This week’s Nature has a review article in it I have been waiting for for some time, and which I suspect may become something of a classic:
Marten Scheffer et al, Early-warning signals for critical transitions Nature 461, 53-59 (3 September 2009) | doi:10.1038/nature08227. Here’s the abstract
Complex dynamical systems, ranging from ecosystems to financial markets and the climate, can have tipping points at which a sudden shift to a contrasting dynamical regime may occur. Although predicting such critical points before they are reached is extremely difficult, work in different scientific fields is now suggesting the existence of generic early-warning signals that may indicate for a wide class of systems if a critical threshold is approaching.
One of the problems with tipping points in complex systems is that straightforward analysis is incredibly unlikely to be precise and accurate about the tipping point’s threshold. A model may happily tell you that a system has a tipping point, bit it will not tell you where it is. In climate terms, you can be sure that there is a point at which the Greenland ice sheet will collapse, but you don’t know how far we are from it. This article reviews work which suggests a way round this. The system itself may tell you when it is getting close to a tipping point through subtle changes in the way its behaviour varies over time — in particular changes associated with “critical slowing”. What follows is my interpretation of the paper, which seems impressively approachable for a piece of mathematics, but which I may nevertheless be getting wrong; any real mathematicians in the audience should feel free to chip in in the comments.
A key symptom of critical slowing are that the system becomes lower to restore itself to its usual state after being perturbed. This means that if the system is fluctuating, its present state will become more closely determined by previous states — its “memory” will increase. In mathematical terms, this is an increase in autocorrelation. At the same time, and seemingly contradictorily, its variance may also increase because it becomes less able to recover from external shocks; that effect appears not to be as well grounded as the autocorrelation, but it does turn up in a lot of models.
As well as slowing down in this way the system will also start to get assymetric, because fluctuations that push it towards the tipping point and those that push it away will not be responded to in quite the same ways. It may also start to “flicker” as it moves back and forth across the boundary between two states before plumping firmly for one or the other. There are also ways of looking at differences over time, which I can’t really sum up: instead I’ll quote an example from the paper dealing with desertification:
Models of desert vegetation show that as a critical transition to a barren state is neared, the vegetation becomes characterized by regular patterns because of a symmetry-breaking instability. These patterns change in a predictable way as the critical transition to the barren state is approached, implying that this may be interpreted as early-warning signal for a catastrophic bifurcation [that being is one of the types of tipping point under discussion]
More on the desert stuff in this fascinating Science paper from 5 years back, one of the authors of which, Max Rietkerk, is also an author on the Nature paper.
How does this work in practice? Here’s an example using data from a 2008 PNAS paper by Dakos et al, on which many of the review’s authors worked.
The top plot is showing calcium carbonate percentages in a deep sea sediment core as a marker for the influence of the carbon cycle on the climate, as discussed in this 2005 Nature paper. The bottom plot is the measure of autocorrelation. As you can see, the time series goes from being not autocorrelated at all to being highly autocorrelated, and then bang. Similar autocorrelations can be seen in front of seven other abrupt climate shifts the PNAS authors looked at. The review looks at similar patterns in the onset of asthma attacks, ecological events, epileptic seizures and sudden stockmarket surges, and as the authors conclude
Flickering may occur before epileptic seizures, the end of a glacial period and in lakes before they shift to a turbid state; self-organized patterns can signal an imminent transition in desert vegetation and in asthma; increased autocorrelation may indicate critical slowing down before all kinds of climatic transitions and in ecosystems; and increased variance of fluctuation may be a leading indicator of an epileptic seizure or instability in an exploited fish stock.
So these processes really do seem to have a lot in common, much of which is related to the mathematical treatments reviewed in the paper. This is not to say everything is settled:
More work is needed to find out how robust these signals are in situations in which spatial complexity, chaos and stochastic perturbations govern the dynamics. Also, detection of the patterns in real data is challenging and may lead to false positive results as well as false negatives.
There are a lot of complexities here to do with how you filter the data, what data you choose, whether all the bifurcations that cause critical slowing are really catastrophic tipping points, and more. There are probably people who think it is all hogwash (and people should feel free to point me towards them). But I must say that after reading the review and feeling I have come a little way towards understanding what is going on, I look forward over the next years to people with climate models that show tipping-point behaviour getting stuck into this sort of analysis looking for precurssors. (Here’s a topical question: what does an autocorelation on the year-by-year arctic sea ice minimum show?) The idea that such mathematical work will ever reach a level where you would feel justified in saying “the Greenland ice tipping point is ten years away” may be far fetched. But you don’t know til you try.
