Clumping is good; controlled clumping is better.

When I pouted last week about the fact that other writers had beaten me to the punch in discussing an interesting recent paper on the fitness benefits of clumping in yeast, I had somehow failed to notice that another, similarly fascinating, paper on a related topic had just come out from the Bassler lab (Nadell and Bassler 2011. A fitness trade-off between local competition and dispersal in Vibrio cholerae biofilms.  PNAS doi:10.1073/pnas.1111147108).  This paper is looking at the formation of biofilms in the bacterium Vibrio cholerae, a nasty little bug that has been a major evolutionary force in the development of modern sewage systems.  One of the factors that makes V. cholerae hard to get rid of is the fact that it can, when it chooses, grow in biofilms; it can produce a structural matrix called extracellular polysaccharide (EPS) in which the bacterial cells are embedded. EPS production has a number of benefits, including offering bacteria from many species the opportunity to collaborate and behave as a community.  The puzzling thing, though, is that these community benefits are available to everyone, not just the bacteria who do the work of producing the EPS.  This is a classic set-up for “cheating”; in theory, if some bacteria can gain the benefits of EPS production without paying the price for it, then those “cheating” bacteria would be expected to grow faster than the poor exploited EPS producers.  At some point, the EPS producers (still struggling to build community, no doubt) would die out, and the whole system would collapse.  The theoretical arguments seem very persuasive, but actually EPS-producing bacteria show no signs of going away.  So clearly we need a new theory.

Kevin Foster and colleagues (including Carey Nadell, the first author of this paper) have been working for some time now on the possibility that EPS production, in addition to its benefits for the community, offers direct benefits to the cells that produce it.  If you simulate the growth of EPS-producing microbes in three dimensions, including the way that nutrients and oxygen diffuse and are consumed, you can see that producing EPS can help a lineage of cells to push itself above the masses and get access to better conditions, incidentally suffocating non-EPS producing cells.  This line of argument suggests that, far from being a happy “all for one, one for all” type commune, microbial biofilms are a balancing act between cooperation and competition — much like some other societies you might be aware of.  It also suggests that, though there are some conditions in which “cheaters” (non-EPS producing cells, though now they look lazy and stupid rather than cunning) can win, especially when a group of cells is colonizing a new area, if a biofilm persists for a long time the EPS-producing cells have a strong advantage.  And a particularly clear prediction from the 3D modeling is that, in a mixture of EPS-producers and non-producers, the EPS-producing lines should end up in skyscraper-like towers (reaching towards better oxygen conditions), suffocating the cheaters.

Feed me, Seymour

The diversity of life is a puzzle for ecologists and evolutionary biologists.  The principle of competitive exclusion suggests that if two species are competing for the same resource, one of them should eventually win and the other should become extinct.  So if you have n different food sources, you should end up with (at most) n different species.  But real biological communities are far more diverse than this analysis would suggest.

Pink sundew. From http://www.biophilia.net/

In this context, I found a recent paper about competition between carnivorous plants and spiders interesting.  (Jennings et al. 2010. Evidence for competition between carnivorous plants and spiders. Proc. R. Soc. B 277 3001-3008 PMID: 20462904).  This paper looked at the dietary habits of the pink sundew, Drosera capillaris, and the wolf spider Sosippus floridanus.  Both eat insects — do they compete?

Trade balances in microbial communities

So this week seems to be turning out to be cooperation week.  We talked about cooperative behavior of the proteins that make up the cytoskeleton on Monday, cooperation in breeding behavior in birds on Wednesday, and now it’s time to talk about cooperative behavior in bacteria.  If only I’d planned it in advance.  Ah well; can’t have everything.

You know, of course, that in the wild bacteria do not typically live in monocultures: different varieties of bacteria both compete and collaborate, and the complex interactions that result are not easy to study.  A number of labs have been working on developing well-defined synthetic communities to ask questions about how communities evolve.  The Silver lab has now taken a rather different approach (Wintermute and Silver 2010, Emergent cooperation in microbial metabolism. Molecular Systems Biology 6: 407 PMID: 20823845), by exploring the interactions among 46 different metabolically impaired strains of E. coli and rationalizing the results in terms of a flux-balance-analysis model of interacting strains.

What interested Wintermute and Silver was the fact that bacterial communities can perform all kinds of important metabolic tricks that individual species can’t manage.  This is not hard to understand, or at least to imagine that you understand: one species finds an efficient way to produce rare metabolite A, another species develops an efficient way to produce rare metabolite B, when you mix the two together they both have the advantages of a supply of both A and B, but they’ve effectively halved the cost of production (making all those enzymes) by sharing.  But is that really how it works?

If you can’t grow it, sequence it

Bacteria live almost everywhere, and use a staggering variety of strategies to get the energy they need to grow.  In the process, they make and recycle all kinds of globally important materials; and we often don’t understand how, biochemically, they do this.  One reason — apart from the sheer overwhelming number of different types of bacteria — is that many bacterial species are hard to culture in the laboratory.  Estimates of the proportion of bacteria that are “unculturable” (or, not cultured yet) range as high as 99%, based on sequencing of 16S rRNAs.   If the microorganism you want to study happens to be among the unlucky 99%, what are you supposed to do?  These days, you have a new option: sequence its genome.

In a paper published this month in PNAS (Lücker et al. 2010 A Nitrospira metagenome illuminates the physiology and evolution of globally important nitrite-oxidizing bacteria. Proc Natl Acad Sci U S A. 107, 13479-13484 PMID: 20624973), Lücker et al. do just that.  Frustrated by their inability to grow a nitrite-oxidizing bacterium — one that grows happily in sewage treatment facilities, what’s more, and therefore has no right to be fussy — they made an enriched preparation of it from sludge, and sequenced it.

Friday Feature: Carboxysome spacing

I promise that not every Friday Feature will be a movie, but since I mentioned the Silver lab’s ambitions to control how cells use light energy in the last post, here is a lovely movie of cyanobacteria growing and dividing, in which you can see the remarkably regular spacing of labeled carboxysomes.  Carboxysomes are where much of the magic of carbon fixation happens: they’re said to be responsible for about 40% of all the carbon fixation on the planet.  Dave Savage got interested in how they work, and, not unnaturally, wanted to see what they look like.  In this movie they are labeled with YFP.

Error

This video doesn’t exist

Savage DF, Afonso B, Chen AH, Silver PA.  2010. Spatially ordered dynamics of the bacterial carbon fixation machinery. Science.  327 1258-61. PMID: 20203050

The remarkable regularity you see is not just an illusion: carboxysomes are evenly spaced along the length of the cell, and their position adjusts as the cell grows (or as new carboxysomes appear) so that the spacing remains regular.  They “wiggle” due to diffusion far less than you would expect them to.  The spacing seems to be determined by the cytoskeleton, using mechanisms that were originally described in connection with the regular spacing of certain plasmids.