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Posts Tagged new science stories

beery bladders & other oddities Alison Campbell Sep 03

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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?

legionella – an intracellular pathogen Alison Campbell Sep 02

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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

picking out the drunks, and other interesting tales Alison Campbell Sep 01

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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 :)

caterpillar drool enhances plants’ calls for help Alison Campbell Aug 31

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ResearchBlogging.org

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

our lives with dogs, & other interesting reading Alison Campbell Aug 24

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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?

fungal parasites & zombie ants Alison Campbell Aug 23

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ResearchBlogging.org

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. 

An external file that holds a picture, illustration, etc.<br /> Object name is pone.0004835.g001.jpg Object name is pone.0004835.g001.jpg

Ants biting the underside of leaves as a result of infection by O. unilateralis. The top panel shows the whole leaf with the dense surrounding vegetation in the background and the lower panel shows a close up view of dead ant attached to a leaf vein. The stroma of the fungus emerges from the back of the ant’s head and the perithecia, from which spores are produced, grows from one side of this stroma, hence the species epithet. The photograph has been rotated 180 degrees to aid visualization.
 
From: Pontopiddan et al. PLoS ONE. 2009; 4(3): e4835. doi: 10.1371/journal.pone.0004835
 
Instead, before an ant actually dies it bites into the surface of whatever plant it’s standing on at the time. Pontopiddan et al. identify this behaviour as the fungus’s extended phenotype: it holds the ant’s corpse in place on the plant for long enough that the fungus can secrete a ‘glue’ that will stick the body there more permanently, which in turn gives time for the fungus to develop its fruiting body (the ’stroma’ & ‘perithecia’ in the images above). What’s more, the team had heard accounts of ‘graveyards’ containing large numbers of dead carpenter ants (cue images of zombie ants staggering along to some formicine cemetery). So they decided to determine whether these graveyards really do exist and, if they do, how various biotic & abiotic factors influenced the distribution of dead ants.
 
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.
 
 
 
 

 
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

 

a solar salamander Alison Campbell Aug 17

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This is a new story & potentially a very exciting one (& I must thank Grant for drawing this story to my attention!). A Nature News item (Petherick, 2010) describes the discovery of green algae apparently living within the cells of salamander embryos. I’ll wait with interest for the published paper, but if this finding’s confirmed then it will be the first recorded instance of endosymbiosis in a vertebrate.

The story’s based on a conference presentation by Ryan Kerney, who noticed that the salamander embryos he was studying were a bright green – and not because of algae living on the tiny animals’ skin. This was exciting stuff. Apparently scientists have known for a while that spotted salamanders & the unicellular alga Oophila amblystomatis have a symbiotic relationship. (In fact, Oophila doesn’t live anywhere else, apart from in association with the eggs of a few other amphibians.) Like most frogs, salamanders lay their eggs in water. Here the animal’s urine provides nitrogenous compounds that promote algal growth, while photosynthesising algae living on & in the jelly surrounding the embryos raise the levels of oxygen in the water, whcih would support a higher respiration rate in the tiny salamanders.

However. Kerney found that the algal cells were actually growing inside the cells of his embryo salamanders. (I suspect he would have rubbed his eyes & looked again, on first spotting this one.) This is unexpected – what you’d anticipate is that any algae somehow getting into a vertebrate’s cells would be pretty quickly picked off by the animal’s immune system, which is able to distinguish between ’self’ and ‘non-self’ cells & pick off any intruders. So an interesting question for future research would have to be, what’s the mechanism that’s allowed the algae to penetrate & survive within the amphibian’s cells – how has it overcome/avoided the animal’s immune response? 

A related question is, how do the algae actually physically get into the salamander cells? The Nature News item suggests this might happen when the cells are releasing nitrogen-rich waste products, but as the release of these compounds from individual cells would be very much on the subcellular scale, it’s hard to visualise how this would provide an opening for the algae.

And of course, do the embryo salamanders gain photosynthates from the algae living within them? Work by Hutchison & Hammen, way back in 1958, showed that salamander eggs that lack algae in their jelly casings hatch more slowly. And it’s been known for a long time (e.g. Cates, 1975) that invertebrates such as corals and jellyfish gain photosynthates from their endosymbionts, as does the sea slug Elysia chlorotica  . But if it turns out that the embryos are actually able to utilise the sugars produced by the photosynthesising algae, this would be a first. There are suggestions in Kerney’s conference paper that this might be happening: micrographs that show salamander mitochondria sitting close to the internalised algae. The next step here would be to demonstrate that sugars released by the algae were indeen being taken up and used by the animal’s mitochondria.

A solar-powered vertebrate? Perhaps – but there’s a lot of work needed here yet.