Image copyright Nature Publishing Group
Cheryl made me aware of the excellent idea of a synchronised posting about women in technology in honour of Ada Lovelace (my image of whom, for what its worth, was set irevocably and doubtless unreliabley by Bruce Sterling and Bill Gibson in The Difference Engine). I said I’d join in, and my subject is Constance Hartt, about whom I know very little, but whose work is of fundamental importance to people trying to understand the evolution of photosynthesis over the past 30 million years or so, and also to opening up the possibility of radical improvements to various crops.
Hartt was a laboratory researcher at the Hawaiian Sugar Planters Association Experiment Station, and her assiduous work on the biochemistry of sugar cane in the 1930s and 1940s convinced her that, for that plant at least, the primary product of photosynthesis is malate, a four carbon sugar. Later carbon-14 studies showed that she was right — and led to an interesting conundrum. Why did some plants — most plants, indeed, and almost all algae — make a three carbon sugar, phophoglycerate, while sugar cane and, it later became clear, various other grasses made a four-carbon sugar?
The answer lies in the process of photorespiration. The enzyme which fixes carbon into phosophglycerate, rubisco, is very ancient and rather easily confused — left to itself it will sometimes grab oxygen molecules rather than carbon dioxide molecules, and instead of making phosphoglycerate makes phosphoglycolate. This is no good to man nor beast nor, most tellingly, plant: recycling the phosphoglycolate made accidentally in this process of photorespiration into a form of carbon that can be used for further photosynthesis takes energy, and thus making less phosphoglycolate in the first place is a good thing. The malate-initiated photosynthesis that Hartt was instrumental in discovering is an evolutionary response to that problem: malate is part of a clever biochemical/physiological supercharger that concentrates a great deal more carbon dioxide into the cells where rubisco is doing its thing, thus making it less likely to commit that costly error with the oxygen.This supercharging system is known as C4 photosynthesis, the 4 denoting the number of carbons in malate; the regular sort of photsynthesis is called C3 in contrast.
C4 photsynthesis confers various advantages: in particular, it makes plants more efficient in their use of water. The mechanisms that concentrate carbon dioxide mean that the pores through which it is taken up, the plant’s stomata, don’t have to be as wide open as they would be otherwise, and thus less water is lost. C4 plants resist various sorts of stress better, including direct sunlight and salty ground. The mechanism has evolved independently many, many times over the past 30 million years or so, mostly but not entirely in the grasses, which either have a propensity for the sorts of physiological re-design that is required or are particularly prone to finding themselves in the sort of niches where this approach helps, or both. Sugar cane is not the only domesticated or agriculturally relevant example — there’s also maize and sorghum, and for energy crops switch grass and miscanthus, among others. There is now considerable interest in building the pathway into some grasses that have not learned it naturally — most importantly rice. C4 rice, with higher water use efficiency and other extra hardiness, might have considerably higher yields than traditional varieties while needing less water (my colleague Emma wrote a little about this not so long ago, though her words are behind the Nature paywall).
This knowledge and potential all flows from the work of Hartt and her colleagues in Hawai’i. It was small scale stuff, and more or less by defintition the team was isolated form the mainstream. Their work was for some time almost forgotten, and may still not be as well remembered as it should be; the elucidation of the C4 pathways took place in Australia a decade or so later, and that work tended, afterwards, to eclipse the discovery work done in Hawai’i. The secondary sources that I have say little about Hartt, other than noting the devoted careful work she invested in the subject, and giving the impression that the team she worked in, led by a sweet sounding Quaker called Hugo Kortschak, was a friendly and happy one.
Do I think she is a great unsung scientist? Well unsung, yes. Great, probably not. But whenever one looks into the history of science — or indeed into the way it goes today — one sees that you do not need to be great to matter, to discover, to move the story on, or to fulfill yourself through it. She and her colleagues, tucked away far from the mainstream, trying to do some good, discovered something of profound importance for science, and perhaps, in time, for technology and humanity. What more is needed?
Update: Gary has some wise words on the subtleties of C3 and C4. His point that C4 plants tend to be protein poor is a good one (though in a higher CO2 world that might even out a bit, as the rubisco content in C3 plants will drop whereas in C4 you’d expect it to stay the same, ceteris paribus) and reminds me of Arnold Bloom‘s idea that photorespiration might help with nitrate assimilation. His bigger point is that ceteris paribus is a poor way to see the world, and that to concentrate on any single factor, such as C3 v C4, is to overlook a great deal that you should probably be paying attention to. And that’s true.
