Of Pronghorn and Predators

A male pronghorn, photographed on Antelope Island, Utah.


Bee hives, with their regularly arranged honeycombs and permanently busy workers may seem like the picture of order. But look closer, and hives are often abuzz with secret codes, eavesdropping spies and deadly alliances.

Bees release alarm pheromones that draw small hive beetles towards the hive.African honeybees are victimised by the parasitic small hive beetle. The beetles move through beehives eating combs, stealing honey and generally making a mess. But at worst, they are a minor pest, for the bees have a way of dealing with them.

They imprison the intruders in the bowels of the hive and carefully remove any eggs they find. In turn, the beetle sometimes fools the bees by acting like one of their own grubs, and gets a free meal instead of imprisonment. In Africa, both species have found themselves in an evolutionary stalemate.

But in 1998, American beekeepers spotted the beetle in hives of their local European-descended honeybees. These insects are gentler versions of their aggressive African relatives, and in them, the beetles found more vulnerable victims.

In the last decade, they have spread through hives on the East Coast, causing much more destruction than they normally get away with. In some cases, the damage is so severe that the bees are forced to abandon their hive. As the bees suffer, so do the economically vital crops they pollinate.

Now, scientists from the International Centre of Insect Physiology and Ecology and the University of Florida have uncovered the secrets behind the beetle's destructive ability.

Small hive beetles  hunt down beehives by hijacking their communications. When bees are stressed or confronted by threats, they release alarm pheromones into the air to alert their hive-mates of impending danger. But the beetles can also detect these chemical signals and use the bees' own early warning system to locate their hives.

Baldwyn Tonto and colleagues found that the beetles are sensitive to much lower levels of these pheromones than the bees themselves are, and can detect a much wider ranger of airborne chemicals from the hive. With their superior senses, the beetles can home in on beehives before the bees themselves can sense the alarm.

But that's not the whole story. Tonto found that honeycombs infested by beetles, but free of worker bees, were emitting a strange smell. It mimicked the bees' alarm pheromones and strongly attracted even more beetles. But it wasn't coming from the parasites themselves.

Instead, the source of the smell was a type of yeast that hitches a ride with small hive beetles into the bees' home. Tonto found that the fungus was fermenting the pollen collected by the bees, and releasing chemicals that closely mimic the beetle-attracting alarm pheromones.

Domesticated European honeybees have been bred into helplessness against the small hive beetle.The beetles' keen sensitivity to the bees' chemical messages allows them to initially home in on a hive. As they arrive, they bring the yeast along for the ride and distribute it among the hive's pollen stores. The yeast ferments the pollen and releases chemicals that mimics the bee's alarm pheromone, attracting even more beetles .

Soon, the infection reaches critical mass, and the bees are forced to abandon their homes. They leave behind a sizeable store of pollen and honey, ideal breeding grounds for the unwitting partnership of yeast and beetle.

But the yeast also exists in Africa, where it is similarly spread to hives by hive beetles. Why does the alliance not wreak such havoc there? Tonto believes that domestication is the answer. Because of years of selective breeding, the European honeybee is a slightly dopier version of the African bee - more docile and less prone to swarming.

It faces a larger number of pests and problems that prevent it from concentrating on imprisoning invading beetles. And its poor sensitivity to its own alarm chemicals allows the beetle-yeast alliance to gain a strong foothold before the bees recognise the threat.

With bee populations mysteriously dying off across America, the threat of the small hive beetle and its fungal partner may be even more pressing than before.

Reference: Torto, Boucias, Arbogast, Tumlinson & Teal. 2007. Multitrophic interaction facilitates parasite-host relationship between an invasive beetle and the honey bee. PNAS 104: 8374-8378.

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Capable of reaching speeds exceeding 70 kilometers per hour, the pronghorn (Antilocapra americana) is one of the fastest mammals on earth. No large North American carnivore can match it for speed – some conservationists have go so far as to suggest importing cheetahs to special parks to reinstate the evolutionary race between pronghorn and extinct big cats – yet every year many pronghorn fall prey to a canid more often considered a pest than a consummate hunter. Wolves, cougars, bears, and even eagles all prey upon pronghorn from time to time, but it is the coyote that kills more individuals than any other, especially in the northern range of Yellowstone National Park.

