Wednesday, October 14, 2009

ELECTRIC FISH PLUG IN TO COMMUNICATE

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Just as people plug in to computers, smart phones and electric outlets to communicate, electric fish communicate by quickly plugging special channels into their cells to generate electrical impulses, University of Texas at Austin researchers have discovered.

The fish generate electric fields to navigate, fight and attract mates in murky streams and rivers throughout Central and South America. They do so at night, while trying to avoid predators such as catfish that sense the electric fields.

Generating electricity is costly (ask any homeowner paying for air conditioning during a hot summer), and the fish are using a dimmer switch to save energy by turning their electrical signals up and down, says Harold Zakon, professor of neurobiology.

Zakon, Michael Markham and Lynne McAnelly published their findings on the electric fish in PLoS Biology on Sept. 29.

They found that the dimmer switch comes in the form of sodium channels the fish insert and remove from the membranes of special cells, called electrocytes, within their electric organs. When more sodium channels are in the cell membrane, the electric impulse emitted by the electric organ is greater.

The scientists also show that the process is under the control of hormones. And it is maintained through a day-night circadian rhythm and can change rapidly during social encounters.

"For a vertebrate animal, this is the first account that brings the whole system together from the behavior down to the rapid insertion of channels and in such an ecologically meaningful way," says Markham, a research scientist in the Zakon laboratory. "This is part of the animal's every day activity and it is being regulated very tightly by a low level molecular change."

Markham says the rapidity of the action is particularly stunning.

"This is happening within a matter of two to three minutes," he says. "The machinery is there to make this dramatic remodeling of the cell, and it does so within minutes from the time that some sort of stimulus is introduced in the environment."

The electric impulse can likely be produced so quickly because a reservoir of sodium channels is sitting in storage in the electric cells. When serotonin is released in the fish brain, it initiates the release of adrenocorticotropic hormone from the pituitary gland. This gooses the mechanism that puts more sodium channels in the membrane.

"It's kind of like stepping on the gas in a car sitting there with its engine already running," says Zakon.

When the fish are inactive, they remove the sodium channels from the cell membranes to reduce the intensity of the electric impulse.

The electrocytes in the fishes' electric organ are made of modified muscle cells. This is significant because the vertebrate heart, which is also a muscle, can also add sodium channels to its cells to help it pump faster. The electric organ and heart are discharging constantly, and both organs are energetically costly.

"One big question for us in the future is, did this mechanism evolve once a long time ago or is this a case of convergent evolution, where the vertebrate heart evolved the ability to traffic these channels and then the electric organ evolved the same ability independently?" says Zakon.

University of Texas

IN AMOEBA WORLD, CHEATING DOESN'T PAY

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Cheaters may prosper in the short term, but over time they seem doomed to fail, at least in the microscopic world of amoebas where natural selection favors the noble.

But why? Shouldn't "survival of the fittest" give the sneaky cheaters an edge? Not necessarily, as it turns out amoebas that cooperate for the benefit of all – and even die for the cause – bring their own genetic weapons to the fight.

Researchers from Rice University and the Baylor College of Medicine (BCM) are peeling back the layers of strategy that determine how colonies of social amoebas resist the efforts of cheaters to alter the balance of power.

In work appearing today in Nature, Rice evolutionary biologists Joan Strassmann and David Queller join forces with BCM geneticist Gad Shaulsky to determine how altruistic mutants help preserve cooperative behavior by single-celled amoebas.

In the paper titled "Cheater-resistance is not futile" ("Star Trek" fans take note), they found Dictyostelium discoideum, amoebas that thrive on rotting vegetation in forest soil, mutate to keep "cheaters" at bay, forcing them out of the reproductive chain.

Dictyostelium fascinate researchers because so many of them willingly give up their lives to save others of their colony – a characteristic seen at all rungs on the ladder of life, but only recently studied at the genetic level. Commonly known as slime molds, these amoebas are not slimy and are not molds. They are independent, bacteria-munching creatures that live alone until the food at a particular location runs out.

When that happens, thousands of amoebas clump into a slug and move as a unit towards heat and light – signposts for food. When they reach their destination, amoebas at the front of the slug sacrifice themselves, turning into a dead, cellulose stalk. The rest of the amoebas pile on, combining to produce spores that sit precariously atop the stalk until wind, insects or other outside forces can carry them to a better place. The whole construct, known as a fruiting body, looks like a tiny balloon on a string.
However, during the journey some Dictyostelium do their best to stay in the back of the slug, thus avoiding the fate of the 20 percent of colony-dwellers that die for the good of the collective. The cheaters quite happily take Gen. George S. Patton's advice to heart: Good soldiers don't die for their country, they make others die for theirs.

By that logic, the researchers noted the cheaters should dominate. But altruistic amoebas – at least those that survive – seem to know when there's a fink in the ranks, and draw upon weapons in their genetic code to keep cheaters at bay.