Image from Flickr user _Wiedz, used under a creative commons licence
Filed under: Warning: contains molecules
Here’s something which follows on from this post about what happens when viruses infect photosynthetic bacteria in the oceans and also from this post about Craig Venter, I guess, in that he is one of the authors of the paper I’m talking about, and the fishing of vast numbers of DNA sequences out of the ocean on which this work depends is something that he has pioneered.
As I was saying in that previous post, viruses which attack photosynthetic bacteria don’t just carry “viral” genes — genes that code for the components of the virus. They code their own versions of “bacterial” genes — genes that the bacteria use in their everyday existence — too. Why bother? Obviously the bacteria already have their own copies of the bacterial genes, and by carrying these genes the viruses are making their genomes bigger and thus more costly to reproduce, which you would think was a bad thing. The answer must be that getting the bacteria to read the viral versions of the genes and thus produce the proteins they encode helps the virus reproduce.
Now a paper by Itai Sharon and a number of co-authors, mostly at the Technion in Israel, published in the new ISME Journal offers further evidence on the matter. They worked with DNA samples from the open ocean, and one of the things they were looking for was those which contained parts of the D1 protein, which is central to photosynthesis. They found a great many copies of versions of the D1 protein from viruses (which could be identified because they were flanked by viral, as opposed to bacterial, genes), and found that they differed systematically from the normally expressed native bacterial versions in two particular parts of the sequence.
The researchers interpret this in the same way that the authors of the Nature paper I blogged about before (people from Penny Chisholm’s lab at MIT, largely) do in a paper they published last year in PLoS Biology. That study showed that in some cases there is a marked preference among the viruses for forms of the D1 protein that look like the forms which some of their hosts keep in reserve for times of stress. It looks quite likely that these viral proteins undergo less turnover than the normal proteins. I imagine they probably pay for this in terms of increased damage and lower efficiency in the long run, but make up for that by requiring less maintenance effort. That’s a good short-term trade-off for a cell with other stresses to deal with — and its a neat trick to steal if you’re a virus that wants to devote as much of your host cell’s capabilities as possible to making more virus. The details of the differences between viral forms of the protein and the common bacterial forms seem to bear this analysis out.
This is not just a quirky thing. Bacterial photosynthesis counts for a significant part of total ocean productivity, and a few percent of those bacteria will, at any given time, be under viral control, and probably expressing viral photosynthesis proteins. The idea that a measurable chunk of the earth’s primary productivity is in the hands of the viruses strikes me as quite a cool one.
Filed under: Warning: contains molecules
About a day after I posted on excited geology my esteemed colleague Phil Ball pointed out this paper in GRL to me about the possibility that soil bacteria share electrons with each other through networks of nanowires — an idea that would always seem extremely cool and in the circumstances seemed steeped in syncronicity too. Phil looked into the work and wrote us a fine news story for this week’s Nature. Excerpt:
Last year, Gorby and his colleagues discovered that Shewanella oneidensis bacteria can grow long filaments, just 100 nanometres (a hundred millionths of a millimetre) thick, which conduct electricity (Y. A. Gorby et al. Proc. Natl Acad. Sci. USA 103, 11358–11363; 2006). The researchers presented evidence that the microbes use these ‘nanowires’ to shunt electrons produced during metabolic reactions onto the surface of mineral grains in the soil, to be taken up by metal ions. Without an electron acceptor, the bacteria cannot function properly and die. The researchers found that several other bacterial species also produce such nanowires.
Oxygen molecules act as convenient electron dumps for bacteria that lie near the soil surface. But little air penetrates to some environments, such as deep lake sediments or waterlogged soils. Now, Gorby and his team think they have found evidence that the bacterial nanowires can link up into a network, conducting electrons to the aerated surface. The researchers filled plastic columns with wet sand infiltrated with a nutrient compound (lactate), and allowed S. oneidensis to grow in this ‘fake soil’. Only the top of the column was in contact with air.
Electrodes inserted at various heights up the columns revealed that, after about ten days, electrical charge was coursing up the column. Gorby’s team examined the sand under a microscope and found that it was threaded by a web of filaments between the bacterial cells. These are wires that provide the pathways for electron transport up to the surface, they suggest.
In contrast, when the team grew a colony of mutant cells that could spawn only very thin, frail and non-conducting filaments, the electrodes in the column remained uncharged.
Phil goes on to note some caveats about the work, notably from Derek Lovley at University of Massachusetts, Amherst, and it does seem quite possible that this sort of wiring is not a major feature of the real world. Redox shuttles in biofilms may be a much more central phenomenon. But it’s definitely thought provoking. For some context to that thought, try “Microbial ecology meets electrochemistry: electricity-driven and driving communities“, a recent review in the ISME journal by many hands, including that of Ken Nealson, quoted in Phil’s piece. And if this wired-up stuff is for real, what are the implications, not just for natural phenomena, but for technologies like the microbial fuel cells (subscription) my colleague Charlotte Schubert wrote about last year? (This blog is not devoted to bigging up Nature; but we do do a pretty good job.)
