Beery bladders… yes, OK, if you drink enough beer your bladder will fill up, but that’s not the focus of a delightful post by Scicurious on Neurotic physiology. It’s a tale of how doctors followed their noses to find that several seriously ill patients had yeast infections – and a decidedly beery odour. And no, they hadn’t been drinking contraband after lights-out on the wards.

Lose weight by taking public transport? Sounds almost too good to be true  – but Paul Statt reports that a recent study does seem to show that taking the bus or train is good for you, as well as good for the planet.

And for the ecologists: in ‘War & Fish’ David Malakoff of Conservation Magazine describes the results of a study looking at the impact of World War II on fish stocks in the North Sea. Bombs, mines, torpedos, & the general call-up of fishermen to join the war effort saw an effective cessation of North Sea fishing & a big bounce-back in fish stocks. An argument for marine reseves in that part of the world?

I know I’ve said it before, but you really do learn something new every day :) I was browsing through my collection of Science alerts & an item about Legionella caught my eye. Legionella pneumophila is the bacterium that causes Legionnaires’ disease, so named because it was first identified when several people attending a 1976 meeting of the American Legion came down with a serious form of pneumonia. But what I didn’t know was that this bacterium is able to grow inside the cells of those affected with it – it’s what’s known as a ‘facultative’ intracellular pathogen (where ‘facultative’ means that it doesn’t have to live this way & can also live outside of the host’s cells). This raises a couple of interesting questions – how does it manage to avoid being digested by the cells it infects, and how does it get the various bits & pieces that it needs in order to survive & reproduce?

In the wild, Legionella is a free-living bacterium, although it must replicate within species of Amoeba. As a human pathogen L.pneumophila is picky about which cells it lives in, going for the immune cells that go around cleaning up both the detritus of dead host cells & also any pathogens that they detect (Diez et al. 2010). In the normal way of things, anything swept up by a macrophage is taken into the cell by a process called phagocytosis: the item is engulfed by the cell and enclosed in a membranous ‘bubble’ that pinches off from the macrophage’s cell membrane. This bubble, called a phagosome, then fuses with little membrane-bound sacs full of digestive enzymes & its contents are promptly digested.

But if a macrophage – or an amoeba – gobbles up a Legionella bacterium that sequence of events is never completed. The phagosomes containing L.pneumophila never fuse with lysosomes (those bags of digestive enzymes) and instead, the bacteria happily grow & reproduce inside their host cells. This is no accident – the Legionella cells produce enzymes that inhibit the fusion of lysosome & phagosome. What’s more, Diez et al. comment that the phagosomes containing these bacteria are closely associated with the host cell’s endoplasmic reticulum & in addition the phagosome membranes contain ribosomes – this is interesting because it suggests that a) the ‘bacterial’ phagosomes may be obtaining materials via the endoplasmic reticulum, & b) that there is protein synthesis happening on the phagosome’s membrane.

This stands to reason as the metabolic demands of a replicating intracellular bacterium will be quite specific and the only way they can be met is by hijackng normal processes in the host cell. Often this movement involves little membrane-bound sacs (vesicles) that bud off the endoplasmic reticulum.  One way that  L.pneumophila manages this is by ‘recruiting’ a specific enzyme, a ’small GTPase’, to the outer surface of the phagosome membrane (Muller et al, 2010). . Small GTPases regulate a whole range of cellular functions – the relevant one here is vesicle transport, although they’re also involved in things like cell division & formation of a nucleus. By regulating vesicle transport the bacterium gains access to the nutrients it needs for its own growth and cell division. In fact, Legionella produces around 60 different proteins that either alter various regulatory pathways in the host cell – including preventing digestion of the bacterial interloper – or are secreted into that host (Cazaket et al. 2004).

Of course, it’s all well & good growing inside a host cell, where you are to some degree protected from the rest of the animal host’s immune system. But eventually the Legionella must escape & spread, & to do this the host cell needs to die. Diez & his colleagues note that in the test-tube Legionella can induce apoptosis in macrophages, & suggest this is done by blocking the actiion of a protein that nromally inhibits cell death. Lose enough macrophages in this way, & you’ll come down with the symptoms of legionellosis.

