Mighty Dons Of Science News

As­tro­no­mers have re­ported find­ing as many as six plan­ets, not many times heav­i­er than Earth, or­bit­ing two near­by Sun-like stars.
The ob­jects, which in­clude two that are about 5 and 7.5 times as heavy as Earth, are rais­ing sci­en­tists’ hopes that it will be just a few years that plan­ets very much like ours turn up.

Image from a sci­en­tists' an­i­ma­tion of the 5-Earth-mass plan­et 61 Vir B, or­bit­ing the star 61 Vir­gi­nis. This plan­et moves in a tight, 4-day or­bit around its star. Half of the plan­et sur­face is much hot­ter than the oth­er half be­cause one side al­ways faces the star. (Cour­tesy U. Hert­ford­shire)

The re­search­ers, led by Ste­ven Vogt of the Un­ivers­ity of Cal­i­for­nia, San­ta Cruz, and Paul But­ler of the Car­ne­gie In­sti­tu­tion of Wash­ing­ton, said the two “super-Earths” are the first ones found around Sun-like stars.

“These de­tec­tions in­di­cate that low-mass plan­ets are quite com­mon around near­by stars. The dis­cov­ery of po­ten­tially hab­it­a­ble near­by worlds may be just a few years away,” said Vogt. As­tro­no­mers claim they’re over­com­ing past dif­fi­cul­ties in find­ing smaller plan­ets, which are more like ours in size and are con­sid­ered like­li­er to be hab­it­a­ble than large plan­ets.

The team found the new plan­et sys­tems by com­bin­ing da­ta gath­ered at the W. M. Keck Ob­serv­a­to­ry in Ha­waii and the An­glo-Aus­tral­ia Tel­e­scope in New South Wales, Aus­tral­ia. Two pa­pers de­scrib­ing the new plan­ets have been ac­cept­ed for pub­lica­t­ion in the As­t­ro­phys­i­cal Jour­nal.

Three of the new plan­ets or­bit the bright star 61 Vir­gi­nis, vis­i­ble with the na­ked eye un­der dark skies in the Spring con­stella­t­ion Vir­go. Space sci­en­tists have long been fas­ci­nat­ed with this star, which is a re­la­tive­ly close 28 light years away (a light year is the dis­tance light trav­els in a year). Among hun­dreds of our near­est stel­lar neigh­bors, 61 Vir stands out as be­ing the most nearly si­m­i­lar to the Sun in terms of age, mass, and oth­er es­sen­tial prop­er­ties.

Vogt and col­leagues have found that 61 Vir hosts at least three plan­ets, weigh­ing in the range of about 5 to 25 Earths. All would be ex­treme­ly hot, though, as they are well with­in orbits equi­va­lent to that of Ve­nus.

Re­cent­ly, a sep­a­rate team of as­tro­no­mers used NASA’s Spitzer Space Tel­e­scope to dis­cov­er that 61 Vir al­so con­tains a thick ring of dust at a dis­tance roughly twice as far from 61 Vir as Plu­to is from our Sun. The dust is ap­par­ently cre­at­ed by col­li­sions of comet-like bod­ies in the cold out­er reaches of the sys­tem.

“Spitzer’s de­tec­tion of cold dust or­bit­ing 61 Vir in­di­cates that there’s a real kin­ship be­tween the Sun and 61 Vir,” said Eu­ge­nio Ri­ve­ra of the Un­ivers­ity of Cal­i­for­nia, San­ta Cruz. Ri­ve­ra com­put­ed an ex­ten­sive set of sim­ula­t­ions to find that a hab­it­a­ble Earth-like world could easily ex­ist in the as-yet un­ex­plored re­gion be­tween the newly dis­cov­ered plan­ets and the out­er dust disk.

Ac­cord­ing to Vogt, the plan­etary sys­tem around 61 Vir is an ex­cel­lent can­di­date for study by the new Au­to­mat­ed Plan­et Find­er Tel­e­scope re­cently con­structed at Lick Ob­serv­a­to­ry on Mount Ham­il­ton near San Jose, Ca­lif. “Need­less to say, we’re very ex­cit­ed to con­tin­ue mon­i­tor­ing this sys­tem” us­ing that de­vice, said Vogt, who is the prin­ci­pal in­ves­ti­ga­tor for the tel­e­scope.