While traveling through northern Utah and Wyoming last summer I saw many pronghorn, but, despite their apparent abundance in the area, the Yellowstone population is quite small. Consisting of less than 300 individuals – low enough to put them at risk of being extirpated locally – the Yellowstone population primarily occupies an area along the northern border of the park. As reported last year in Western North American Naturalist by a team of ecologists led by Kerey Barnowe-Meyer, the partially-migratory group often summers in the arid, shrubby land around Gardiner, Montana in the winter but some migrate into Yellowstone during the summer.

A female pronghorn and two fawns, photographed just outside Grand Teton National Park, Wyoming.


You swallow the pill. As it works its way through your digestive system, it slowly releases its chemical payload, which travels through your bloodstream to your brain. A biochemical chain reaction begins. Old disused nerve cells spring into action and form new connections with each other. And amazingly, lost memories start to flood back.

Dementia results in massive neuron loss, but that doesn't mean memories are destroyed.The idea of a pill for memory loss sounds like pure science-fiction. But scientists from the Massachussetts Institute for Technology have taken a first important step to making it a reality, at least for mice.

Andre Fischer and colleagues managed to restore lost memories of brain-damaged mice by using a group of drugs called HDAC inhibitors, or by simply putting them in interesting surroundings.

They used a special breed of mouse, engineered to duplicate the symptoms of brain diseases that afflict humans, such as Alzheimer's. The mice go about their lives normally, but if they are given the drug doxycycline, their brains begin to atrophy. The drug switches on a gene called p25 implicated in various neurodegenerative diseases, which triggers a massive loss of nerve cells. The affected become unable to learn simple tasks and lose long-term memories of tasks they had been trained in some weeks earlier.

Fischer moved some of the brain-damaged mice from their usual Spartan cages, to more interesting accommodation. Their new cages were small adventure playgrounds, replete with climbing frames, tunnels and running wheels, together with plentiful food and water. In their new stimulating environments, the mice returned to their normal selves. Their ability to learn improved considerably, and amazingly, seemingly lost memories were resurrected.

They didn't grow any new neurons, and their brains remained the same size. But Fischer found that they did have many more synapses - the connections between nerve cells - than brain-damaged peers. Even though they had lost a substantial number of neurons, their enriched environments triggered the surviving cells to re-wire themselves.

These experiments suggest that many lost memories are in fact not lost at all, but misplaced. The dead neurons take important connections with them and the survivors, though incommunicado, still retain latent traces of memory. When they are jolted into action and form new networks, these trace memories are reinstated. And that provides genuine hope for people affected by dementia, Alzheimer's and other conditions.

It would be a touch silly to suggest putting such people in the equivalent of a large playpen. But Fischer also found a group of drugs called HDAC inhibitors that have the same effect - the molecular equivalent of a stimulating environment.

HDACs or histone deacetylases control whether genes are switched on or off by altering other proteins called histones. DNA winds around histones like spools, which serves to package this long and unwieldy molecule into a compact and more manageable form.

HDACs change the histones so that they wrap more tightly around DNA and render its genetic code unreadable. Any genes contained in these stretches of DNA are silenced. Drugs like sodium butyrate (SB) neutralise HDACs, freeing DNA from the repressive grip of histones.

Any silenced genes can now be freely switched on and among these, are genes that allow the brain's neurons to sprout new synapses. The details still need to be ironed out, but the results are clear - just like mice housed in fun cages, those treated with SB regained lost memories.

Naysayers might point out that these results are all very good for mice, but are a long way off benefiting people. But while our brains outclass those of mice, we appear to store memories in very similar ways. New experienced are initially encoded among the neurons of the hippocampus, only to be transferred into deeper and long-term stores about three or four weeks later.