"In some ways it's no surprise that resistance to cheaters has evolved," said Strassmann, Rice's Harry C. and Olga K. Wiess Professor and co-author of the paper with Queller, the Harry C. and Olga K. Wiess Professor of Ecology and Evolutionary Biology; Shaulsky; BCM professor Adam Kuspa; Lorenzo Santorelli, who earned his doctorate at Rice, worked on the project at BCM and is now a postdoctoral fellow at Oxford; and primary author Anupama Khare, a graduate student in Shaulsky's BCM lab.

"In this study Anu has demonstrated so clearly and cleanly such a response to cheaters at the molecular level," said Strassmann.

The researchers found that cheater cells inserted into a population of mutants would "select" Dictyostelium strains that contained a particular resistor gene. Strong cheaters would push a high percentage of altruistic cells – for whom resistance was indeed futile – to the front of the slug, where they would do their duty and die. But a small percentage of resistant amoebas refused to be pushed around, and over successive generations of growth those resistant strains came to dominate. By the sixth cycle of spore production and germination, the resistant mutants had increased their numbers 100-fold, to the detriment of the cheaters.

"Think of them as the firebreaks that prevent the flames from spreading," said Shaulsky.

Repeated experiments suggested the presence of cheaters inevitably gives rise to cheater-resistant mutations and that such spontaneous mutations were in fact the most robust (more so than when researchers inserted resistant genes into "wild" strains of Dictyostelium). By and large, the mutants retained their altruistic characteristics. "It's very interesting that these resisters are noble, in the sense that they themselves do not exploit their ancestor," said Strassmann.

And when resistors, cheaters and wild strains were mixed evenly, the researchers found to their surprise that the cheater-resistant strains afforded extra protection to the otherwise-defenseless wild amoebas – a kind of molecular inoculation.

Queller noted the results are the latest in an ongoing collaboration between Rice and the Shaulsky and Kuspa groups at BCM. "It shows how productive and innovative cross-disciplinary collaborations can be," he said.

Rice University

SAN ANDREAS AFFECTED BY 2004 SUMATRAN QUAKE

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U.S. seismologists have found evidence that the massive 2004 earthquake that triggered killer tsunamis throughout the Indian Ocean weakened at least a portion of California's famed San Andreas Fault. The results, which appear in the journal Nature, suggest that the Earth's largest earthquakes can weaken fault zones worldwide and may trigger periods of increased global seismic activity.

"An unusually high number of magnitude 8 earthquakes occurred worldwide in 2005 and 2006," said study co-author Fenglin Niu, associate professor of Earth science at Rice University. "There has been speculation that these were somehow triggered by the Sumatran-Andaman earthquake that occurred on Dec. 26, 2004, but this is the first direct evidence that the quake could change fault strength of a fault remotely."

Earthquakes are caused when a fault fails, either because of the buildup of stress or because of the weakening of the fault. The latter is more difficult to measure.

The magnitude 9 earthquake in 2004 occurred beneath the ocean west of Sumatra and was the second-largest quake ever measured by seismograph. The temblor spawned tsunamis as large as 100 feet that killed an estimated 230,000, mostly in Indonesia, Sri Lanka, India and Thailand.

In the new study, Niu and co-authors Taka'aki Taira and Paul Silver, both of the Carnegie Institution of Science in Washington, D.C., and Robert Nadeau of the University of California, Berkeley, examined more than 20 years of seismic records from Parkfield, Calif., which sits astride the San Andreas Fault.

The team zeroed in on a set of repeating microearthquakes that occurred near Parkfield over two decades. Each of these tiny quakes originated in almost exactly the same location. By closely comparing seismic readings from these quakes, the team was able to determine the "fault strength" -- the shear stress level required to cause the fault to slip -- at Parkfield between 1987 and 2008.

The team found fault strength changed markedly at three times during the 20-year period. The authors surmised that the 1992 Landers earthquake, a magnitude 7 quake north of Palm Springs, Calif. -- about 200 miles from Parkfield -- caused the first of these changes. The study found the Landers quake destabilized the fault near Parkfield, causing a series of magnitude 4 quakes and a notable "aseismic" event -- a movement of the fault that played out over several months -- in 1993.

The second change in fault strength occurred in conjunction with a magnitude 6 earthquake at Parkfield in September 2004. The team found another change at Parkfield later that year that could not be accounted for by the September quake alone. Eventually, they were able to narrow the onset of this third shift to a five-day window in late December during which the Sumatran quake occurred.

"The long-range influence of the 2004 Sumatran-Andaman earthquake on this patch of the San Andreas suggests that the quake may have affected other faults, bringing a significant fraction of them closer to failure," said Taira. "This hypothesis appears to be borne out by the unusually high number of large earthquakes that occurred in the three years after the Sumatran-Andaman quake."

Rice University

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