The sec­ond new sys­tem found by the team fea­tures a plan­et weigh­ing the equiv­a­lent of about 7.5 Earths and or­bit­ing the star HD 1461, anoth­er near per­fect twin of the Sun about 76 light-years away. The plan­et, des­ig­nat­ed HD 1461b, is about half­way be­tween Earth and Ura­nus in weight. The re­search­ers said they can­not tell yet if it’s a scaled-up ver­sion of Earth, com­posed largely of rock and iron, or wheth­er, like Ura­nus and Nep­tune, it is made mostly of wa­ter.

At least one and pos­sibly two ad­di­tion­al plan­ets al­so or­bit the star, the group said. Ly­ing in the con­stella­t­ion Ce­tus, HD 1461 can be seen with the na­ked eye in the early eve­ning un­der good dark-sky con­di­tions.

The Lick Car­ne­gie Exoplan­et Sur­vey Team led by Vogt and But­ler uses ve­locity mea­sure­ments from ground-based tel­e­scopes to de­tect the “wob­ble” in­duced in a star by the gravita­t­ional tug of an or­bit­ing plan­et. In the past year, im­prov­ing meth­ods have made it ev­i­dent that plan­ets or­bit­ing the Sun’s near­est neigh­bors are ex­tremely com­mon: cur­rent in­dica­t­ions are that fully half of near­by stars have a de­tectable plan­et with mass equal to or less than Nep­tune’s, But­ler said.

The Lick-Car­ne­gie Exoplan­et Sur­vey Team has de­vel­oped a pub­licly avail­a­ble tool, the Sys­tem­ic Con­sole, which en­ables mem­bers of the pub­lic to search for the sig­nals of ex­tra­so­lar plan­ets by ex­plor­ing real da­ta sets. This tool is avail­a­ble on­line at www.ok­lo.org.

De­spite pop­u­lar con­cep­tions about the hor­mone tes­tos­ter­one, in wom­en, at least, the sub­stance ac­tu­ally may pro­mote fair, con­cil­ia­to­ry be­hav­ior, re­search­ers say.

But the myths about tes­tos­ter­one are so pow­er­ful that wom­en in a study started act­ing less fairly if they thought they had re­ceived a dose of it, wheth­er they had or not.

Such are the find­ings of a study ap­pear­ing in the Dec. 8 ad­vance on­line is­sue of the re­search jour­nal Na­ture.

Test­os­terone is often called the “male” hor­mone and is po­pu­lar­ly asso­ciated with aggres­sion. Wom­en have some test­os­terone also, though.

Ernst Fehr of the Un­ivers­ity of Zu­rich, Switz­er­land, and col­leagues set up a bar­gain­ing game in which fe­male par­ti­ci­pants were giv­en a pill ei­ther of tes­tos­ter­one or of a neu­tral sub­stance, called a pla­ce­bo.

Those that re­ceived tes­tos­ter­one showed a “sub­stan­ti­al in­crease in fair bar­gain­ing be­haviour,” lead­ing to better so­cial in­ter­ac­tions, the re­search­ers wrote. But wom­en who thought that they re­ceived tes­tos­ter­one, wheth­er or not they ac­tu­ally did, “be­haved much more un­fair­ly” than those who thought that they re­ceived pla­ce­bo.

So, the neg­a­tive, an­ti­so­cial con­nota­t­ion of in­creas­ing tes­tos­ter­one lev­els seems to be strong enough to in­duce neg­a­tive so­cial be­hav­iour even when the bi­o­log­i­cal re­sult is ac­tu­ally the op­po­site, the sci­en­tists re­marked.

Ev­i­dence from an­i­mal stud­ies does show that tes­tos­ter­one causes ag­gres­sion to­ward oth­er mem­bers of the spe­cies, Fehr and col­leagues wrote. Pop­u­lar wis­dom tends to as­sume hu­mans work the same way. But it has been un­clear wheth­er this is cor­rect.

Stud­ies have in­deed found that male and fe­male pris­on­ers with vi­o­lent his­to­ries have high­er sal­i­vary tes­tos­ter­one lev­els than nonvi­o­lent pris­on­ers, the re­search­ers not­ed. But this does not show that the tes­tos­ter­one ac­tu­ally caused the vi­o­lence.

A com­pet­ing idea, they ob­served, is that tes­tos­ter­one mo­ti­vates peo­ple to seek high so­cial sta­tus. De­pend­ing on the situa­t­ion, they may try to achieve that ei­ther through vi­o­lence or through fair­ness.

In the con­text of the ex­pe­ri­men­tal bar­gain­ing game, fair­ness tended to help pro­tect so­cial sta­tus, ac­cord­ing to Fehr and col­leagues.