Four years ago, a man who had been barely conscious for almost 20 years began to move and speak again. His nerves, badly damaged by a car crash, had started to re-wire themselves and form new connections, in the same way that Fischer's rats did. The possibilities are there; it's just the method that needs refinement.

At the moment, the biggest problem with Fischer's approach is that it's akin to shooting at a fly with a shotgun. HDAC inhibitors have far-reaching effects on a multitude of different genes. It's fortunate that these include genes that lead to brain re-wiring, but such a scattershot approach is prone to collateral damage.

Documenting the full actions of HDAC inhibitors is vital. It will allow scientists to understand what side effects such treatments would have in people, while designing more sophisticated drugs with a narrower range of targets.

Reference: Fischer, Sananbenesi, Wang, Dobbin & Tsai. 2007. Recovery of learning and memory is associated with chromatin remodelling. Nature doi:10.1038/nature05772

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To understand the population dynamics of the Yellowstone pronghorn and which predators posed to greatest threat to them, Barnowe-Meyer and colleagues monitored the movements and mortality of adult females and newborn fawns. During the winters of 1999-2001 and  2004-2006 the team darted adult females and placed tracking collars on them (which would also notify the scientists when the animal died) and in the spring of 1999-2001 they similarly tracked new fawns (taking care to make sure they did not place the baby pronghorn at increased predation risk). When an individual was killed the team went out to inspect the carcass and recorded whatever useful information remained about what kind of animal had killed the pronghorn, thereby providing an outline of what kinds of predators were taking pronghorn and with what frequency.

The trouble with a carcass in Yellowstone is that it does not last for long. Beyond the damage done by the attacking predator, scavengers can quickly obscure clues about what kind of animal made the kill. Nevertheless, the team was able to authenticate the cause of death in 22 cases of adult mortality, with 13 of those being attributed to predators (eight were undetermined and one was due to complications during birth). Of those thirteen the predator breakdown looked like this: 5 coyotes, 3 cougars, 1 wolf, and 4 undetermined predators. The sample was small, but, based upon the incidents in which the killer could be identified, coyotes appeared to be the most significant predators of pronghorn.

The sample of pronghorn fawns was also small, but showed a similar pattern. Of 28 tagged fawns, four survived, eight disappeared, and two died of unknown causes, leaving 14 cases of predation. Of this subset, six were killed by coyotes, five were scavenged (and may have been killed by) coyotes, one was killed by a large bird of prey, and two were killed by an unknown predator. Once again, coyotes appeared to be the most significant predator of the pronghorn, especially since they frequented the kind of habitat which pregnant females preferred for giving birth to and raising their fawns. The other predators took pronghorn opportunistically as the herbivores migrated between Wyoming and Montana, but coyotes preyed on them consistently.

What remains unknown, however, is how the predation of pronghorn by coyotes has been influenced by the reintroduction of wolves to Yellowstone in the 1990’s. Coyotes are mesopredators – second-tier carnivores whose populations are controlled by apex predators – and it has been proposed that the existence of wolves in northern Yellowstone acts as a check on the number of coyotes in the area. Then again, it may be that coyotes avoid the rugged, more forested habitats which are home to other predators in favor of more open areas, thus placing adult female pronghorn and their fawns at increased predation risk. At present, the effect of wolves and top-level predators on coyotes in Yellowstone is still poorly known, but figuring out how coyotes have responded to the reintroduction of wolves may help conservationists manage what is left of the Yellowstone pronghorn population.

A male pronghorn, photographed on Antelope Island, Utah.

Blogging on Peer-Reviewed ResearchPeople seem inordinately keen to pit nature and nurture as imagined adversaries, but this naive view glosses over the far more interesting interactions between the two. These interactions between genes and environment lie at the heart of a new study by Rose McDermott from Brown University, which elegantly fuses two of my favourite topics - genetic influences on behaviour and the psychology of punishment.

<Regular readers may remember that I've written three previous pieces on punishment. Each was based on a study that used clever psychological games to investigate how people behave when they are given a choice to cooperate with, cheat, or punish their peers.