C.Cazalet, C.Rusnick, H.Bruggemann, N.Zidane, A.Magnier, L.Mz, M.Tichit, S.Jarraud, C.Bouchier, F.Vandenesch, F.Kunst, J.Etienne, P.Glaser & C.Buchrieser (2004) Evience in the Legionella pneumophila genome for exploitation of host cell functions and high genome plasticity. Nature Genetics 36: 1165-1173. doi: 10.1038/ng1447

E.Diez, Z.Yaraghi, A.MacKenzie & P.Gros (2000) The neuronal apoptosis inhibitory protein (Naip) is expressed in macrophages and is modulated after phagocytosis and during intracellular infection with Legionella pneumophila. Journal of Immunology 164: 1470-1477   

M.P.Muller, H.Peters, J.Blumer, W.Blankenfeldt, R.S.Goody & A.Itzen (2010) The Legionella effector protein DrrA AMPylates the membrane traffic regulator Rab1b. Science 329 (5994): 946-949. doi: 10.1126/science.1192276

A week or so back, one of the weekend papers ran a story on just how many beers someone needed to drink before they’d be legally too drunk to drive. The Significant Other & I were staggered to find that the answer was, A Lot. (Around 9, as I recall.) Speaking for myself, about 2 would do it for me – after that, I wouldn’t feel safe to drive. And yet, as Christian Jarrett points out in BPS Research Digest, most people are hopelessly bad at recognising the signs of inebriation in others.

Those of you preparing for Level 3 or Scholarship exams at the end of the year will (among other things) be learning about human cultural evolution. Some of the evidence for the development of culture comes in the form of carvings, including of the human form – the various ‘Venus’ figurines are a good example. Over at Gambler’s House, teofilo presents information on another type of representation: human effigy vases.

And on Deep-Sea News,  Kevin Zelnio writes about a beautiful arthropod fossil, new to science but very old in the scale of arthropod evolution. Just occasionally palaeontologists find spots (lagerstatten) where the fossil assemblages are rich and amazingly well-preserved. From one such site in China comes Yicaris, an ancient crustacean, and one that’s probably very close to the point at which crustacea diverged from the other arthropod lineages. (The late Stephen Jay Gould would have loved this one!)

I do like being on leave – it’s nice to have the chance to roam the science blogs more widely :)

A while ago now I discussed how some plants are able to warn others when they’re under attack by grazing animals. Now it seems that these responses and interactions are even more subtle – a new paper describes how signalling chemicals in tobacco plants can be altered by the grazers’ saliva (Allmann & Baldwin, 2010).

As I described in that earlier post, plants demonstrate a number of responses to grazing. They may produce chemicals that directly harm the grazing animal in some way: poisons, maybe, or substances that inhibit the animal’s digestive processes. Other, volatile, chemicals allow communication with other plants – they signal the presence of herbivores and stimulate those plants receiving the signal to produce defensive chemicals in advance of any grazing attack. And it appears that some of these volatiiles can attract predators that in turn feed on the grazers.

Allmann & Baldwin studied the ‘herbivore-induced volatiles’ (or HIPVs) released by tobacco plants (Nicotiana attenuata) that were being munched on by caterpillars (Manduca sexta). They were interested to see if any of these compounds functioned in attracting specific predators on the caterpillars, something that’s been seen in lab experiments but hasn’t been well-documented in the field.

HIPVs can very considerably, depending not only on the plant & animal species involved but also with various abiotic environmental factors and on the passing of time. The authors identified compunds known as terpenoids as most likely to be involved in attracting predators, because they’re released – after a delay of at least a few hours and up to a day or more – from the whole plant & not just the damaged tissues. The time delay would give opportunity for the plant to manufacture chemicals specific to the particular grazer attacking them. ‘Green-leaf volatiles’ (GLVs), on the other hand , are released from leaves as soon as they’re damaged. With no time for them to be modified by the plant, this class of compounds would provide generalised information about just where on the plant the caterpillars are located: a wasp attracted by the terpenoids could then use the GLVs to home in on their target.

However, it turns out that things are more complex, & more subtle than that.

