Mighty Dons Of Science News

Artist'sren­der­ing of what HD 131488's in­ner plan­e­tary sys­tem might look like as two large rocky bod­ies col­lide. In­set il­lus­trates the lo­ca­tion of HD 131488's dust belts (top) and com­pa­ra­ble re­gions to our own So­lar Sys­tem (bot­tom). HD 131488's hot in­ner dust belt has si­m­i­lar sep­a­ra­tions from its host star as the ter­res­tri­al plan­et zone around our Sun while the star's cool dust belt has si­m­i­lar sep­a­ra­tions from its host star as the Kuiper Belt re­gion in our So­lar Sys­tem. Al­so shown for our So­lar Sys­tem are the or­bits of Ju­pi­ter, Sat­urn, Ura­nus, and Nep­tune.</font> (Cour­te­sy Gem­i­ni Ob­serv­a­to­ry)

A far-off so­lar sys­tem seems to be form­ing from a strange dust whose make­up is un­like that of our and oth­er so­lar sys­tems, as­tro­no­mers say.

The researchers at the Univers­ity of Cal­i­for­nia Los An­ge­les found ev­i­dence for the forma­t­ion of young, rocky plan­ets from dust cir­cling a star some 500 light-years away. A light-year is the dis­tance light trav­els in a year

“Un­til now, warm dust found around oth­er stars has been very si­m­i­lar in com­po­si­tion to as­ter­oi­dal or com­et­ary ma­te­ri­al in our So­lar Sys­tem,” said the uni­vers­ity’s Carl Melis, who led the re­search while a grad­u­ate stu­dent.

But this case is diff­er­ent, he said.

“Typic­ally, dust de­bris around oth­er stars, or our own Sun, is of the ol­i­vine, py­rox­ene, or sil­ica va­ri­e­ty, min­er­als com­monly found on Earth,” he noted. But this ma­te­ri­al “is not one of these dust types. We have yet to iden­ti­fy what spe­cies it is.”

Melis re­ported the find­ings last Wednes­day at the annual Amer­i­can As­tro­nom­i­cal So­ci­e­ty meet­ing in Wash­ing­ton, D.C.

The star, known as HD 131488, ap­pears to be sur­rounded by warm dust in a re­gion called the ter­res­tri­al plan­et zone, where tem­per­a­tures are si­m­i­lar to those on Earth, Melis said. He added that the dust seems to harbor rocky, emb­ry­onic planets that have re­cently coll­ided.

“What makes HD 131488 truly un­ique is the un­iden­ti­fied dust spe­cies re­leased from the col­lid­ing bod­ies as well as the pres­ence of cold dust far away from the star,” said as­tron­o­mer Ben­ja­min Zuck­er­man of the univers­ity, a co-author of the re­search. “These two char­ac­ter­is­tics make HD 131488 un­like any oth­er star with ev­i­dence for mas­sive quanti­ties of dust in its ter­res­tri­al plan­et zone.”

The re­search­ers an­a­lyzed the warm in­ner dust through in­fra­red im­ag­ing and spec­tros­co­py us­ing an in­stru­ment called T-ReCS on the Gem­i­ni South tel­e­scope in Chil­e. Spec­tros­co­py is the anal­y­sis of the com­po­si­tion of ob­jects us­ing the spec­trum of light they give off.

Melis and his team ar­gue that the most plau­si­ble ex­plana­t­ion for the un­usu­al abun­dance of warm dust is a re­cent col­li­sion of two rocky plan­e­tary mass bod­ies.

While the mys­te­ri­ous warm dust lies at a dis­tance from HD 131488 that is com­pa­ra­ble to the Earth-Sun separa­t­ion, the team al­so found cool­er dust about 45 times fur­ther out. This out­er dusty re­gion is anal­o­gous to the Kuiper Belt in our own So­lar Sys­tem where many mi­nor plan­ets or­bit the Sun just be­yond the or­bit of Nep­tune.