McDermott reasoned that the way people behave in these games might be influenced by the genes they carry and especially one called monoamine oxidase A (MAOA), which has been linked to aggressive behaviour. Her international team of scientists set out to investigate the effect that different versions of MAOA would have in a real situation, where people believe that they actually have the chance to hurt other people.

MAOA encodes a protein that helps to break down a variety of signalling chemicals in the brain, including dopamine and serotonin. It has been saddled with the tag of "warrior gene" because of its consistent link with aggressive behaviour. A single fault in the gene, which leads to a useless protein, was associated with a pattern of impulsive aggression and violent criminal behaviour among the men of a particular Dutch family. Removing the gene from mice makes them similarly aggressive.

These are all-or-nothing changes, but subtler variations exist. For example, there is a high-activity version of the gene (MAOA-H), which produces lots of enzyme and a low-activity version (MAOA-L), which produces very little. The two versions are separated by changes in the gene's "promoter region", which controls how strongly it is activated.

A few years ago, British scientists found that children who had been abused are less likely to develop antisocial problems if they carry the MAOA-H gene than if those who bear the low-activity MAOA-L version. An Italian group has since found the same thing. It is a truly fascinating result for it tells us that the MAOA gene not only affects a person's behaviour, but also their reactions to other people's behaviour.

But both studies had a big flaw - they measured aggression by asking people to fill in a questionnaire. Essentially, they relied on people to accurately say how belligerent they are and we all know that many people like to talk big. McDermott wanted to look at actions not claims.

To that end, she recruited 78 male volunteers and sequenced their MAOA gene to see which version they carried (just over a quarter had the low-activity version). The volunteers played out a scenario where they believed that they could actually physically harm another person for taking money that they had earned. Their weapon of retribution? Spicy sauce.

Use the Sauce, Luke

She told the recruits that they would be paid according to how well they answered a vocabulary quiz. They were allegedly paired with anonymous online partners, who would then decide how the jackpot would be split. In reality, their partner was a computer, the game was fixed so that all players in any given round earned the same money, and the computer would always choose to keep either 20% or 80% of the total.

When the volunteers were told about their share, they could punish their "partner" by forcing them to drink a teaspoon of unpleasantly spicy sauce. They had an armory of ten teaspoons of hot sauce and any that hadn't been used could be traded in for cash - that way, the players were actually forfeiting money in order to dole out retribution.  This went on for four rounds, with a new fake "partner" on every one. (Incidentally, only 8 people were suspicious that they weren't actually forcing sauce upon a partner and they were excluded from the results. Everyone was debriefed later, for ethical purposes.)

McDermott found that the activity of the MAOA gene did affect the volunteers' propensity for punishment and its influence depended on how strongly they were provoked. When the fictitious partner took just 20% of the money, MAOA had little bearing on the volunteers' desire to punish. But when they lost 80% of their winnings, people with the low-activity version were more likely to mete out saucy punishment than those with the high-activity one.

The MAOA gene did have a more general effect - overall, those with the low-activity version behaved more aggressively than those with the high-activity one. And after the first round, even if their partner had taken a paltry 20%, the MAOA-L carriers were slightly more likely to use the sauce. So this variant seems to be linked to aggressive tendencies, but much more so after aggravation - a classic case of nature via nurture.


If anything, the experiment underestimated the true extent of aggressive behaviour among MAOA-H carriers. With a finite supply of hot sauce, and no option for buying more,  McDermott had set an upper limit to aggressive behaviour, which many of the recruits eventually hit. Indeed, when 80% of the money was taken from them, 44% of the MAOA-L carriers used up their entire sauce supply, while just 19% of the MAOA-H carriers did.

You talkin' to me?

McDermott's study clearly demonstrates that the low-activity version of MAOA is linked to belligerent tendencies, which lead to actual aggressive behaviour in real situations. The reasons behind this link are still unclear, but an earlier study suggested that individuals with MAOA-L are overly sensitive to threats or challenges that other people would shrug off, and overreact to them.