In the “ul­ti­ma­tum game,” as it was called, two play­ers are pre­sented with a sum of mon­ey, which they can keep if they can agree on how to split it. The catch is that just one play­er gets to pro­pose—and only on­ce—how it should be di­vid­ed. The oth­er play­er must ac­cept or re­ject that of­fer. “Fair” of­fers, such as an even split, tend to be more readily ac­cepted than “un­fair” of­fers where the pro­pos­er tries to keep most of the mon­ey. Fehr and col­leagues sug­gested that tes­tos­ter­one mo­ti­vat­ed play­ers to pro­pose “fair­er” of­fers in or­der to avoid the so­cial af­front of re­jection.

Humans and mice have previously unknown and potentially critical differences in one of the genes responsible for Duchenne muscular dystrophy (DMD). Researchers writing in the open access journal BMC Biology have found that two major features of a key DMD gene are present in most mammals, including humans, but are specifically absent in mice and rats, calling into question the use of the mouse as the principal model animal for studying DMD.

Roland Roberts led a team of researchers from King's College London, UK, and was funded by the Muscular Dystrophy Campaign. The team made the discovery while studying α-dystrobrevin, a component of the dystrophin protein complex that is disordered in DMD. Roberts said, "Two previously unrecognized features (a gene switch or promoter and a novel binding site for the adaptor protein syntrophin) are encoded by the α-dystrobrevin gene of almost all four-legged animals except mice. We assume that this tardy recognition of key features of a gene that has been intensively studied since its discovery 13 years ago is due to the predominance of the mouse as the model organism for studying DMD and the specific destruction of these parts of the gene in the mouse."

A major consequence of these findings is that mice (and their rat and hamster relatives) are likely to be particularly poor models in which to study the effects of DMD on the brain. Roberts added, "The brain is the major site of α-dystrobrevin expression and we now know that the mouse is missing more than 50% of the brain α-dystrobrevins. The fact that there are fundamental differences between the brains of mice and humans potentially limits our understanding of the role of dystrobrevins and DMD-related complexes in this organ. In fact, almost all of our knowledge of the function of α-dystrobrevin has been gleaned from the mouse."

DMD is a fatal skeletal myopathy, causing loss of muscle tissue throughout the body. It is also associated with substantial neurological effects including learning difficulties, night blindness, defective color vision and a suggestion of personality disorders, so studying the mechanisms in the brain underlying these effects is crucial.

A chemical culprit responsible for the rapid, mysterious death of phytoplankton in the North Atlantic Ocean has been found by collaborating scientists at Rutgers University and the Woods Hole Oceanographic Institution (WHOI). This same chemical may hold unexpected promise in cancer research.
A photomicrograph of an Emiliania huxleyi cell. The black spots within the cell are the virus, which contains a previously unknown lipid that is killing phytoplankton in the North Atlantic. (Credit: V. Starovoytov and A. Vardi, Rutgers University)

The team discovered a previously unknown lipid, or fatty compound, in a virus that has been attacking and killing Emiliania huxleyi, a phytoplankton that plays a major role in the global carbon cycle.

"Emiliania huxleyi is the rock star of phytoplankton," explains Kay Bidle, Rutgers assistant professor of marine science in the Institute of Marine and Coastal Sciences. "It blooms all over the oceans, and we can easily see it by satellite. We know that these blooms are frequently infected with viruses, and this virus is specific to this phytoplankton."

"The lipids are the key ingredient in the virus that causes the phytoplankton to die," says WHOI scientist Benjamin Van Mooy. "We have a completely different lipid molecule that, as far as we know, is unknown to science."

E. huxleyi grows rapidly in the North Atlantic, "in these big blooms that you can actually see from outer space," Van Mooy says.

"But," adds Van Mooy, "they die just almost as quickly as they start out, and we're not sure why. They die after a few days."

Bidle and Assaf Vardi, a postdoctoral investigator in his laboratory and the study's lead author, had been examining the interaction between the virus and the dying phytoplankton and had developed ideas for how this process works. After Vardi heard lipid expert Van Mooy give a talk in Santa Fe, N.M., he suggested the collaboration between WHOI and Rutgers.

"I saw Ben's talk on marine microbes and lipids…[and] I ran after him," said Vardi. "We told him about our ideas" involving the virus's effect on the phytoplankton.

"They studied the viruses and I study lipids," Van Mooy said. "It seemed like a good mix."