The researchers found that leaves that had been snipped, to simulate grazing, produced a particular mix of GLVs. But when they collected GLVs from plants that had been nibbled by M.sexta caterpillars, the ratio of diffferent GLVs changed over time. The next step was to snip more leaves (on a new set of plants), treat the wounds with either water or caterpillar drool, & again collect the volatile compounds that the leaves released. The result: caterpillar saliva, but not water, had a lasting effect on the ratio of GLVs. Some complex chemical analyses showed that the saliva wasn’t stimulating a change in metabolic pathways within the plant, so the next question was, was there a compound in the saliva that was acting directly to modify the original volatile compounds released by a damaged leaf? Further experiments suggested that the answer was ‘yes’ – and that it was quite a specific enzyme; saliva from other species of caterpillars didn’t have the same effect.

Because of this species-specific effect, Allmann & Baldwin then wondered whether the modified green-leaf volatiles might actually function in attracting carnivores (in this case, the wasp Geocoris) that prey specifically on Manduca sexta caterpillars. To test this one, they first mixed lanolin with different ratios of GLVs (iincluding the ‘original release’ & saliva-modified mixes). They then attached M.sexta eggs to the undersides of leaves low on the stems of tobacco plants, and placed cotton swabs with the different lanolin/GLV mixes close by. And waited. And discovered that the eggs were much more likely to be predated by Geocoris if they were sitting next to a cotton swab wafting saliva-modified GLVs into the air, basically waving a flag signalling that Manduca eggs (or young caterpillars) were there for the taking. So it wasn’t just the terpenoids (that other class of signalling compounds) that were calling in the predators, after all.

All this works well for the plants, but you have to wonder – why do Manduca caterpillars produce this salivary compound? On the face of it, it’s actually maladaptive: by altering volatile plant chemicals in a way that clearly identifies the presence of these caterpillars to their predators, it surely places the caterpillars at a selective disadvantage. Allmann & Baldwin suggest that the modified green-leaf volatiles may have some antimicrobial function that in some way enhances caterpillar survival. Now that’s an intriguing suggestion for future investigation :) And a reminder that plant and animal interactions are often far more complex than they might first appear.

Allmann S, & Baldwin IT (2010). Insects betray themselves in nature to predators by rapid isomerization of green leaf volatiles. Science (New York, N.Y.), 329 (5995), 1075-8 PMID: 20798319

X-rays were discovered in 1895 by Wilhelm Roentgen, a discovery that was to bring him the first Nobel Prize for physics. (No, I’m not really going to trespass on Marcus’s territory! Well, not for long.) Like many other scientists of the time, Roentgen was experimenting with electtrifying the thin gases in vacuum tubes. One night he noticed that a fluorescent screen at one end of his lab glowed each time he ran a current through his vacuum tube. The screen continued to glow when Roentgen placed sheets of card, copper, or aluminium between tube & scrreen, but stopped when these were replaced by lead. This must have been startling enough, but he must really have been blown away to see the bones of his hand show up on the screen when his hand passed through the invisible rays emitted from the electrified vacuum tube. Roentgen had discovered X-rays.

Today X-rays are used in a wide range of applications. The structure of DNA was elucidated through X-ray diffraction photographs. Airport security systems use them to detect various proscribed items in travellers’ baggage. (Recent developments in this area have led to concerns that customs officers might see more of a traveller than modesty might permit.) And of course there are the medical applications of X-rays, along with their more sophisticated spin-off, the CT (or computerised tomography) scan. CT scans are a signifcant medical tool, but they’ve also allowed scientists to examine some truly ancient indiviuals: CT scans of a Homo  floresiensis cranium have been used to build a ‘virtual endocast’ that models the indivdiual’s brain & has been used to attempt to determine its affinities.

And where is this heading? Well, I now have a lovely X-ray of my left foot that shows very clearly what happens when your little toe connects at speed with a door jamb. The proximal phalanx of my little toe (that’s the toe bone closest to the bones of the foot itself) is in 2 quite distinct parts. Ouchy ouch ouch! I must wear a moon shoe for the next few weeks,and the dog is Not Pleased. Not pleased at all.

Your immune system is a wonderful, complex, multipartite mechanism that usually allows you to fight off the attentions of the various pathogenic organisms (bacterial, fungal, and viral) that you’ll meet during your life. I say ‘usually’ because it’s not always successful on its own, and even where it is, you can be laid low for quite some time – think of flu, but also think of measles, mumps, smallpox, polio… This is where vaccination comes in: this ‘primes’ your immune system so that it can react far more rapidly when it encounters the actual pathogens themselves. NB for a taste of some ‘alternative’ thinking on this concept, try this thread over on SciBlogsNZ.

