Field of Science

Bacterial Fossils



Cyanobacteria fossils - from Berkeley university page


Maybe not quite as impressive as dinosaurs...








Guest Post - Survival of the fittest?


Post - survival of the fittest?





a) no antibiotic stress, bacteria naturally produce indole.
b) dead and dying bacteria fail to produce indole






I for one welcome our glowing overlords...








Glowing pixelated space invaders!

This is why I went into science :p

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...


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

Follow me on Twitter! in red

Got back from the conference last night, absolutely shattered. I had a great time, and the presentation was really well recieved, everyone seemed to love our coloured bacteria and it was my first time doing a conference presentation to Grad students. I met some new friends, and got the chance to visit Venice on the way back.

While I was away, red happened!

I'm still holding out for the glowing green myself...

To find out more visit the Cambridge iGEM team wiki.

I have a lot of stuff to catch up on, but if anything particularly amazing has happened on the internet while I've been away (other than Bora moving house - which I know about already and wish him the best of luck) drop me a note or stick it in the comments.

Bacterial Lightbulbs


So in the mean time, have a bacterial lightbulb:






Bacteria vesicles - SGM series

ResearchBlogging.orgThe SGM autumn conference is now over - thanks to everyone who tweeted it so people like me could catch up on events without actually going. I've just got two more topics of my own little personal blog-conference to go, and this one is going to be on bacterial vesicles rather than secondary metabolism because it suddenly struck me that I don't actually know much about outer membrane vesicles, and this might be a good opportunity to explore them.

So this is the penultimate post in my SGM topic series: Bacterial vesicles.

The first thing to note about them is that they only form in Gram negative bacteria, which have an outer membrane covering a small glycopeptide layer (Gram positive bacteria have no outer membrane and a very large glycopeptide layer). The top layer simple peels off into a little vesicle, taking periplasmic proteins with it, as shown below (diagram from the reference):

The mechanism for vesicle formation is largely unknown, but it is found in both pathogenic and non-pathogenic strains of bacteria, and used for several different purposes. In pathogenic bacteria the vesicles often contain virulence factors, which can destroy or damage host cells. in the wild, they may also bind to or destroy other bacteria. In less-virulent strains they have been shown to act as a method of removing misformed or unwanted proteins from the periplasmic space (the space between the two membranes). They can also play a part in antibiotic resistance, it's not yet certain how but my guess is that they pump the antibiotic into the periplasmic space then vesicle it off to stop it just diffusing back in again.

When first discovered, the vesicles were thought to be a by-product of bacterial death, after all, why else would little bits of membrane with bacterial proteins inside be found floating around a large colony? However work done on pathogenic bacteria (which get more funding) and biopsies of infected tissues showed the vesicles playing an important part in infection. They are produced during the stationary phase of growth, the same period when bacteria start to produce most of their virulence factors and secondary metabolites. In an infected organism, this phase is after the bacteria has set off an inflammation reaction, and once it has multiplied in the site of infection.

Factors that affect the formation of vesicles include oxygen stress, the availability of iron (finding a regular iron source inside human bodies is a regular problem for bacteria) and the composition of the outer membrane (suggesting that at least some of the mechanism is mechanical). It is a ubiquitous process carried out across a range of Gram negative species.

As well as being used offensively, some vesicles were also shown to carry DNA between bacteria, although it's not at all clear how, or how the DNA gets into the periplasm in the first place. P. aeruginosa are also capible of transferring antibiotic resistant enzmyes between bacterial cell using the vesicles. This is not totally an act of complete altruism, as P. aeruginosa carries out much of it's infectious cycle as a biofilm, which requires lots of cells to form.

As I said, the actually mechanism for the formation of the vesicles is not yet established, so there's probably quite a lot of work to do with imaging their formation, genetics to find out any genes involved, and a mixture of genetics and protein work to discover more about what goes inside the vesicles. It looks like an interesting area of research, with the potential for some quite amazing imagery-work, and I look forward to reading more about it.


Kuehn MJ, & Kesty NC (2005). Bacterial outer membrane vesicles and the host-pathogen interaction. Genes & development, 19 (22), 2645-55 PMID: 16291643

Surviving in the stomach - SGM series

The fifth post now in the SGM series, and this one focuses on Acid Stress. As I covered in a previous post, bacteria are able to survive in a number of adverse conditions, so this post will focus on just one of them, high acidity. Particularly the high acidity within the human stomach.