Their paper is published in the Nov. 6 issue of Science., E. huxleyi performs photosynthesis -- "just like plants," says Van Mooy. "They suck up carbon dioxide." In doing so, they reduce the amount of CO2 released into the atmosphere. They form a calcium carbonate shell, also helping to regulate the carbon cycle.

If viruses are killing off phytoplankton, this can increase greenhouse emissions, Van Mooy suggests. "That's important because if viruses infect a whole bunch of cells, then they can't perform photosynthesis, they can't take up carbon dioxide."

In April 2008, Van Mooy's team visited the sites of E. huxleyi blooms during a research cruise between Woods Hole and Bermuda and collected samples for lipid analysis back in the laboratory.

They immediately recognized lipids that were just like those in virally infected E. huxleyi cells grown by the Rutgers team. Helen Fredricks, a research associate with Van Mooy, carried out the lipid analyses at WHOI. "Seeing this viral lipid appear during the course of infection was amazing, and then we found it in the ocean too. We were celebrating in the lab that day."

Adds Vardi: "Viruses are really important players in regulating phytoplankton blooms. We zoom into the bloom and try to understand the interaction between the viruses and host, which is this really important, cosmopolitan, bloom-forming species."

After isolating the viral lipids, the team found that the lipids alone were able to bring about the symptoms of viral infection in the phytoplankton. "The lipids themselves act just like the virus," says Van Mooy. "We can cause the phytoplankton to die by just giving the lipids."

This alone was enough to excite the team. "Now we have a biological marker that we can go out on a ship and look for and identify where this [infection of phytoplankton] is happening and learn how to study it better," Van Mooy says.

But there may be other, even farther-reaching implications. Both the virus and the newly found lipid deal their deadly blow by causing the upper-ocean plants to commit cellular suicide. As a major focus of their research at Rutgers, Bidle's lab has found that "programmed cell death" is an important process in the fate of marine phytoplankton and in the demise of blooms in the oceans. Bidle's group had previously found that successful infection of E. huxleyi induced, and actually required, the programmed cell death pathway.

But programmed cell death is not unique to phytoplankton. It is a common and healthy process in all kinds of cells, including human cells.

According to Vardi, "These lipids can induce programmed cell death in many organisms, including animals and plants. They also enrich in plasma membrane, and they are the port of the cell, where pathogens get in and out of the cell. This is important in viral diseases."

There is also a potential connection with cancer. If a healthy cell is stressed or damaged, usually it will kill itself with programmed cell death. But cancer cells have a defect: "They don't kill themselves," says Bidle.

"It's a critical aspect of cancer research, because cancer cells have figured out a way to turn off the programmed cell death pathway," he says. "In cancer studies, they try to figure out ways to reactivate those pathways."

The lipid may help shed light on why cancer cells are unable to commit suicide. Someday, the researchers say, it might suggest ways to correct that defect. Right now, the lipid is only known to be effective in algae, but in the future, the team is hoping to test the effectiveness of their molecule in experiments with cancer cells.

"There's a long way to go between here and curing cancer," Van Mooy says, "but the potential exists that this molecule could have therapeutic applications in the treatment of human disease, including cancer. Hopefully this paper will pique the interest of other investigators."

More immediately, scientists hope to learn more about the central role phytoplankton -- and viruses -- play in regulating climate. Bidle says this is a particularly interesting virus. "It appears that the virus has…borrowed, copied actually, the genes for this lipid from the host," he says. "Similar genes are still on the host, but the virus has figured out a way to take those genes and put them into its own genome, and alter them enough to make them more toxic."

"We find the biosynthetic pathway for this unique lipid encoded in the virus genome, not only in the host, and this has never been described before in any other virus," Vardi says. "We knew that [lipids] were important, but we were really intrigued about why the virus contained these genes. And what is the role of the pathway in the co-evolution of programmed cell death in the host and virus."

Van Mooy sees it as a struggle between two mighty forces. "The phytoplankton are at one end of the boxing ring and they're taking up carbon dioxide, and the viruses are at the other end, and they're out to kill them. And how that works out controls how much carbon dioxide is taken up.

"We're very interested in understanding what controls these phytoplankton," he says. "I didn't know that much about viruses until I started working on this project and the Rutgers researchers didn't know that much about lipids. So now we're both really onto something here. We're continuing to collaborate. "We have found other interesting lipids from these viruses," says Van Mooy.

"There are probably more out there. And who knows what kind of activities they may be involved with. They may hold a cure for a human disease or they may play unknown role in…phytoplankton.