Now, all multicellular animals have some form of immune system. Ours offers two modes of defence: an ‘innate’ immune system, plus the ‘adaptive’ system involving antibody production in response to the multitude of antigens we face each day. At the other end of the scale, things like jellyfish & sea anemones have only the innate component. For example, Hydra (a freshwater version of the more familiar sea anemones, greenish in colour due to the presence of green algae in the cells lining its gut) lacks any physical mechanisms to keep out pathogens – no thick skin, or anything along those lines. But its epithelial cells release antimicrobial chemicals & antiproteinase enzymes when they detect external antigens.

What about plants? They too have innate defence systems, including mechanical barriers against infection – waxy cuticles, and bark (cork), and also the trichomes (hairs) that you find on many leaves - that . But bark can split, & cuticles can be pierced eg by insect mouthparts – what do plants do then? It seems that when plants detect an invading organism, they release high levels of salicylic acid (the active ingredient in aspirin) in the affected tissues. This induces programmed cell death in the affected tissues, which restricts the spread of the pathogen, and also activates immune responses elsewhere in the plant – this in turn means the plant is now primed to resist futher attacks on other tissues. Salicylic acid isn’t the only chemical resonse to infection; it turns out that plants also produce an enzyme called nitric oxide synthase, which catalyses production of nitric oxide (NO) after an infection.

Now, a pathogen that can evade an organism’s immune system for any length of time is going to be at a selective advantage, and so you get a form of arms race, where hosts with the ability to detect & respond to such a pathogen are in turn likely to have better odds of survival, & so on. Some strains of the bacterium Staphylococcus, for example, are able to wrap themselves in strands of the protein fibrin (which they obtain from the host’s blood), which may make them much harder for the host’s immune cells to destroy. (Alas for the patient – this ability is also linked to clotting; Not Good at all.)

Like animals, plants use ‘pathogen-associated molecular patterns’, or PAMPS, as the basis for identifying pathogens (de Jonge et al., 2010), so a pathogen that can somehow hide these from a plant would be at an advantage. The range of potential PAMPS – detected by receptors on the plant cell surface - includes lipopolysaccharides, peptidoglycans, a protein called flagellin, sugars typically found in fungal cell walls – & chitin, a major constituent of cell walls in fungi. Plants with damaging mutations in these receptors would potentially be more susceptible to attack by bacteria & fungi.

De Jonge & his colleagues studied  the cause of leaf mould in tomatoes, a fungus called Cladosporium fulvan. When this fungus is moving into the inside of a leaf, among the proteins it releases is one that protects the fungal cells from plant enzymes called chitinases, which would otherwise break down the fungus cell walls. Actually there’s more to it than that – when chitinases hydrolyse fungal cell walls, this releases molecules that appear to act as PAMPs & so stimulate the plant’s immune defences.

Another protein, called Ecp6, seemed to be needed for the fungus to be really effective at infecting tomato plants. Looking this more closely, the team found that Ecp6 doesn’t affect chitinase release but appears to tidy up other proteins released by the fungus, so that they aren’t floating around & able to be detected by the plant’s defences. So, because the host’s immune system doesn’t kick in, C.fulvan is able to grow more rapidly within the plant’s tissues. And It turns out that the genes controlling Ecp6 production are widespread in fungi – perhaps one outcome of the plant-fungus arms race. (And other example of how plants are considerably more complex than many of us would think.)

de Jonge R, van Esse HP, Kombrink A, Shinya T, Desaki Y, Bours R, van der Krol S, Shibuya N, Joosten MH, & Thomma BP (2010). Conserved fungal LysM effector Ecp6 prevents chitin-triggered immunity in plants. Science (New York, N.Y.), 329 (5994), 953-5 PMID: 20724636

I have a dog. As a result, papers to do with dogs tend to catch my eye :) On his blog Neuroanthropology, Greg Downey reviews an upcoming book by Pat Shipman and discusses humanity’s long relationship with canines. Beginning with the point that “the first animals domesticated were not food sources, but a fellow predator and scavenger: the wolf (dogs being descendants of wolves, even a subspecies by some reckoning). Clearly, domestication wasn’t first about eating the animal…” Our current relationship may have begun as a commensal one, with wolves following nomadic human hunter-gatherers – unfortunately this sort of thing doesn’t exactly leave traces in the fossil record. A long post, but well worth reading (especially for those of you currently studying human cultural evolution as part of your NCEA L3 biology).

