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Ophiocordyceps unilateralis infected ant from random web search.

Parasite causes zombie ants to die in an ideal spot
Contact: Kevin Stacey, kstacey@press.uchicago.edu  |  University of Chicago Press Journals  |  11-Aug-2009

A study in the September issue of The American Naturalist describes new details about a fungal parasite that coerces ants into dying in just the right spot—one that is ideal for the fungus to grow and reproduce. The study, led David P. Hughes of Harvard University, shows just how precisely the fungus manipulates the behavior of its hapless hosts.

When a carpenter ant is infected by a fungus known as Ophiocordyceps unilateralis, the victim remains alive for a short time. The fungus, however, is firmly in the driver’s seat. It compels the ant to climb from its nest high in the forest canopy down into small plants and saplings in the understory vegetation. The ant then climbs out onto the underside of a low-hanging leaf where it clamps down with its mandibles just before it dies. There it remains, stuck fast for weeks.

After the ant dies, the fungus continues to grow inside the body. After a few days, a stroma—the fungus’s fruiting body—sprouts from the back of the ant’s head. After a week or two, the stroma starts raining down spores to the forest floor below. Each spore has the potential to infect another unfortunate passerby.

Scientists have known for over one hundred years about this parasite’s ghastly ability to turn unsuspecting ants into zombies. But Hughes and his colleagues chronicle the amazingly precise control the fungus has over its victim.

At a field site in a Thai forest, Hughes’s team found that the infected carpenter ants are almost invariably found clamped onto the undersides of leaves that are 25 centimeters (about 10 inches) from the ground below. What’s more, most of the dead ants were found on leaves sprouting from the northwest side of the plant. Interestingly, the researchers found that temperature, humidity and sunlight in these spots are apparently optimal for the fungus to grow and reproduce. When the researchers placed leaves with infected ants at higher locations, or on the forest floor, the parasite failed to develop properly.

“The fungus accurately manipulates the infected ants into dying where the parasite prefers to be, by making the ants travel a long way during the last hours of their lives,” Hughes said.

But getting the ant to die in the right spot is only half the battle, as the researchers found when they dissected a few victims.

“The fungus has evolved a suite of novel strategies to retain possession of its precious resource,” said Hughes.

As the fungus spreads within a dead ant’s body, it converts the ant’s innards into sugars which are used to help the fungus grow. But it leaves the muscles controlling the mandibles intact to make sure the ant keeps its death grip on the leaf. The fungus also preserves the ant’s outer shell, growing into cracks and crevices to reinforce weak spots. In doing this, the fungus fashions a protective coating that keeps microbes and other fungi out. At that point, it can safely get down to the business of claiming new victims.

Carpenter ants apparently have few defenses against the fungus. The most important way they avoid infection seems to be staying as far away from victims as possible. That may be part of the reason why these ants make their nests in the forest canopy, high above fungal breeding zones. Carpenter ants also seem to avoid blazing their foraging trails under infected areas. This too might be an adaptive strategy to avoid infection, but more study is needed to confirm it, Hughes says.

The mechanisms and cues the fungus uses to control an ant’s behavior remain unknown. “That is another research area we are actively pursuing right now,” Hughes says. Whatever the mechanisms, this much is clear: O. unilateralis has evolved highly specialized abilities to get unsuspecting ants to do its bidding.

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Sandra B. Andersen, Sylvia Gerritsma, Kalsum M. Yusah, David Mayntz, Nigel L. Hywel‐Jones, Johan Billen, Jacobus J. Boomsma, and David P. Hughes, “The Life of a Dead Ant: The Expression of an Adaptive Extended Phenotype.” The American Naturalist, September 2009.

This story is important because it challenges the current “Clovis first” settlers in America and the entire trans-siberian land bridge migration of humans into the Americas. Perhaps, evidence will prove 2 migrations into the Americas, a western one via the land bridge and and eastern one from Europe either following the edge of the ice or straight across the water.

The Debra L Friedkin site lies just outside Austin. Image BBC

Stone tools ‘demand new American story’
By Paul Rincon and Jonathan Amos Science reporters, BBC News  |  24 March 2011

The long-held theory of how humans first populated the Americas may have been well and truly broken.

Archaeologists have unearthed thousands of stone tools that predate the technology widely assumed to have been carried by the first settlers.

The discoveries in Texas are seen as compelling evidence that the so-called Clovis culture does not represent America’s original immigrants.

Details of the 15,500-year-old finds are reported in Science magazine.

A number of digs across the Americas in recent decades had already hinted that the “Clovis first” model was in serious trouble.

But the huge collection of well-dated tools excavated from a creek bed 60km (40 miles) northwest of Austin mean the theory is now dead, argue the Science authors.

“This is almost like a baseball bat to the side of the head of the archaeological community to wake up and say, ‘hey, there are pre-Clovis people here, that we have to stop quibbling and we need to develop a new model for peopling of the Americas’,” Michael Waters, a Texas A&M University anthropologist, told reporters.

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Viruses may by one of the environmental triggers that allows a latent, or dormant potential to become manifest. The study of latent genetic potential is called epigenetics. Epigenetics will forever end the nature vs nurture debate by showing how nature and nurture both affect the genome.

The Insanity Virus
11.08.2010  |  discovermagazine.com  |  by Douglas Fox

Schizophrenia has long been blamed on bad genes or even bad parents. Wrong, says a growing group of psychiatrists. The real culprit, they claim, is a virus that lives entwined in every person’s DNA.

Steven and David Elmore were born identical twins, but their first days in this world could not have been more different. David came home from the hospital after a week. Steven, born four minutes later, stayed behind in the ICU. For a month he hovered near death in an incubator, wracked with fever from what doctors called a dangerous viral infection. Even after Steven recovered, he lagged behind his twin. He lay awake but rarely cried. When his mother smiled at him, he stared back with blank eyes rather than mirroring her smiles as David did. And for several years after the boys began walking, it was Steven who often lost his balance, falling against tables or smashing his lip.

Those early differences might have faded into distant memory, but they gained new significance in light of the twins’ subsequent lives. By the time Steven entered grade school, it appeared that he had hit his stride. The twins seemed to have equalized into the genetic carbon copies that they were: They wore the same shoulder-length, sandy-blond hair. They were both B+ students. They played basketball with the same friends. Steven Elmore had seemingly overcome his rough start. But then, at the age of 17, he began hearing voices.

The voices called from passing cars as Steven drove to work. They ridiculed his failure to find a girlfriend. Rolling up the car windows and blasting the radio did nothing to silence them. Other voices pursued Steven at home. Three voices called through the windows of his house: two angry men and one woman who begged the men to stop arguing. Another voice thrummed out of the stereo speakers, giving a running commentary on the songs of Steely Dan or Led Zeppelin, which Steven played at night after work. His nerves frayed and he broke down. Within weeks his outbursts landed him in a psychiatric hospital, where doctors determined he had schizophrenia.

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An elegantly simple explanation of how a differential gear works.