defence

Crickets forewarn their offspring about predators before they're born

edyong — Tue, 09 Feb 2010 08:30:40 +0000

Crickets forewarn their offspring about predators before they're born

Mothers can teach their children much about the world, but some mothers can do it without ever meeting their young. Take the field cricket Gryllus pennsylvanicus. A female cricket isn't exactly a caring mother. Once she lays her eggs, she abandons them to their fate. But amazingly, she can also forewarn her young of the dangers they might face. If a pregnant female is exposed to a wolf spider, her experiences affect her unborn young. When they hatch, the baby crickets are more likely to freeze when they smell wolf spiders nearby.

If mothers sense a threat in their environment, there are clear advantages in being able to prepare her young to face those threats. Over the last decade or so, scientists have discovered that many animal and plant mothers do exactly this, even before their young are born. If pregnant water fleas are exposed to the smell of a predatory midge, they produce young that are armed with larger "crowns-of-thorn", defensive spiky helmets that make them difficult mouthfuls. In the same way, aphids produce more winged offspring if they sense danger. Even the humble radish can generate a generation with sharp, spiky hairs.

In all of these examples, the adaptations are physical ones. The case of the crickets, documented by Jonathan Storm and Steven Lima at Indiana State University, is the clearest example yet of mothers preparing their young for life by influencing their behaviour. Physical defences wouldn't do much good here, for even the largest of crickets are easy pickings for spiders.

Storm and Lima bred crickets that had never seen a wolf spider before. They placed pregnant females in cages with wolf spiders whose killing fangs had been disabled with wax. After a while, the females were removed and allowed to lay their eggs. Storm and Lima collected the hatchlings and placed them in plastic arenas lined in paper saturated with the faeces and silk lines of wolf spiders.

Compared to youngsters born to naive mothers, those born to females with experiences of spiders were 27% more likely to freeze when surrounded by their silk or droppings. If the arenas were lined with clean paper, or paper saturated with cricket odours, the youngsters didn't behave any differently - it was only the spider smells that kept them still.

This small difference in behaviour often meant the difference between life and death. Storm and Lima placed the young crickets in naturalistic environments, complete with hiding places. When spiders were introduced, the forewarned youngsters spent about twice as long in their refuges and they survived for much longer.

The same thing happens in the wild. Storm and Lima collected pregnant female crickets from areas where wolf spiders are known to prowl, and others that are free of these hunters. Just as in their lab experiments, the hatchlings were more wary of spidery smells if their mothers lived in areas where spiders roamed. And it's clearly the mother's experiences that change her offspring's behaviour. When Storm and Lima exposed the eggs or nymphs of naive females to the scent of spiders, the youngsters' behaviour weren't affected.

Predators are likely to pose constant threats to a prey species from generation to generation. As such, Storm and Lima think that these sorts of pre-natal parental tip-offs should be fairly common in nature. It's just that we haven't looked very hard for them yet. In other possible examples, pregnant skinks that smell snakes on the air produce young that flick their tongues out more often when snakes around.

For now, we don't know how the mother crickets manage to tip off their young. Their behaviour could be changed through "epigenetic" means, by adding molecular tags onto their DNA that change the way specific genes are used and controlled. A mother could also convey information to her unborn young with hormones. By placing the right balance of hormones into her eggs, she could influence the development of her offspring's defensive behaviour.

Reference: Storm, J., & Lima, S. (2010). Mothers Forewarn Offspring about Predators: A Transgenerational Maternal Effect on Behavior The American Naturalist, 175 (3), 382-390 DOI: 10.1086/650443

Image: by Cody Hough

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edyong Tue, 02/09/2010 - 03:30

Tiger moths jam the sonar of bats

edyong — Fri, 17 Jul 2009 07:30:32 +0000

Tiger moths jam the sonar of bats

Bats view the world in echoes, timing the reflections of their own ultrasonic calls to navigate and hunt. This biological sonar, or echolocation, has made them masters of the night sky; it's so sensitive that some species take moths and other insects on the wing, while others pluck spiders from their webs without entangling themselves in silk. But with such an efficient technology, it was only a matter of time before their quarry developed countermeasures.