N.Cates (1975) Productivity and organic consumption in Cassiopea and Condylactus. Journal of Experimental Marine Biology and Ecology 18(1): 55-59. doi:10.1016/0022-0981(75)90016-7

V.H.Hutchison & C.S.Hammen (1958) Oxygen utilisation in the symbiosis of embryos of the salamander, Ambystoma maculatum and the alga, Oophila amblystomatis. Biological Bulletin 115: 483-489.

A.Petherick (2010) A solar salamander. Nature News published online 30 July 2010, doi:10.1038/news.2010.384  

but surely if it does no harm… Alison Campbell Aug 16

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ResearchBlogging.org

There’s a lot been written in the blogosphere around what’s known as ‘complementary & alternative medicine.’ (I would argue that there’s no such thing – if it works ie improves/cures the patient’s health, then it’s medicine). In any debate around the use of CAM someone is likely to say that at least it does no harm. For things like homeopathy you could argue that since the client is swallowing only water or sugar pills, with no active principle present, then they’re highly unlikely to come to harm (witness the 10-21 homeopathic ‘overdose’). The counterargument here is that if the patient relies solely on homeopathy for anything beyond self-limiting conditions then there is in fact considerable potential for harm.

With other ‘treatments’ the potential for harm is more apparent. And in some cases the harm can be real. In the latest issue of the New Zealand Medical Journal, Brian Kennedy & Lutz Beckert report on the case of a woman whose acupunturist  left her with a case of pneumothorax. This is not a trivial problem: pneumothorax is where air builds up within the chest cavity, in the space round a lung, as the result of chest trauma or due to a spontaneous breach in the lung itself – or in this case, because an acupncture needle pierced the lung. This puts pressure on the lung, & as a result the lung collapses. (Pneumothorax has also had medical applications – in Sonja Davies‘ autobiography, Bread & Roses, she describes it as a treatment for tuberculosis. Apparently collapsing the affected lung makes it more difficult for the tuberculosis bacilli to survive & grow, so the lung has a chance to recover.)

In the case described by Kennedy & Beckert, the patient “became acutely short of breath, following introduction of an acupuncture needle into the right side of her chest posteriorly. She developed ‘tightness’ … and associated chest pain” & very sensibly left the clinic, went home, & called an ambulance when her symptoms (typical of pneumothorax) got worse. An X-ray showed that her lung has collapsed, & doctors used a needle to remove 450ml of air from the pleural space around the lung. The next morning the pneumothorax had recurred, which meant surgery to inset a ‘drain’ into htr chest wall. After the lung reinflated the drain was removed (& presumably the opening was sealed) & she went home a day later.

Madsen, Gotzsche & Hrobjartsson (2009) performed a meta-analysis of clinical trials looking at acupuncture as a treatment for pain. They looked at data from a total of 3025 patients who received either ‘real’ acupuncture, ’sham’ (placebo) acupuncture, & no treatment. Their conclusions: there was “a small analgesic effect of acupuncture …, which seems to lack clinical relevance and cannot be clearly distinguished from bias. Whether needling at acupuncture points, or at any site, reduces pain independently of the psychological impact of the treatment ritual is unclear.” (As Orac comments, on a related study, “the larger and better designed the study, the less likely it is to find a treatment effect greater than placebo due to the treatment.”)

Given the following that acupuncture appears to have, people will no doubt continue to seek it out for various ills, regardless of the fact that it performs no better than placebo. In which case, they need to be aware that adverse events like the one described by Kennedy & Beckert, although very rare, can still occur. (These authors list ”transmission of diseases, needle fragments left in the body, nerve damage, pneumothorax, pneumoperitoneum [air in the abdominal cavity], organ puncture, cardiac tamponade [accumulation of fluid around the heart] and osteomyelitis [a bone infection]” as major adverse events, albeit extremely rare ones.) They conclude that as these events are generally associated with poorly-trained practitioners, if people do seek out acupuncture treatment they should choose their practitioner carefully – and if treatment involves acupuncture of the chest wall, then the client should be warned about the risks of pneumothorax by the practitioner concerned.

But as Darcy says over on SciBlogs, why go down this route at all?

Brian Kennedy, & Lutz Beckert (2010). A case of acupuncture-induced pneumothorax The New Zealand Medical Journal, 123 (1320) http://www.nzma.org.nz/journal/123-1320/4258

M.V.Madsen, P.C.Gotzsche & A.Hrobjartsson (2009) Acupuncture treatment for pain: systematic review of randomised clinical trials with acupuncture, placebo acupuncture, and no acupuncture groups. BMJ 338: a3115

azolla & endosymbiosis Alison Campbell Aug 01

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ResearchBlogging.org

There are other photosynthesisers besides Volvox, living in our fishpond. Bigger plants include waterlilies, various sedges, & Elodea. And at this time of year the surface is covered by a carpet of duckweed, but when summer comes the Azolla will tend to take over. Sometimes called ‘water fern’, Azolla contains an endosymbiont, a cyanobacterium (blue-green alga) that lives within the plant’s ‘body’ but not within its cells (Ran et al. 2010).