Jason Goldman writes The thoughtful animal.He’s just discussed a paper looking at some intriguing behaviour in the Galapagos marine iguana. These reptiles are non-vocal, communicating among themselves through visual & olfactory signals. But – they appear to respond appropriately to alarm calls by mockingbirds, becoming more vigilant when the birds’ calls indicate that a predator’s on the prowl. This sort of interspecific eavesdropping’s not unknown, but it’s a first in a species that doesn’t itself use sounds to communicate.

And at Tetrapod zoology, Darren Naish has a fascinating article about the strikingly ugly turtle, the matamata. Its weird looks are matched by its unusual feeding behaviour, for it catches prey not by snatching & biting but by inhaling it, expanding its throat to rapidly draw in large volumes of water along with whatever happens to be swimming in it at the time. How neat is that?

Parasites are ubiquitous. I remember watching a video (years ago, while I was teaching at secondary school) about parasites that make humans their home. Lice, eyelash mites (yes, really!), various intestinal worms… I tell you, I had psychosomatic itching for days after seeing that! Then I got my hands on Carl Zimmer’s wonderful book, Parasite Rex – as well as learning all sorts of stuff about parasites & how they live, I also had it brought home to me that parasites aren’t just some sort of passive, undesirable house guest – in many cases they actively influence the host’s behaviour in ways that enhance the parasites’ ability to complete their life cycles.

I was alerted to a recent paper in this area by a blog post from another Kiwi blogger: his sub-header was ‘zombie ants controlled by parasitic fungus for 48 million years’, which reall y took my fancy (the link will take you to a story in the Guardian, of which more later in this post). The authors of this paper (Pontoppidan et al. 2010) point out that it’s not just a case of the parasite affecting individual ants – they can structure the entire host population in terms of its distribution in time and space & thus influence their own distribuiton: the parasite’s ‘extended phenotype’, if you will.

The authors kick off by listing some rather dramatic ways in which other host species are influenced by their parasites, such as behavoural changes that make them more susceptible to predation, thus enabling the parasite to move to its next host; or effectively drowning themselves, which lets the adult stage of the parasite reproduce. (Their full list’s available in the PLoSOne paper.) All this raises interesting questions about just how this manipulation of host behaviour is achieved, & the effects of such parasitism on the species’ population as a whole (it’s obviously a Bad Thing for the indivdiuals concerned). Pontoppidan & her colleagues asked a further topic: the impact of infection on the host species’ distribution in space & time. They chose to look at the fungal parasite Ophiocordyceps unilateralis , and a tropical species of carpenter ants (Camponotus leonardi.).

This is really cool stuff (in a gruesome sort of way). An ant picks up the sticky fungal spores by walking over them on the forest floor; fungal hyphae then penetrate the unfortunate animal’s cuticle & extend throughout its body. It can be just a few days from infection until death. Once the ant’s dead, the fungus grows a ‘fruiting body’ out the back of its host’s head. This produces large spores, too big & heavy to spread on the wind. Instead they fall to the forest floor, produce & release secondary spores, a hapless ant comes along… and the cycle repeats itself. So far, so good (for the fungus), but the really interesting part is that the ants don’t die just anywhere, nor do they simply turn up their toes & drop dead on the ground. 

To do this they spent more than 5 weeks & >500 person-hours in a Thai rainforest, looking for ants. (This wasn’t quite needle-in-a-haystack territory as these ants can be >4mm long, but still…) In all this time they found 2243 dead ants in their study plots (the great majority of which were Camponotus leonardi), but only 2 live C.leonardi. But there were lots of living ants from other species, doing what ants do, in the study area – which suggested that leonardi was definitely the main host for Ophiochordyceps unilateralis. It was 3 weeks before they saw an active trail of leonardi, which descended one tree & travelled only 5m on the ground before heading up another trunk, followed by yet another descent before disappearing into the canopy again. That trail led to a single leonardi nest, high in the canopy (20-25m above ground), with a network of trails running along twigs & branches & extending up to 100m from the nest.

