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This is a figure summarising the quorum sensing mechanism in Vibrio cholerae.

In this video by Bonnie Bassler, she explains how quorum sensing can be targeted to control infections.

At 15:09 she explains why cqsA- mutants show more dramatic effect when external CAI1 is added - because we are not fighting against the endogenously produced autoinducer1.

My question : But won't endogenously produced autoinducer help in controlling virulence, as the more the auto inducer lesser the virulence ? Why should we be fighting against endogenously produced autoinducer 1 ?

  • $\begingroup$ I haven't watched the video and I don't know the details, but doesn't induction of virulence depend upon auto-inducer in these systems? $\endgroup$
    – Alan Boyd
    Commented Mar 7, 2014 at 18:23
  • $\begingroup$ its true the compound (homoserine lactone?) is produced by the individual cells already. but yes we can engineer the bacteria to be non virulent, but in general the problem is not the stuff coming out of the labs, but the stuff that's out there already. $\endgroup$
    – shigeta
    Commented Mar 7, 2014 at 18:25
  • $\begingroup$ @AlanBoyd Yes it is usually that, but Vibrio Cholerae has exactly the opposite mechanism - it switches off virulence when in large numbers and activates genes that help it go out of the body via diarrhea. $\endgroup$
    – biogirl
    Commented Mar 7, 2014 at 19:28
  • $\begingroup$ @biogirl but isn't diarrhea = virulence in this case since it is the main pathological effect? $\endgroup$
    – Alan Boyd
    Commented Mar 7, 2014 at 20:25
  • $\begingroup$ @Alan yeah you are right but when it is in large number it activates a gene for chopping off the protein by which it was attached. $\endgroup$
    – biogirl
    Commented Mar 8, 2014 at 2:52

1 Answer 1


First of all I find quorum sensing to be generally facinating, so I'm happy to see the topic brought up here.

Dr. Bassler has many papers on the subject, but I think one of the most relevant ones to this question is here.

Regarding your question, you have the right idea, but you're missing the point of her comment. The Western shows a more dramatic difference in cqsA- bacteria because they are not inhibiting themseleves (as you suggested). Thus the lower concentrations have much higher levels of the toxin produced because the only CAI-1 being provided is the synthetic one. This makes the ramp up in administered CAI-1 seem more drastic because you start at a higher level.

I hope that makes since, if I can find an open writes version of the Western, I'll come back and give further analysis on it.

Regarding @AlanBoyd 's comments, V. cholerae is different because it seeks to create an acute infection, not a persistent one. Cholera toxin is what causes the majority of diarrhea and virulence from cholera. V. cholera produces the toxin until it's inhibited by ether auto-inducer (which should be after the pt already has massive diarrhea), then it switches to produce enzymes which detach it from the gut. The pt still has diarrhea at this point, cholera just doesn't need to make any more toxin for it to continue. To do so would probably waste energy, and not help the bacteria make it back to a water supply.

  • $\begingroup$ Thanks u ! And to add to your last point , if it secrets excessive toxin it might also kill the host before it has chance to escape. $\endgroup$
    – biogirl
    Commented Mar 8, 2014 at 4:33
  • 1
    $\begingroup$ i would want to add a point that V. cholerae is not an obligate pathogen.. Being a mild alkalophile, it cannot tolerate the stomach acidity. Infection happens only if there are too many bacteria. $\endgroup$
    Commented Mar 8, 2014 at 9:45

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