This cyanobacterium is actually a fairly recent fellow-traveller for the fern. Almost all eukaryotes (with the exception of Archaezoans like Giardia) contain intracellular endosymbionts – the mitochondria. These & the chloroplasts of plants formed as the result of endosymbiotic events that occurred perhaps two billion years ago, when the free-living ancestors of these organelles were engulfed by other prokaryote cells but for some reason weren’t digested. Instead, they continued to do their thing, churning out sugars (in the case of the proto-chloroplasts) & ATP well in excess of what the ‘host’ could generate alone (mitochondria). Lyn Margulis developed this endosymbiotic theory for the origins of mitochondria & chloroplasts on the basis of a range of observiations: both organelles contain their own, circular, DNA & (just like bacteria) are able to manufacture their own proteins; their ribosomes & tRNA molecules are like what you’d find in bacteria; and they’re enclosed in a double membrane. Interestingly, many of the genes that would once have been on that circular chromosome of a mitochondrion or chloroplast have ended up in the ‘host’ cell’s nucleus – the host can to some degree control the organelles’ functioning. (Ran et al. note that the chloroplast genome is one of the smallest known, at only 150-200,000 base pairs long.)

Ran & his colleagues were keen to delve further into the process of endosymbiosis as it relates to chloroplasts in plants. To do this, they chose to study a cyanobacterium living inside a species of Azolla – inside, but outside the actual Azolla cells, tucked away into litle ‘cavities’ in cells on the water fern’s upper surface. While there are other symbioses between plants & cyanobacteria, this one’s unusual on two counts: the cyanobacterium involved can’t grow outside the host, & it’s passed on from one generation of Azolla to the other (’vertical transmission’). The oldest fossils of Azolla date back 140 million years, & it’s possible that this endosymbiotic relationship goes back that far in time, The team hypothesised that “… genome reduction may… act on cyanobacteria in symbiosis with plants”, mirroring what appears to have happened in the evolution of chloroplasts.

Figure 1 from Ran et al. (2010): A) fronds of Azolla filiculoides;. B) Close up of the upper surface of an Azolla branch. C) Light micrograph of the cyanobiont. The larger cells represent nitrogen-fixing heterocysts. Scale bar = 5 µm. D) Transmission electron micrograph of the cyanobiont. E) A snap-shot in the vertical transmission process of the cyanobiont between Azolla plant generations, using fluorescence microscopy. Pairs of megasporocarps (blue) develop at the underside of the cyanobacterial colonized Azolla leaves. Filaments of the motile cyanobacterial cell stage (red), the hormogonia (h), are attracted to the sporocarps, gather at the base and subsequently move towards the tip, before entering the sporocarps via channels (white arrows). Once inside the sporocarp the hormogonia differentiate into individual thick walled resting spores (or akinetes; ak), seen as the intensively red fluorescing small inoculum on top of the megaspores (sp).

The team sequenced the cyanobacterium’s genome – and found it to be ‘eroding’. Thirty-one percent of its genes are pseudogenes (they’re either not transcribed, or they don’t produce functional proteins), & there are a lot of transposons – ‘jumping genes’ - in the genome. Significantly, some of the genes that are essential for a free-living bacterium have been ‘pseudogenised’, which means that the cyanobacterium must be dependent on the Azolla for things like DNA repair proteins. The ‘DNA replication initiator’ gene is also pseudogenised,  which is important as it means that Nostoc azollae can divide & grow only very slowly. And the same is true for genes involved in glycolysis and taking nutrients into the cell.

On the other hand, the cyanobacterial genes involved in nitrogen fixation are still functioning well ie the cyanobacterium is able to differentiate to produce heterocysts, where nitrogen-fixation occures, meaning that the symbiont is a key source of nitrogen for its plant host. There’d be quite strong selection pressure for continuing this endosymbiotic relationship: nitrogen is a limiting factor for plant growth, and the host (the Azolla) would gain a big selective advantage over competitors that lacked N-fixing endosymbionts.

The team conclude that over time, the Nostoc azollae genome will erode to the point that ‘ulimately may cause NoAz to resemble a plant organelle (devoted to nigtrogen fixation) more than a free-living organism.’  They also point out that for such organelles to evolve, there would initially have to have been some form of vertical transmission process (seen in this example) & eventually  the symbiont would become intracellular.

So perhaps, in the relationship between Azolla filiculoides and its cyanobacterial partner, we are looking at the evolution of a fully endosymbiotic relationship.

