Until quite recently it was thought that this was pretty much the only way to get bacteria to divide, until 1999, when the sequences of two Chlamydia species turned out not to contain genes for FtsZ. As Chlamydia are intracellular parasites (which I covered in more detail here) it was at first thought that they might be using some host proteins to complete the cell division, but after the discovery of an FtsZ-less free living archaea, and several more bacteria, it became apparent that the FtsZ-centric model of cell division (shown diagrammatically above) wasn't covering the behaviour of all bacteria.
In the archaeal species (in fact the entire archaeal kingdom Crenarchaea) the cell division was found to be based on a completely different cytoskeletal system. By screening for genes that were turned on at the onset of cell division, a three-gene operon was found to be involved. These genes coded for homologues of eukaryote vesicle trafficking proteins and their regulators, and it was suggested that they formed curved filaments which could pinch off sections of the membrane, forming new archaea. Although the method is similar, the 3D structure of the archaeal proteins is very different to that of FtsZ; the two proteins are not related, but have been coerced into doing the same job.
As well as finding bacteria without FtsZ, it was also discovered that taking a strain of Mycoplasma genitalium and removing the FtsZ didn't stop cell division and in fact showed the same growth kinetics as the wild type. The division mechanism in this case relied on the fact that Mycoplasma move by adhering to a surface and pulling their way along it (in a lab this will be on a glass or plastic surface). To pull their way forward they use a 'terminal organelle', a little protrusion that attaches to the surface and pulls the cell along (figure from the reference).
Erickson, H., & Osawa, M. (2010). MicroCommentary: Cell division without FtsZ - a variety of redundant mechanisms Molecular Microbiology DOI: 10.1111/j.1365-2958.2010.07321.x
The diagram above shows Mycoplasma without FtsZ undergoing cell division. You can clearly see not one, but two little terminal organelles at either end of the long stretched cell. What's happening is that in the absence of proper organised proteins to sort out cell division the bacteria has taken matters into its own hands, and sent two terminal organelles determinedly heading off in opposite directions. The bacteria is literally tearing itself apart, splitting into two by ripping in half and letting the membrane close up behind.
It has been suggested that this might be an older method of cell division, used before FtsZ entered the Mycoplasma. It's certainly a lot more brutal than FtsZ-mediated division, and the bacteria has to spend a lot more time in stationary phase recovering from it. As this method only works in bacteria that can attach and hang onto surfaces, it is unlikely to be use by the Chlamydia species (the mechanism for their cell division is still unknown, although some work has been done with L-form bacteria). In the archaeal species it may even be the other way around, that the new filamentous system evolved to be even more efficient that FtsZ in certain species, and so the FtsZ has been dropped entirely.
All of this builds up a picture of just how diverse even simple systems like cell division can be within the bacterial kingdom. And, in my mind at least, is a compelling argument for not just working with model organisms...
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