Some insects gained ears; others simply rely on outmanoeuvring their attackers. But one group, the tiger moths, play bats at their own game. When attacked, they unleash ultrasonic clicks of their own to jam the calls of their pursuers, disrupting their ability to accurately gauge distances or even feigning echoes off non-existent objects.

This technique has been suggested ever since moths were first discovered to click several decades ago, but Aaron Corcoran from Wake Forest University has found the first conclusive evidence that moths actually do this. They pitted moths of the species Bertholdia trigon) against four big brown bats (Eptesicus fuscus) against each other over the course of three days, in gladiatorial arenas surveyed by high-speed infrared cameras and ultrasonic microphones.

When the three bats were pitted against moths in flight, they only managed to snag B.trigona on around one in five attempts. Even if the moths were tethered onto a stump, the bats still fumbled their approach at the last minute. A related moth species that doesn't click fared much worse and almost always succumbed to the bats.

Tiger moths make their clicks using an organ called a tymbal, and by cutting this away, Corcoran managed offer muted individuals to the bats. Deprived of their organic castanets, the vast majority of moths were eaten, proving that the clicks were the cause behind the bats' failure. That also rules out the possibility that the clicks advertise the fact that the moths are unpalatable or poisonous, for the bats were all to happy to munch away on their silenced prey. Indeed, after the moths start clicking, the bats carry on with their attack - they just fail to actually close the deal. That too suggests that the clicks aren't off-putting in themselves.

Over the course of a week, the bats didn't become any worse or any better at capturing clicking moths. This implies that they don't need to learn anything about the defence, which again rules out the idea that the noises advertise a poor taste. It also rules out the idea that the clicks are meant to startle approaching bats, for experienced animals would soon become accustomed to that and learn to carry through with the chase. That didn't happen, even if it was the same moth and the bats were having another shot, seconds after a failed attempt

The only remaining possibility is that the bats were jamming the bats - it's the sort of defence that is neither enhanced nor diminished by experience on the part of the bat, which is exactly what the data showed. The bats' behaviour also supported this theory. When they take other moths, their attack follows a regular pattern - approach the target, track its movements, and swoop in for the kill, all accompanied by their own distinct style of sonar pulse. But bats attacking clicking moths become confused, going back and forth along their chain of attack.

It's clear that not all species of tiger moths click to jam bat sonar, and Corcoran suggests that originally, the noises did evolve to signal a foul taste. Indeed, some moths mimic each others' sounds to fool hungry bats. That, however, was a relatively simple defence and one that could be easily penetrated through experience. It was a stepping-stone to the more sophisticated jamming technique, the latest countermeasure in the arms race between bat and moth.

Reference: Science 10.1126/science.1174096

More on bats and moths: Moths mimic each others' sounds to fool hungry bats

edyong Fri, 07/17/2009 - 03:30

Correlated noise is the bane of any ranging system. It isn't that it makes the solution harder to find, but rather that the solution may be wrong, and if multiple solutions are seen they can't all be right.

Pure evil. That's what moths are. Does it shock me they control the powers of darkness? Not one bit.

Yeah, jamming my arse. If you pause the first video just right, you can spot the moment where the moth hits the bat with black magic.

Fascinating. I feel sorry for the moths getting things cut out of them for the experiment. Not pleasant. But the second comment reminded me of one of my children's views on moths.

There's just something about this sentence that reminds me of cheesy old science fiction movies (or current Saturday offering from SyPhy( nee SciFi)): "They pitted moths of the species Bertholdia trigon) against four big brown bats (Eptesicus fuscus) against each other over the course of three days, in gladiatorial arenas surveyed by high-speed infrared cameras and ultrasonic microphones." ... but don't you have an extra "against" phrase in there?

Retrocyclins: a defence against HIV, reawakened after 7 million years

edyong — Wed, 29 Apr 2009 06:30:21 +0000

Retrocyclins: a defence against HIV, reawakened after 7 million years

HIV is an elusive adversary. The virus is so good at fooling the immune system that the quest for an HIV vaccine, or even a countermeasure to resist infections, has spanned two fruitless decades. But maybe a defence has been lurking in our genomes all this time.

Nitya Venkataraman from the University of Central Florida has managed to reawaken a guardian gene that has been lying dormant in our genomes for 7 million years. These genes, known as retrocyclins, protect monkeys from HIV-like viruses. The hope is that by rousing them from their slumber, they could do the same for us. The technique is several safety tests and clinical trials away from actual use, but it's promising nonetheless.