They even have unusually high levels of activity in their dorsal anterior cingulated cortex (dACC) - a part of the brain that has been linked to feelings of distress after social rejection or confrontation. That gels nicely with what McDermott herself found - MAOA's influence on behaviour is stronger in situations when people have been provoked or challenged.

This fascinating work adds a deeper dimension to other studies that use psychological games to understand how punishment contributed to the evolution of cooperation. Influenced by their genes, some groups of people may use very different strategies than others and the relative success of these will depend on how frequently they are used in the population. For example, if everyone was a pacifist, carriers of MAOA-L might gain an advantage by acting more aggressively than normal (I stress again that it's a question of degree - MAOA-L carriers aren't destined to be violent thugs). But if everyone carried MAOA-L, its advantage would soon disappear.

Many studies tend to focus on "altruistic punishment", where people take a personal hit to punish others for the good of the group. But in this experiment, those who paid to punish received no returns on their "investment" - they were acting out of spite, which McDermott describes as the "neglected ugly sister of altruism".

Spite has been investigated recently in a study which showed that students from 16 cities around the world varied greatly in their tendency to punish others spitefully or "antisocially". That study attributed the differences to how the various societies felt about free-loading and how strongly respected the rule of law. But it would be equally interesting to see if the low activity version of MAOA was more common in some of these countries than in others.

Reference: PNAS to be published this week. DOI:10.1073/pnas.0808376106

Image: Tabasco sauce by Andrew Dunn

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Female and infant pronghorn are not the only individuals to be killed by coyotes. Male pronghorn, despite their armaments, can also fall prey to the mesopredators, and one recent case identified a unique risk suffered only by the males. Much like elk, male pronghorn often fight with their horns, and every now and then two males become irrevocably stuck. As reported by Jennifer Chipault and Dustin Long in The Southwestern Naturalist, at about 8 PM on October, 2 of 2006 two male pronghorn in Vermejo Park Ranch, Colfax County, New Mexico were found locked together – the horn of one was stuck on the head or neck of the other such that they were nearly nose-to-nose. One was already in a bad state, lying on its side and breathing shallowly, and the other made frequent attempts to free himself.

The naturalists observed the pronghorn intermittently throughout the night, but they were not the only ones watching. At about 2 AM on October 3rd several coyotes were seen in the vicinity of the stuck pronghorn. The coyotes did not immediately attack, perhaps being deterred by the presence of the human observers, but when the researchers left and checked back at the site at about 6:30 AM there was little left of the pronghorn which had been lying on the ground. What remained of it was still attached to the other male. As the researchers described the scene:

The pronghorn on the ground had been partially consumed; all that remained was the head and four limbs held together by dorsal skin, backbone, pelvis, and ribcage. The head of the carcass was still attached to the head of the live, standing pronghorn, which pulled, twisted, and within ca. 1 min freed himself from the carcass.

Is the great speed of the pronghorn attributable to an evolutionary “arms race” with the extinct, fleet-footed cat Miracinonyx? Perhaps, but it would be a mistake to consider the relationship between pronghorns and their predators as only a matter of speed. Infant and female pronghorn are vulnerable to much slower predators during the fawning season, and male pronghorn may inadvertently grapple their way into very vulnerable positions. Pronghorn are not withering away while waiting for a long-lost superpredator to reappear and kickstart their evolution – they continue to be actors in the Darwinian “struggle for existence” in which the rules, and competitors, are subject to change at any time.

Kerey Barnowe-Meyer, P.J. White, Troy Davis, and John Byers (2009). Predator-Specific Mortality of Pronghorn on Yellowstone’s Northern Range Western North American Naturalist, 69 (2), 186-194 DOI: 10.3398/064.069.0207

Chipault, J., & Long, D. (2010). Pronghorn (Antilocapra americana) Locked in Fight Becomes Prey of Coyotes (Canis latrans) The Southwestern Naturalist, 55 (2), 283-284 DOI: 10.1894/TAL-07.1

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