L.Ran, J.Larsson, T.Vigil-Stenman, J.A.A.Nylander, K.Ininbergs, W-W.Zheng, A.Lapidus, S.Lowry, R.Haselkorn & B.Bergman (2010). Genome erosion in a nitrogen-fixing vertically transmitted endosymbiotic multicellular cyanobacterium PLoS ONE, 5 (7) : 10.1371/journal.pone.0011486

how a little green ball of cells controls where it’s going Alison Campbell Jul 29

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ResearchBlogging.org

In one of our first-year biology labs the students spend a bit of time looking down the microscope at various algae & protozoa. Some of their samples come from a container of interestingly weedy water from my fishpond. Not only is the pond covered with duckweed & Elodea, but it turns out to have a wide range of tiny unicellular plants & animals, & some not quite so tiny, such as Volvox.

Actually that pond has a whole thriving ecosystem. We must be doing something right, because the goldfish keep breeding like, well, goldfish, & every year we see the split husks of mayfly & dragonfly nymphs, adhering to the reeds where the animals climbed to make the final moult into their adult forms. And I suspect that either the nymphs, or the bigger goldfish, eat a lot of newly-hatched little fish, because at first we see large numbers of them – little bigger than animated eyelashes – but then each year we end up with just 1-2 new additions to the goldfish family. But I digress…

Volvox is a colonial green alga. Someone in the class will almost always spot one, bumbling relatively slowly across their slide in the company of Paramoecium, Euglena, Spirogyra, & other members of that microcosmic world. However, Volvox can grow up to 2mm across & dwarfs the other organisms swimming with it.

An individual Volvox is a hollow ball of cells, interconnected by strands of cytoplasm. (Apparently you can sometimes find things like rotifers going along for the ride, living within the ball.) The individual cells are often described as ‘Chlamydomonas-like’ (Ueki et al. 2010), as they are very similar in appearance to the unicellular alga Chlamydomonas, including the presence of a light-sensitive ’eyespot’ & a pair of flagella.

Now, the presence of the flagella leads to an interesting question. Like Chlamydomonas, Volvox is motile, moving around as a result of the beating of all those whip-like flagella. Which makes a lot of sense, as the ability to move towards a light source would give a considerable adaptive advantage to a green alga, which needs light in order to photosynthesise. But for this to happen the beating of all those flagella (several thousand of them, in the bigger organisms) must be coordinated. How is this achieved, in an organism that’s basically a ball of cells?

Ueki et al. (2010) studied Volvox rousseletti in an attempt to answer this question, by exposing the organisms to light stimuli & looking to see what happened in terms of flagellar action & the way in which individual cells responded to light. It seems that Volvox, despite the appearance of a homogeneous ball of cells, actually has a recognisable anterior & posterior end, or ‘pole’. The researchers found that the ‘beat frequency’ of flagella changed when a Volvox was exposed to light, & in addition the ‘effective stroke’ – that is, the stroke causing movement in a particular direction - was reversed,

What’s more, they found that the front (anterior) half of the organism was more responsive to light than the posterior half, such that only the anterior cells responded to light in a way that changed its pattern of movement. This could be related to the size of those light-sensitive eyespots: bigger on the anterior half, grading to either tiny, or absent altogether, at the posterior pole.

How does all this work in a way that sees Volvox show positive phototaxis, consistently moving towards a light source? Well, there’s a tendency for these balls of cells (the authors call them ’spheroids’) to rotate gently as they move through the water, especially when they’re not exposed to a directional light source. This is because, on any given cell, both flagella beat in the same direction, towards the posterior pole, & addition they ‘beat in parallel planes pushing the [Vollvox] in the posterior-anterior direction’ (Ueki et al. 2010). Overall, the effect is to propel the organism along in a generally forward direction while at the same time rotating gently on its axis – it actually looks as if it’s rolling along, which is where the Latin name comes from.. However, if this rotation turns the anterior half towards a point source of light, the flagella on those illuminated anterior cells reverse the direction of their beat. The result: the direction of rotation is reversed. This brings other anterior cells into the light & their flagella in turn reverse their direction of beat, Meanwhile the posterior cells just keep right on beating, & the overall effect of this is a slightly erratic movement towards the light. (Just think of the complicated lighting, camera, & microscopy setup needed to capture all this!)

Reading this paper has made me view those little green pond-wanderers in quite a different light, a view I’ll have to share with next year’s algal-lab class :-)

Ueki, N., Matsunaga, S., Inouye, I., & Hallmann, A. (2010). How 5000 independent rowers coordinate their strokes in order to row into the sunlight: Phototaxis in the multicellular green alga Volvox BMC Biology, 8 (1) DOI: 10.1186/1741-7007-8-103

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