“The hot dust al­most cer­tainly came from a re­cent cat­a­stroph­ic col­li­sion be­tween two large rocky bod­ies in HD 131488’s in­ner plan­e­tary sys­tem,” Melis said. But the cool­er dust “is probably left over from plan­et forma­t­ion that took place far­ther away from HD 131488.”

HD 131488 lies in the di­rec­tion of the con­stella­t­ion Cen­tau­rus and is three times heav­i­er and 33 times more lu­mi­nous than our own Sun. The star is part of a ma­jor, south­ern-hem­i­sphere star form­ing re­gion known as the Upper-Cen­tau­rus-Lupus as­socia­t­ion whose mem­bers are be­lieved to be about 10 mil­lion years old. By con­trast, the Sun and Earth are about 4.6 bil­lion years old..

In adult fe­male mice, switch­ing off one gene seems to start turn­ing the ovaries in­to tes­ti­cles and trig­gers the pro­duct­ion of male hor­mones at nor­mal male levels, sci­en­tists say.

The cu­ri­ous find­ings have led two re­search­ers to re­mark in a pub­lished pa­per that, bi­o­log­ic­ally speak­ing, fe­males may be en­gaged in a life­long “bat­tle to sup­press their in­ner ma­le.”

Both pa­pers ap­pear in the Dec. 11 is­sue of the re­search jour­nal Cell.

The new results echo a pre­vious study that found that fe­male ovar­ian tissues in mice start to con­vert to male-like tis­sues in the ab­sence of sig­nals from es­tro­gen, a fe­male sex hor­mone. That stu­dy ap­peared in the Dec. 17, 1999 is­sue of the jour­nal Science.

In the newer re­search, N. Hen­ri­ette Uh­len­haut of the Eu­ro­pe­an Mo­lec­u­lar Bi­ol­o­gy Lab­o­r­a­to­ry in Hei­del­berg, Ger­ma­ny, and col­leagues were stu­dy­ing genes that dur­ing de­vel­op­ment are re­spon­si­ble for con­vert­ing glands called go­nads in­to ei­ther ovaries or tes­ti­cles, de­pend­ing on the sex.

Ovaries produce eggs, the fe­male sex cells, while tes­ti­cles produce sperm.

Uh­len­haut and col­leagues ge­net­ic­ally en­gi­neered mice in which the ac­ti­vity of a called Fox2L could be chem­ic­ally sup­pressed in the ovaries.

Fox2L, in turn, is a reg­u­la­tor gene that in­flu­ences the lev­el of ac­ti­vity of an ar­ray of oth­er genes. Among oth­er things, it keeps in check genes that tend to pro­mote tes­ti­cle de­vel­op­ment, ac­cord­ing to Uh­len­haut’s group.

Switch­ing off Fox2L had the im­me­di­ate ef­fect of in­creas­ing the lev­el of ac­ti­vity of some of these “tes­tis-specific” genes, the sci­en­tists re­ported. Crit­i­cal among these, they iden­ti­fied one called Sox9.

Con­com­i­tant with the boost in Sox9 ac­ti­vity was a “re­pro­gram­ming” of cer­tain ovar­i­an cell lin­eages in­to what ap­peared to be tes­tis cell lin­eages, Uh­len­haut and col­leagues found. Mean­while, the mod­i­fied ovaries be­gan pro­duc­ing nor­mal ma­le-like lev­els of the hor­mone tes­tos­ter­one.

“Our re­sults show that main­te­nance of the ovar­i­an phe­no­type [form] is an ac­tive pro­cess through­out life,” the sci­en­tists wrote.

It’s un­clear wheth­er the find­ings would trans­late to hu­mans, but be­cause mice share over 90 per­cent of their genes with hu­mans, it very of­ten hap­pens that mouse pro­cesses have par­al­lels in hu­mans.