Retrocyclins are the only circular proteins in our bodies, and are formed from a ring of 18 amino acids. They belong to a group of proteins called defensins that, as their name suggests, defend the body against bacteria, viruses, fungi and other foreign invaders. There are three types: alpha-, beta- and theta-defensins. The last group is the one that retrocyclins belong to. They were the last to be discovered, and have only been found in the white blood cells of macaques, baboons and orang-utans.

In previous experiments, Venkataraman's group, led by Alexander Cole, showed that retrocyclins were remarkably good at protecting cells from HIV infections. They are molecular bouncers that stop the virus from infiltrating a host cell. The trouble is that in humans, the genes that produce retrocyclins don't work. Over the course of human evolution, these genes developed a mutation that forces the protein-producing machinery of our cells to stop early. The result is an abridged and useless retrocyclin.

But aside from this lone crippling mutation, the genes are intact and 90% identical to the monkey versions. Now, Venkataraman has awakened them. She found two ways to fix the fault in human white blood cells, one involving gene transfer and the other using a simple antibiotic. Either way, she restored the cells' ability to manufacture the protective proteins. And the resurrected retrocyclins did their job well - they stopped HIV from infecting a variety of human immune cells.

Venkataraman says that we can think of retrocyclin deficiency as "an inherited disorder, albeit one with an incidence of 100%. To "cure" it, she created corrected versions of the faulty human retrocyclin genes and loaded them into white blood cells. Using glowing antibodies designed to stick to retrocyclins, she saw gleaming evidence under the microscope that the cells had made their own stock of these proteins. She even managed to purify the rekindled proteins themselves.

This clearly tells us that our cells have all the right machinery needed to actually make retrocyclins - it's just that the instructions have a typo in them. Most importantly, the restored proteins worked. They prevented HIV from infecting up to 80% of the cells, and even reduced the levels of virus in cells that had already been infected.

Obviously, gene transfer techniques like this are hardly practical for poor African nations where HIV is most rampant. For retrocyclins to really play a role in the fight against HIV, we need a cheaper and easier way of reactivating them. And Venkataraman thinks she has found one - a group of antibiotics called aminoglycosides.

In bacteria, these drugs work by blocking them from creating proteins. But in the more complex cells of animals, they do something different - they react with the protein-making machinery of our cells so that they make slightly more mistakes than usual. Normally, that would be a bad thing but for retrocyclins, it's an unexpected boon. It means that the machinery barrels straight through the mutation that causes retrocyclins to be built half-finished. It doesn't stop prematurely, and produces a full-length protein.

Venkataraman found that one of these drugs, tobramycin, was especially good at restoring retrocyclins, and did so in both white blood cells and actual vaginal tissue. The drug slashed the rate of HIV infection by about 50% - a respectable figure but clearly a smaller one compared to the sizeable benefits bestowed by the gene transfer method. On the plus side, the technique didn't seem to harm the cells in any way.

These results are promising ones indeed, and Venkataraman thinks that with more work, aminoglycoside-based creams could be used to prevent HIV infections in the real world.

HIV kills by infecting the very cells that are meant to defend us from infections and destroying them. But retrocyclins are something it hasn't encountered before. Humans lost the ability to create these guardians millions of years ago and by reawakening them, we could have a new but ancient weapon against this sneakiest of foes.

Reference: Venkataraman, N., Cole, A., Ruchala, P., Waring, A., Lehrer, R., Stuchlik, O., Pohl, J., & Cole, A. (2009). Reawakening Retrocyclins: Ancestral Human Defensins Active Against HIV-1 PLoS Biology, 7 (4) DOI: 10.1371/journal.pbio.1000095

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edyong Wed, 04/29/2009 - 02:30

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genetics

Medicine & Health

New drugs & treatments

Very interesting, it's always facscinating what you can learn by studying the differences between similar species...something that is recognized all too infrequently in discussions about the value of animal research.

