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  • Joe Hanson 12:17, 26 March 2012 (EDT):In addition to the "run state" phenotypes, are there any known genetic mutations that provide intermediate E. coli flagellar activity? Are there any "slow" flagellar mutations or dominant negatives known? I am certainly not asking this as a way to get help with our group's class project.
  • --Erik Quandt 10:30, 2 April 2012 (EDT): There have been several igem projects aimed at controlling flagellar activity. The 2010 Denmark Team sought to produce a "hyperflagellated" that would produce more flagella and be more motile. They did this by overexpressing the flgDC operon, flgDC regulates the expression of genes required for flagellar assembly. Perhaps "slow" cells could be engineered by reducing the number of flagella produced? A mutation in the PomA (MotA homolog) gene from Vibrio alginolyticus was found to confer a slow phenotype [1]. Mutations to either MotA or MotB would likely have the biggest effects on motility speed [2]...

Other groups have tried to control the expression of the motor protein MotB in order to control the rotation of the flagella in response to quorum sensing signals bacterial relay race. Bacillus subtilis has a protein EpsE that acts as a flagellar "clutch" which regulates the rotation of the flagella [3].

  • Jeffrey E. Barrick 17:49, 1 April 2012 (EDT): Listeria's form of locomotion is the coolest I've seen. It zooms around like a comet inside mammalian cells by hijacking actin polymerization (the same mechanism by which amoeba and white blood cells crawl around).



  1. Blair2008 pmid=18566286
  2. Kojima2000 pmid=10809720
  3. Blair2003 pmid=12788496