Field of Science

Bacteria that tear themselves apart

This post was chosen as an Editor's Selection for ResearchBlogging.orgBacterial cell division is one of those fairly well studied areas, where time and much study has come forth with a nice standard model. One of the main proteins involved is FtsZ, which seperates one bacteria into two by forming a ring of protein around the middle of the bacteria and tightening it shut as shown below (figure from Nature paper):

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).

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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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

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9 comments:

Psi Wavefunction said...

...or rather, diversifying the models. One still has to have some sort of model organisms to do any dev + cell biol work. Also, about time bacteria get treated as real organisms, just like the big popular stuff, as opposed to mere bags of biochemistry!

Lab Rat said...

@Psi: I don't know...models are great, sure, but I think it's a good idea sometimes to do a bit of concentrated research on a random bacteria, not make a new model, just take a look at all the diversity you could be missing.

And yes! Bacteria are waaay more than just little bags of biochemistry, although I have to admit as a current synthetic biologist I am treating them a bit like that at the moment ...

Mike Lisieski said...

Weren't all model organisms studied for their own right in the first place? It's not like we could have developed model bacterial systems without first knowing something about bacteria, nor genetic models in fruit flies without first knowing something about fly biology, etc. Because we can never predict what the applications of biological research will be before it is done, it behooves us to simply try to do as much general biological research as possible, because without this, modeling of any sort would soon dry up.

Psi Wavefunction said...

@Lab Rat It would be awesome to do research on just random bacteria. And eukaryotes. It would truly kick ass.

Problem: cell biology doesn't work that way. Unfortunately, before even doing any cell biology work on an organism, plenty of work must first be put in to learn to work with it, culture it, do crosses, etc. It takes time, and is not easy. So considering the amount of effort (and time and money) that must be invested into an organism before it becomes suitable for further research, it is unsurprising most of the effort has been concentrated on a handful of models.

What would be fantabulous is if the models were well-distributed, both phylogenetically and also in terms of lifestyle -- ie, not all parasites. Parasites are fucking diverged, and thus hard to generalise from. Apparently some people have yet to catch on...

Lucas Brouwers said...

FtsZ-less division sounds.. painful!
If the tearing division really is older, the associated signals and processes could maybe shed some light on the origins of the different mechanisms.
Is the tearing mechanism initiated by the same 'Hey-I-am-ready-to-divide' signalling system as in FtsZ division, for example?

Lab Rat said...

Regarding model organisms: Yes, they did start out just as randomly studied organisms, but time and positive feedback means that they are now used almost exclusively for some problems, despite in many cases being severely under-representative of what the rest of the kingdom are like. Model organisms are a great way to quickly get a lot of (potential) generalisable points about a large group, which is necessary when funding is limited.

Their usefulness is a whole nother post I think!

@Lucas: I don't think theirs been enough research into FtsZ-les division for that to be answered! There's clearly some kind of signal though, and given that the Micoplasma were dividing at the same time and rate (allowing for 'recovery time') regardless of whether or not the cell had FtsZ I think it's a safe bet they use the same signal.

diseaseoftheweek said...

At the recent Australian Society for Microbiology conference there was a number of talks about this stuff. One of the ones that stuck with me was how peptidoglycan is laid down by different species during/after cell division. Even species like Staphylococcus and Streptococcus which look very similar use entirely different division and peptidoglycan synthesis machinery.

Lab Rat said...

@diseaseoftheweek: Ooh...I've recently been getting into peptidoglycan organisation during cell division (especially with lipid evolution type things) so will definitely be looking that up!

diseaseoftheweek said...

I just looked it up. The guys name is Prof. Simon Foster from the Uni of Sheffield, UK. Nice guy and really good presenter too.