There are many different bacteria with acid stress survival techniques, all bacteria that ever visit the stomach need to be able to cope with the low pH. Listeria monocytogenes is a bacteria that anyone whose every looked into pregnancy will know about, as although it does not often cause human dieases it can have potentially fatal effects on an unborn fetus. The bacteria are found in un-pasteurized cheeses and dairy produce, and apparently one of the reasons for this is that the food surrounding them helps to protect them against the acidity of the stomach.

Soft cheese - now with added Listeria!

There are various different ways that a bacterial cell can survive acid stress (which is distinct from surviving in constant acidic conditions). Regulatory systems for acid stress have been found, such as the two component EvgS/EvgA system in E. coli, which turn on a large number of acid-stress related genes when sensing low pH in the surrounding environment. In Bacillus cereus, which hides out in warm rice (and is the reason you have to re-heat takeaways to piping hot the next day at work) acid stress conditions were shown to induce a number of typical bacteria cellular responses - two component systems, alternative sigma factors (which lead to changes in the proteins being produced) and excess proteases and chaperones to get ensure more correctly folded proteins (harder in an acidic environment).

With the Listeria however, it was discovered that they were actually getting a lot of help from their surrounding food. Certain amino-acids, such as glutamate, are used by the bacteria to neutralize stomach acid and it turns out that cheese is quite high in glutamate. Also, a fair amount of acidity is used in the cheese making process, which helps the bacteria practice at their acid-resistance; essentially any bacteria in contaminated cheese will have already run an acidity gauntlet which stands it in good stead for the experience it will get in your stomach.

This work is also interesting as it shows that it's not just the amount of consumed bacteria that can lead to stomach poisoning, it's also dependent on the surrounding nutritional environment of your stomach. Eating Listeria in non-glutamate containing food is less likely to lead to an infection, unless you also like tomato juice (very high in glutamate) and drink that at the same time. As well as being interesting from a scientific view this is also very useful diet advice for people susceptible to certain bacterial infections. An understanding of how bacteria work within specific metabolic environments will allow better dietary advice about foods to keep away from.

There is no paper for this, so I'm working mostly off the press release, which can be read here. As I didn't attend the talk at the SGM conference, I'd welcome any corrections of any facts I may have either omitted or misinterpreted. Having read the abstract I'm kindof gutted I didn't get to this talk, it looks fascinating.

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Studying Streptococcus - SGM series











Xtreme bacteria! - SGM series

This is the third post in the SGM series and this one is about Extremophiles. There were lots of talks in this topic, so instead of a serious research-analysis post, this will just be a quick run-down of some of the more interesting bacteria that were covered:

Award for : Survival under extreme acidity
This award is presented to the Natranaerobiales species that live in sun-heated salt lakes in the Middle East and Africa. These can grow at conditions of Ph 3.7 and also manage to survive at 66 degrees Celsius, by using specially modified proteins to carry out vital cellular tasks.

Award for: Coldest temperature - thermophiles
Theremophiles are bacteria that are found only in very hot temperatures, so researchers were rather surprised when an experimental heating up of arctic ice to 50 degrees stimulated a range of dormant thermophiles to spring to life. What the bacteria were doing there, what kind of global warming event they were waiting for, and why researchers were heating up arctic ice to 50 degrees anyway remains to be discovered...

Award for: Resistance to radiation
This award collected on behalf of all radiation resistant bacteria by Deinococcus radiodurans. Recent work in these bacteria revealed that there is a mechanistic link between resistance to radiation, protein protection and (rather weirdly) manganese accumulation. Apparently surplus manganese in cells can help against reactive oxygen species.

Award for: Survival at greatest pressure range
The deep-sea bacteria Photobacterium profundum is not only able to survive at 15 degrees C, but also lives at a pressure of 28MPa (atmospheric pressure being 0.1MPa). Any eukaryotes living at that pressure tend to unfortunately explode when brought to the surface, but these bacteria are able to survive fine at normal pressures. (Scientific aside - their cell surface lipopolysaccharide composition is thought to help with the cold survival. Mutants that are cold sensitive have a lower concentration of smooth LPS than the cold-adapted parents).