Hobby horses aside, this is an exciting result. The authors of the above study mention a new drug called PTC-124 (a.k.a. Ataluren) that acts in a similar way to the aminoglycosides. This drug has the benefit of being a lot less toxic than the antibiotics (important for long term use) and has performed well in phase II clinical trials for Duchenne Muscular dystrophy and Cystic Fibrosis.

http://www.muscular-dystrophy.org/research/news/626_the_latest_news_fro…
http://www.cff.org/research/DrugDevelopmentPipeline/#CFTR_MODULATION

If the longer term monitoring and larger trials of PTC-124 for FC and DMD continue to indicate that it is safe and effective trials against HIV might start sooner than we might expect for such a novel approach.

Really friggin' cool, man. I bet abbie is drooling...

That is seriously cool, and your explanation was lucid and easy to follow. Thanks!

This came to my mind:

Genetic Mutation Immunity to Bubonic Plague and HIV http://is.gd/vmdF

HIV Protection CCR5 Chemokine Receptor Mutation http://is.gd/vmfx

Natural selection and resistance to HIV [PDF] http://is.gd/vmh2

Evaluating plague and smallpox as historical selective pressures for the CCR5-Delta-32 HIV-resistance allele [PDF] http://is.gd/vmhF

The geographic spread of the CCR5 HIV-resistance allele
http://is.gd/vmm5

So tobramycin will allow translation other human pseudogenes (the authors elude to this in the discussion). Are there some potential side effects here?

Wow. The title to this post was an attention grabber and the content lived up to the title. This is exciting. Thank you for sharing it.

Are there some potential side effects here?

Vitamin C production? :-) Or maybe the vomeronasal organ might start working again.

BTW, you mean allude, as shown by the "to" that follows it.

Ed,
The one thing that is very questionable is using aminoglycosides in eukaryotes to "release" the retrocyclin. Aminoglycosides work by affecting the 30s subunit of the prokaryote ribosome. Eukaryotes--which includes the cells of humans--lack a 30s ribosome. You probably already know, but that is why antibiotics kill bacteria in us an don't kill us. Humans have 80s ribosomes, consisting of 40s and 60s subunits. Because we don't have 30s ribosome subunits, how would this be able to do anything to eukaryotic cells?
Thanks.

Mick, there's an equivalent site on the eukaryotic ribosome that the aminoglycosides bind to weakly. From the paper:

In bacteria, aminoglycosides bind strongly to the decoding site on the 16S rRNA, thereby hindering protein synthesis [26]. However, in eukaryotes, aminoglycosides bind to the eukaryotic decoding site with low affinity and induce a low level of translational misreading, which suppresses the termination codon through the incorporation of an amino acid in its place.

Tim Read, there are theoretical risks associated with this approach, but so far research looks promising.

Using aminoglycoside antibiotics for treatment of HIV is probably not a realistic option, while they are very useful as antibiotics they cause side effects in some patients that get more common and more serious the longer they are taken for. While they are benificial if taken for a few days or weeks they are probably appropriate for treating HIV where they will probably need to be taken for several years (and at the very least for several months).

However the paper above also mentions a new drug named PTC-124 that has been developed to have the same property of allowing the translational machinery to read through premature stop codons. PTC-124 has successfully completed Phase IIa clinical trials for the treatment of Duchenne muscular dystrophy and Phase II trials for Cystic Fibrosis, and so far indications are that it is far less toxic than the aminoglycosides. It is now in longer (2 years) and larger (>100 participants) Phase IIb trials.

http://www.muscular-dystrophy.org/research/news/626_the_latest_news_fro…

If further research continues to support the reactivation of retrocyclin as a means of combatting HIV, and clinical trial results for PTC-124 for CF and DMD continue to be positive, than PTC-124 may start to look like a very promising new anti-HIV drug.

Far away from something tangible, buy looks very very promising. Very good post.
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The obvious problem here is that we don't know the consequences of reactivating a gene that has been switched off for 7 million years. First, there might very well be a reason why it was switched off in the first place (i.e. it may have provided some kind of selective advantage).

Second, if the gene has indeed been dormant for 7My, we humans have evolved a lot during this time, and the reactivated gene might well interact badly with the new machinery that emerged while it was asleep.

This is amazing! thanks!

The answer to the concerns about the effect of restarting retrocyclin production in humans is a familiar statement that infuriates marketeers, politicians and pundits: We need more data. Between the "This has questionable consequences, do DON'T DO IT!" people and the "We gotta DO SOMETHING!" crowd, hardly anyone favors spending what it will take to actually answer the question.