to survey the surrounding and keep a record of number so as to decide what next. Several classes of such signal molecules have now been identified. So if there are a large number of molecules I need to classify that right? Ok. So here it is. 1st group is amino acids and short peptide derivatives, commonly utilized by Gram-positive bacteria and 2nd group is fatty acid derivatives, called homoserine lactones (HSLs) utilized by Gram-negative members.
Another system that communicates is the toxin antitoxin system.
First understand 3 points-
1. The mazEF locus of Escherichia coli is located in an operon together with the upstream relA gene which encodes an antitoxin/toxin system which is supposed to play a role in programmed cell death under stress and starvation conditions at high cell densities.
2. Escherichia coli mazEF-mediated cell death is a population phenomenon requiring a quorum-sensing molecule called the extracellular death factor (EDF).
3. Any stressful condition that prevents the expression of the chromosomally borne mazEF module will lead to the reduction of MazE in the cell, permitting toxin MazF to act freely.
So what sense does the above 3 make? You guessed it right! At high population densities the E coli produces EDF which activates the mazEF and induces cell death. This helps other cells to survive and keep the population in control at low energy availability and high density. Now what if we can cheat the talk???? He he he.. That’s what exactly happens in action of Rifampicin unlike previously thought. Rifampicin was thought to arrest the growth of bacterial cultures by generally inhibiting cellular transcription by interfering with the activity of its primary target, RNA polymerase. But now we know rifampicin arrests the growth of bacterial cultures by inhibiting cellular transcription by interfering with the activity of its primary target, RNA polymerase. The activation of MazF requires the quorum sensing factor Extracellular Death Factor (EDF).
So the take home message is that by using specific death inducing factors (EDF in above case) along with other antibiotic we could actually reduce the antibiotic resistance. The quorum sensing being a vital phenomenon, the bacteria would evolve resistance slowly, though of course I do think resistance will come.
1. Hanna Engelberg-Kulka,* Idan Yelin and Ilana Kolodkin-Gal. Activation of a built-in bacterial programmed cell death system as a novel mechanism of action of some antibiotics; Communicative & Integrative Biology May/June 2009 2:3, 211-212
2. Ilana Kolodkin-Gal and Hanna Engelberg-Kulka. The Extracellular Death Factor: Physiological and Genetic Factors Influencing Its Production and Response in Escherichia coli; J Bacteriol. 2008 May; 190(9): 3169–3175.