 

On the basis of these observations, the team hypothesised that ants of this particular species actively avoid descending to the forest floor unless it’s the only way to reach a new resource. (You can see how natural selection might achieve this: a colony where too many ants go down to the ground on an everyday basis is likely to lose large numbers of foragers.  So if there’s a genetic underpinning for such behaviour, a queen passing on a ‘go to ground’ gene would end up losing lots of her daughters & thus her nest would be at a competitive disadvantage to other colonies.)  It turns out that there is some evidence supporting this hypothesis: in an area of forest where the parasitic fungus isn’t present, C.leonardi is commonly found at ground level.

 

When the research team went on to look at just where the dead ants were found, it appeared that the bodies weren’t randomly distributed. Instead they were in large aggregations (the ‘graveyards’) of up to 26/m2, separated by corpse-free zones. The now-deceased had bitten onto the undersides of leaves, on average about 30cm above the ground – an example of how the fungus influences its host’s behaviour. The distribution of dead ants appeared to be related to temperature & absolute humidity – things which could influence the survival of fungal spores & thus the chances of an individual ant picking up the infection.

 

Zombie jokes aside, this really is a fascinating example of the complexity of ecosystem interrelationships. And their longevity.  It also turns out that this particular parasitic relationship may have been in place for a very  long time indeed. The ‘death bite’ leaves a characteristic scar on a leaf, and in a separate paper David Hughes & colleagues describe finding just such a scar on a leaf dating back 48 million years, from rocks in what is now Germany.

 

‘Release the fossilised ant army’, indeed!

 

 

 

 

Hughes, DP,  Wappler , T & Lanadeira, CC (2010) Ancient death-grip leaf scars reveal ant-fungal parasitism. Biology Letters. Published online before print August 18, 2010, doi: 10.1098/rsbl.2010.0521

 

Pontoppidan MB, Himaman W, Hywel-Jones NL, Boomsma JJ, & Hughes DP (2009). Graveyards on the move: the spatio-temporal distribution of dead ophiocordyceps-infected ants. PloS one, 4 (3) PMID: 19279680

 

On Thursday I was privileged to spend several hours (actually, a lot of the day as we didn’t finish until about 8.45pm) judging the Waikato regional science fair. I always enjoy doing this as you get to speak with some wonderful young people who are doing some really good science. (It acts as something of an antidote, especially this year as I’d just written a few posts on pseudoscience -that MMS one among them - and was being to worry about the state of science understanding out there.) These young scientists are passionate about what they are doing and every year I learn something new. F’r instance, I overheard Marcus discussing the finer points of trebuchets with the builder of a modern-day form, & now I know why they were on wheels… 

Anyway, all the best projects we looked at had something in common – they demonstrated a good knowledge of the science underpinning their work. And they asked – & attempted to answer – scientific questions about the phenomena they were investigating. That sort of questioning is why projects based solely on what the judges tend to call ‘product testing’ probably won’t make it to the podium. ‘Product testing’ is where the question that forms the basis of the study is along the lines of “is X better than Y?” You can have a lot of fun, & learn some cool techniques, answering that one, but a more interesting question, one that takes the project further & brings it into the realm of science, is why X might be better than Y. That’s why the project on Hawkes Bay fossils that my friend Lynley & I did back in 1971 was never going to win a prize, because it was simply a collection. Mind you, we had heaps of fun doing it, & we learned from the experience! And it’s why my brother’s one on the aerodynamics of paper darts in a home-made wind tunnel did rather well, because he looked into the science of why one dart might fly better than another. And he had fun doing it, too :) 

Which is something that all the exhibitors I spoke with the other day said – that they’d had great fun working on their projects. And that’s how it should be. If it was done as a task, out of duty, or because they’d been told they just had to – that has the potential to take away the enjoyment, the fun, the sheer joy of discovery (the things that keep you going through the tedious bits). Which would be a shame, if the result was turning someone away from the sciences.

So keep it up, everyone, & I’ll look forward to sharing your excitement & discoveries again next year :)

Those of you owned by cats will appreciate how accurate this is :)

(From i can haz cheezburger)