It would seem “tes­tic­u­lar de­vel­op­ment is ac­tively re­pressed through­out the life of fe­ma­les,” added An­drew Sin­clair and Craig Smith of the Mur­doch Chil­dren’s Re­search In­sti­tute in Mel­bourne, Aus­tral­ia, in a pa­per pub­lished in the same is­sue of Cell. Sin­clair and Smith the re­search­ers who in their ar­ti­cle metaphoric­ally sug­gested an “in­ner ma­le” may lurk with­in all fe­ma­les also not­ed the find­ings go against “con­ven­tional wis­dom” that the ova­ry and tes­tis are “ter­mi­nally dif­fer­en­ti­ated,” or ir­re­versibly de­vel­oped to their ma­ture state.

Sci­en­tists have found that pri­ons in­fec­tious mol­e­cules that cause fa­tal brain dis­eases can evolve in a Dar­win­i­an fash­ion, though they lack any DNA or si­m­i­lar ma­te­ri­al.

The study from Scripps Re­search In­sti­tute in Ju­pi­ter, Fla. found that pri­ons can de­vel­op many muta­t­ions. Muta­t­ions that help the pri­ons to with­stand threats then tend to per­sist in a “popula­t­ion” of pri­ons, while oth­er pri­ons are de­stroyed. This even­tu­ally leads the pri­ons to de­vel­op adapta­t­ions such as drug re­sist­ance.

The pro­cess in oth­er words would seem to be analogous to the way that liv­ing things evolve, ac­cord­ing to Dar­win­ist prin­ci­ples. Vi­rus­es, too which are of­ten con­sid­ered non-liv­ing can evolve. But un­like pri­ons, vi­ruses have in com­mon with life forms that they con­tain DNA or closely re­lat­ed mol­e­cule, RNA.

The prion study was pub­lished in the Dec. 31 is­sue of the re­search jour­nal Sci­ence Ex­press, an ad­vance, on­line edi­tion of the jour­nal Sci­ence.

Pri­ons con­sist of pro­teins, large mol­e­cule com­posed of many smaller mo­lec­u­lar sub­units of so-called ami­no acids. Pro­tein mol­e­cules have dif­fer­ent char­ac­ter­is­tics de­pend­ing on the pre­cise ar­range­ment of their sub­units. This in­cludes dif­fer­ent ways the pro­tein’s parts can be folded about with re­spect to each oth­er.

Many of the pri­on “muta­t­ions” boil down to dif­fer­ent fold­ing ar­range­ments, said Charles Weiss­mann, head of Scripps Flori­da’s De­part­ment of In­fec­tol­ogy, who led the stu­dy. These var­i­ous fold­ings play an anal­o­gous ev­o­lu­tion­ary role in pri­ons to dif­fer­ent DNA se­quences, or codes, in the ev­o­lu­tion of liv­ing things.

“On the face of it, you have ex­actly the same pro­cess of muta­t­ion and adaptive change in pri­ons as you see in vi­rus­es,” he ex­plained.

In­fec­tious pri­ons short for pro­tein­a­ceous in­fec­tious par­t­i­cles are as­so­ci­at­ed with some 20 dif­fer­ent dis­eases in hu­mans and an­i­mals, in­clud­ing mad cow dis­ease and a rare hu­man form, Creutzfeldt-Jakob dis­ease. All are un­treat­able and even­tu­ally fa­tal. Pri­ons, which are com­posed solely of pro­tein, are clas­si­fied by dis­tinct strains, orig­i­nally char­ac­terized by their in­cuba­t­ion time and the dis­ease they cause.

Pri­ons ex­ist in a nor­mal, healthy form, pro­duced nat­u­rally in mam­ma­li­an cells, called cel­lu­lar pri­on pro­tein or PrPC. The dis­ease pro­cess be­gins when pri­ons take on an abnor­mal, mis­folded form. A nor­mal pri­on that comes in­to con­tact with a mis­folded one may as a re­sult be­come mis­folded it­self. This zom­bie-like pro­cess may even­tually lead to the creation of huge as­sem­blies of these mis­folded pro­teins. They stick to­geth­er and cause mas­sive dam­age.