Award for: Best attempt at mimicking a B-list Sci-Fi alien
I'm not sure whether this should be given to the bacteria, or the people who wrote the abstract, but to give you a clue the talk is titled "Dark life in the fracture labyrinth of deep hard rock". Bacteria have been found in rock fissures living in complete darkness with hardly any organic minerals, and using hydrogen as an energy source. Or, in the words of the abstract, "An extreme ecosystem that survives in total darkness feeding by hydrogen from the interior of our planet". If these things weren't tiny blobs that would be a movie already.

Honorable mention: Extreme fungi
This was a microbiology conference, not a bacteriology one, which means that it also covered fungi, algae and protists. Fungi have been found that live at high salt concentrations, both high and low temperatures, acidic and basic conditions, high hydrostatic pressure, high ionizing radiation and in extremely toxic environments.

Honorable mention: The virus's of Haloquadratum
These little guys are getting an honorable mention just because they seem to be the only virus's mentioned in the entire talk. They infect the bacteria Haloquadratum and are thought to have played a role in the development of the bacterium's resistance to high salt levels.

That's all the awards for now! Just four more of the SGM series to go, I'm enjoying writing them, even if the "one post every two days" hasn't quite happened.

How bacteria die - SGM series

ResearchBlogging.orgThis is the second post of my SGM conference series and the topic is Microbial Death. I was very interested in this one as a topic, because the mechanisms that lead to bacterial death aren't something I've covered so much. It's generally assumed that antibiotics screw up whatever they target such that the bacteria can no longer survive, and when they aren't around the bacteria just keep dividing.

There were two talks concerning antibiotics in bacterial death, the first addressing a theory that's been bandied about for a while (and which I've already written about) that antibiotics don't really kill the cell by acting on their target. Instead, they just lead to sufficient damage to set off a series of death events within the bacteria themselves, a common pathway for bacterial cell destruction (first reference).

I think if I could have chosen any one talk to watch it would have been that talk, actually given by Kohanski whose been working on the stuff. I think there would have been some interesting questions as well, as this is somewhat controversial research.

The other antibiotics talk covered something I'd never heard about; the ability of some antibiotics in certain cases to prevent bacterial death. Work done on Microbacterium turberculosis - which causes TB and a related strain (Microbacterium bovis) showed that when in stationary phase (i.e the bacteria were not growing and dividing) the addition of antibiotics that usually kill only growing cells helped to aid cell survival. Antibiotics that targeted both growing and non growing cells did not have this effect. The reason for this is not clear, however comparing transcriptomes between cells both with and without antibiotics showed a difference in protein production on addition of antibiotics. These antibiotics are in someway helping to turn on genes for survival, which are keeping the stationary phase bacteria alive.

Another interesting talk was about the regulation of mutagenesis in bacteria, another idea I love. It's based on the observation that as bacteria start to get stressed they go into a sort of massive meltdown, leading to lots of genetic mutations being generated. It's been suggested that rather than this being a side-effect of the surrounding stress, this is actually a deliberate ploy by the bacteria to give themselves a last ditch attempt at getting out of a stressful situation.

Unlike multicellular organisms, bacteria have no surrounding restraints on their mutation rate - with the exception of bacteria in aggregates the only thing a bacteria will harm by changing it's DNA is itself. This gives bacteria a lot more genetic plasticity. Added to this, changing DNA is one of the main ways bacteria go about improving themselves, and adapting to new conditions. Changing the DNA by wholescale random mutagenesis is a bit extreme, but if you're in a stressful situation anyway it might be worth a shot.

Studies for this have mostly been done on E. coli, usually a lab strain, so I'm not sure how much they translate into bacteria in the wild, which might be better adapted at coping with stress situations, or, given that experimental bacteria are in a privileged nutritional environment, it might just be too risky for wild bacteria to start messing around with their genome. Also there's no concrete mechanism been found for it yet, so increased mutagenesis producing different phenotypes in times of stress may just be a happy byproduct of the usual genetic craziness that goes on when a cell dies.

These two theories both don't have as much supporting science as they could do, but they are new ideas which are still being worked on, and I really like them both.

Kohanski MA, Dwyer DJ, Hayete B, Lawrence CA, & Collins JJ (2007). A common mechanism of cellular death induced by bactericidal antibiotics. Cell, 130 (5), 797-810 PMID: 17803904

Ivana Bjedov, Olivier Tenaillon, Bénédicte Gérard, Valeria Souza, Erick Denamur, Miroslav Radman, François Taddei, Ivan Matic (2003). Stress-Induced Mutagenesis in Bacteria Science, 1404-1409 DOI: 10.1126/science.1082240

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