There’s an interesting paper in Proceedings of the National Academy of Sciences this week which adds a small new twist to a great double-headed mystery concerning the beginning the history of photosynthesis on earth (which thus comes pretty near the middle of Eating the Sun: it’s a book with a rather arcane relation to chronology.) When did photosynthesis of the oxygen producing persuasion start, and why did the oxygen produced not immediately turn up in the atmosphere?
There’s pretty hard-to-doubt evidence that the earth’s atmosphere did not have a significant amount of oxygen in it on a permanent basis before about 2.45 billion years ago. (Some people do manage to doubt this, but they have to work fairly hard in order to do so — most people in the field accept it.) At the same time, shales dug out of a borehole in Australia contain various chemicals that suggest a) that there were cyanobacteria, which produce oxygen, living 2.7 billion years ago and b) that some other creatures were using this oxygen for their own metabolic needs. There are persistent rumours of similar results from even older shales, but as far as I know they haven’t actually made it to publication.
This creates a seeming paradox: how can it be possible to have a biosphere that produces oxygen through photosynthesis and at the same time see no oxygen in the atmosphere. And how can such a state of affairs go on for at least 250 million years, and quite possibly a lot longer. The bottomline of most of the answers to this conundrum is that there was enough other stuff — organic carbon and reduced gases from the mantle — for the oxygen to react with that it could never build up stably in the atmosphere. Only when the supply of this “other stuff” was changed, through some mixture of an increased rate of burial of organic carbon, a lessened flux of reduced gases from the mantle, and an increased oxidation of the atmosphere as a whole due to the escape of hydrogen into space, did it become possible for oxygen levels to rise, at least a little. This fascinating interplay between life and the planet it enlivens is gone into in some detail in the book: David Catling has provided a helpful pdf update on the state of the debate for those who want more.
The new paper, Biosynthesis of 2-methylbaceriohopanepolyols by an anoxygenic phototroph (PNAS doi/10.1073/pnas.0704912104), comes out of the labs of Alex Sessions and Dianne Newman at CalTech, of and from which many good things are heard. The lead author is Sky Rashby, for more on whom see this post; also on the team is Roger Summons of MIT, who with colleagues published the evidence for cyanobacteria at 2.7 billion years ago (Newman has just moved to MIT, too). To some extent this new paper challenges that evidence, in that it removes one strand from it. Cyanobacteria make chemicals called 2-methyhopanes, and until now nothing else has seemed to do so, and so the presence of those chemicals in the ancient shales seemed good evidence for cyanobacteria. The new paper shows that a bacterium called Rhodopseudomonas palustris also makes the molecules in question. R. palustris is a photosynthesiser, too — but not an oxygen producing one (there is a wide range of bacteria that use sunlight this way without producing oxygen). So the idea that there were cyanobacteria present long before there was atmospheric oxygen can no longer rely on the methyhopanes for support.
At first blush, this might seem to give comfort to those who, like Joe Kirschvink, also at Caltech, want to argue that oxygen-producing photosynthesis led to the oxygenation of the atmosphere directly — that an evolutionary transition led directly to a geological one, as outlined in this PNAS paper. But the methyhopanes aren’t the only evidence for an earlier origin. What was particularly interesting about the 2.7 billion year old shales Summons and his colleagues studied was that they contained both what seemed to be evidence of oxygen producing cyanobacteria and what seemed to be evidence of oxygen consumption, in the form of molecules called steranes. Producing steranes is thought by most people to require oxygen. And so it’s not special pleading to say that while cyanobacteria are no longer the only possible source for the 2.7 billion year old 2-methyhopanes, the oxygen requiring steranes in the same sample make them the most likely source, and pretty much require that something photosynthetic somewhere was producing oxygen at the time. (There is also, as I understand it, evidence elsewhere that oxygen-requiring methane eating bugs were around before the oxygen hit the atmosphere. Not all methane eaters require oxygen — but some do, and apparently there are molecular markers that can tell you which sort was present where.)
So the idea of a lag between the evolution of oxygen production and the arrival of free oxygen in the atmosphere has at worst only taken a minor knock; from what I can gather most people in the field are still fairly convinced on the matter. It would take a second dramatic finding — for instance evidence that the steranes in the 2.7 billion year old samples are contaminants — to really throw things into doubt. As far as I know there is no indication that any such second shoe is about to drop.
