There are many species of bacteria with two modes of life: one is motile with swimming propelled by rotating flagella, and the other is sessile as part of a biofilm. What happens when they change from free swimming mode to attached mode?
"Two things typically happen next. Cells stop expressing genes that encode components of the flagellum, and they secrete a sticky matrix of polysaccharides that holds them together on the surface. Once at a surface, swimming may be a hindrance rather than a help, and an inverse relationship between swimming and attachment has been seen in many diverse species. However, the molecular details underlying this arrest in motility have not been fleshed out. Are flagella ejected or dismantled? If not, do they keep rotating until they are jammed by the newly formed matrix?"
A nanotechnology clutch disengages the flagellum's tail from the engine that powers its rotation (source here)
It turns out that neither of these possibilities apply. Recent research by Blair et al. has shown that there is an "off-switch for rotation". This device utilises a special protein, EpsE.
"To determine whether EpsE acts as a brake that locks the motor, or a clutch that leaves the rotor freely spinning, Blair et al. tethered bacteria to a substrate by their filaments and observed rotation of the cell bodies around single flagellar motors. Under the influence of EpsE, cells stopped spinning but continued to undergo free rotational Brownian motion, indicating a clutch mechanism."
This finding has been a surprise:
It had been thought that bacteria slowed down by switching off the genes that make flagella, says Richard Berry, a physicist at the University of Oxford, UK, who studies molecular motors.
"This is a completely unknown thing," he says. "The previous wisdom was that flagella would spin for ever."
With hindsight, the clutch mechanism makes a lot of sense:
"The direct inhibition of motor rotation by EpsE represents a newly discovered control mechanism for bacterial swimming. Bacterial flagella are large protein complexes that require about 40 to 50 genes to assemble. Thus, the most obvious advantage of the EpsE mechanism over transcriptional control of flagellar genes is speed. In B. subtilis, only one protein, EpsE, needs to be expressed to stop the motor. Presumably, this is important if cells are to stay put in the early stages of biofilm formation. However, the advantages of a clutch over a brake mechanism are not so clear. Perhaps free rotation of flagella - or, alternatively, reduced motility during the transition to the EpsE-inhibited state - is important for the formation of well-structured biofilms. Or maybe a clutch is simply easier to make than a brake."
The researchers contrast the strategy of turning off flagellum synthesis with the clutch alternative, and supply one additional consideration - the possible need for reactivation of the flagellar motor:
"The flagellum is an elaborate, durable, energetically expensive, molecular machine and simply turning off de novo flagellum synthesis does not necessarily arrest motility. Once flagellar gene expression is inactivated, multiple rounds of cell division may be required to segregate preexisting flagella to extinction in daughter cells. In contrast, the clutch requires the synthesis of only a single protein to inhibit motility. Furthermore, if biofilm formation is prematurely aborted, flagella once disabled by the clutch might be reactivated, allowing cells to bypass fresh investment in flagellar synthesis. Whereas flagellum expression and assembly are complex and slow, clutch control is simple, rapid, and potentially reversible."
The clutch "solution" is therefore a neat, effective and potentially reversible mechanism. The authors describe it as "simple", which is OK if the meaning is that just one component is needed to disengage the flagellar motor. However, this conceptual simplicity in no way conflicts with understanding this system in terms of complex specified information. The researchers have identified a gene epsE responsible for making the EpsE protein which engages with the critical protein transmitting torque to the flagellum and removing the link to the source of power. The measure of complexity is in the unique shape of the EpsE protein and its ability to engage with the torque-transmitting protein so that power is no longer transmitted. The team is now "looking for a protein that disengages the clutch and reconnects the motor". This would help to disaggregate biofilms and could lead to significant medical applications. One measure of "simplicity" is the ease of finding such a protein. My prediction is that the researchers will not be using the word "simple" to describe this phase of the research. The science community is well aware that nanotechnology successes are achieved only by the application of sophisticated science and intelligent engineering design.
A Molecular Clutch Disables Flagella in the Bacillus subtilis Biofilm
Kris M. Blair, Linda Turner, Jared T. Winkelman, Howard C. Berg, and Daniel B. Kearns
Science 320, 20 June 2008: 1636-1638.
Abstract: Biofilms are multicellular aggregates of sessile bacteria encased by an extracellular matrix and are important medically as a source of drug-resistant microbes. In Bacillus subtilis, we found that an operon required for biofilm matrix biosynthesis also encoded an inhibitor of motility, EpsE. EpsE arrested flagellar rotation in a manner similar to that of a clutch, by disengaging motor force-generating elements in cells embedded in the biofilm matrix. The clutch is a simple, rapid, and potentially reversible form of motility control.
Berry R.M. and Armitage, J.P., How Bacteria Change Gear, Science 320, 20 June 2008: 1599-1600.
Whitfield, J. Bacterial engines have their own clutch, email@example.com, 19 June 2008 | doi:10.1038/news.2008.903
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