Meanwhile, the molecules involved in this identity parade may well prove interesting in and of themselves. The fact that they are present in two different photosynthetic bacteria suggests that they might have a photosynthetic purpose of some sort. What that might be remains to be seen, though there are already some theories. If the genes for the pathway that makes the stuff can be found, then it might be possibleto be more definitive about which bugs use it and under what conditions.
Filed under: Warning: contains molecules
There’s a fascinating paper in this week’s Nature (Lindell et al, Nature, 449, pp 83-86 (2007) doi:10.1038/nature06130) dissecting what must be one of the most frequent fatal biological interactions in the world: the infection of the photosynthetic bacterium Prochlorococcus Med4 by the virus, or “phage”, P-SSP7.
This sounds pretty obscure, but it is a commonplace thing. In fact it is unimagineably commonplace. Prochlorococcus is perhaps the most plentiful organism on the planet — the average millilitre of surface seawater contains about 100,000 of them. A quick and doubtless very dirty calculation suggests that there are more prochlorococcus in the earth’s oceans than there are atoms in your head (sources wiki, madsci, guesswork). In parts of the ocean that are nutrient poor (which is a lot of the ocean) these peculiarly small bacteria — sometimes called picoplankton — dominate primary photosynthetic production.
And while doing so they get a lot of viral infections — perhaps 2-3% of the entire population is torn apart by phages every day (that figure is actually from a paper about synechococcus, but I’m happy to go with orders of magnitude here). This all means that a virus infects one of these bacteria a trillion times every nanosecond. And this process, or rather something functionally very similar, has presumably been happening at a similar rate for billions of years.
As I said, unimagineably commonplace.
So what goes on? A team at MIT and other institutions (including Debbie Lindell, now at the Technion, Penny Chisholm, the scientist who first discovered prochlorococcus, and George Church, high-throughput sequencing guru) has looked into the problem by stopping the process of infection at various stages (by flash freezing the bacteria involved) and then looking to see what genes were being transcribed when.
The virus forces the bacterium to produce copies of itself; if it didn’t, it would be a very poor virus. And the way it gets to work is very familiar, in that it is very like the job that the phage T-7 does on lab favourite E. coli. The deep similarities between the strategies used in the gut (natural habitat of E coli) and the open ocean on bacteria that live in entirely different ways is, the authors point out, remarkable.
At the same time as it’s doing this, though, the virus is also transcribing a small set of genes which, though carried in the viral genome, describe proteins that are used by the bacterial metabolism. One of these proteins is D1, which is the protein at the heart of photosystem II, the molecular machine that strips electrons from water using sunlight and thus drives the whole photosynthetic process. The other proteins are also involved in photosynthesis and the cell’s ability to handle its energy. By making more of these proteins, the virus is giving the bacterial cell an energy boost — at exactly the time that it is also requiring the cell to make copies of teh viral genome, which uses a fair amount of energy.
Meanwhile, control of the genomes having been taken over by the virus (and there’s an ablative absolute unknown to Caesar) most of the bacterial genes are shut off to some extent, meaning the proteins the bacteria would normally be making to keep itself in business don’t get made. But though the activity of 1,716 genes gets turned down this way, the expression of 41 others actually goes up, some immediately after infection, some about two hours later.
Some of this is the bacteria’s attempt to do something about the infection. Some may be caused by the phage for its own purposes. Some of it may be things that were once adapatations against infection but which the virus has evolved to welcome, even to promote. The story is particularly involved with the hli gene family. These genes do something (not entirely clear to me what) to help photosynthesis along and allow the bacteria to deal with high light conditions. They get turned on when the phage first strikes — and then copies carried by the phage itself get turned on. What’s more, some of the versions of hli genes seen in bacterial genomes seem to have been acquired from phages and then put to bacterial use.
This is all fascinating (at least to me). And as the authors say, further work on these lines will probably have implications for understanding how bacterial photosynthesis works at an ecological level and what factors limit it. But it also seems to hint at something bigger or stranger. It is very hard for us to see this other than in terms of one thing attacking another. Its almost impossible to describe without terms of agency on the part of the players. But reading about it in this detail brings with it a sense in which teh infectuion almost feels like a thing in itself — a process to be described in its own terms, not as a struggle between two players. I suppose this feeling is linked to the ideas that drive “systems biology” — that there is a system here, phage+bacterium, that is its own thing, and can’t be reduced to two complex components, that evolves in its own way.
I’ve no idea whether that idea has much use or room for expansion; and it carries a vaguely Cronenbergy vibe I’m not necessarily on for. It just felt hard to avoid. The paper is fascinating regardless.
Image: Lawrence Berkeley Labs