“It was gen­er­ally thought that once cel­lu­lar pri­on pro­tein was con­vert­ed in­to the abnor­mal form, there was no fur­ther change,” Weiss­mann said. “But there have been hints that some­thing was hap­pen­ing. When you trans­mit pri­ons from sheep to mice, they be­come more vir­u­lent over time. Now we know that the abnor­mal pri­ons rep­li­cate, and cre­ate vari­ants, per­haps at a low lev­el in­i­tial­ly. But once they are trans­ferred to a new host, nat­u­ral se­lec­tion will even­tu­ally choose the more vir­u­lent and ag­gres­sive vari­ants.”

Weiss­mann and his col­leagues trans­ferred pri­on popula­t­ions from in­fected brain cells to cul­ture cells. When trans­planted, cell-a­dapted pri­ons de­vel­oped and out-competed their brain-a­dapted coun­ter­parts, con­firm­ing pri­ons’ abil­ity to adapt to new sur­round­ings, ac­cord­ing to the sci­en­tists. When re­turned to brain, brain-a­dapted pri­ons again took over the popula­t­ion.

Weiss­mann said the find­ings have im­plica­t­ions for the de­vel­op­ment of treat­ments. In­stead of de­vel­oping drugs to tar­get abnor­mal pro­teins, it could be more ef­fi­cient to try to lim­it the supply of nor­mally pro­duced pri­ons – in es­sence, re­duc­ing the amount of fu­el for the fire, he pro­posed. Weiss­mann and his col­leagues found some 15 years ago that ge­net­ic­ally en­gi­neered mice de­void of the nor­mal pri­on pro­tein de­vel­op and func­tion quite nor­mally and are re­sist­ant to pri­on dis­ease.

“Find­ing a way to in­hib­it the pro­duc­tion of nor­mal pri­on pro­tein is a proj­ect cur­rently be­ing pur­sued in col­la­bora­t­ion with Scripps Flor­i­da Pro­fes­sor Co­rinne Las­mezas in our de­part­ment,” he said.

In a study that could help clar­i­fy the com­plex rela­t­ion­ships be­tween the brain, en­vi­ron­ment and be­hav­ior, re­search­ers have found that four-month-old in­fants’ tem­per­a­ment pre­dicts some as­pects of their brain struc­ture 18 years lat­er.

Sci­en­tists at Mas­sa­chu­setts Gen­er­al Hos­pi­tal in Charles­town, Mass., stud­ied 76 eighteen-year-olds that, at four months of age, had been cat­e­go­rized in pre­vi­ous re­search as “high-reac­tive” or “low-reac­tive.” High-reac­tive gen­er­ally means shy and in­hib­ited, while low-reac­tive means out­go­ing and un­in­hib­ited.

The in­ves­ti­ga­tors used a form of brain scan­ning known as struc­tur­al mag­net­ic res­o­nance im­ag­ing, which em­ploys mag­net­ic field and ra­di­o waves to pro­duce clear and de­tailed pic­tures of the brain.

Adults with a low-reac­tive in­fant tem­per­a­ment showed great­er thick­ness in a brain struc­ture called the left or­bitofrontal cor­tex, the sci­en­tists found. This re­gion has been im­pli­cat­ed in pro­cess­ing of emo­tions and of self-monitoring.

On the oth­er hand, the adults pre­vi­ously cat­e­go­rized as high-reac­tive, showed great­er thick­ness in the right ven­tro­me­dial pre­fron­tal cor­tex, the re­search­ers re­ported. This brain ar­ea has been linked to im­pulse con­trol, with great­er size linked to more self-con­trol, and with the anal­y­sis of so­cial situa­t­ions.

“To our knowl­edge, this is the first demon­stra­t­ion that tem­per­a­mental dif­fer­ences meas­ured at four months of age have im­plica­t­ions for the ar­chi­tec­ture of hu­man cer­e­bral cor­tex last­ing in­to adult­hood,” the re­search­ers wrote in the stu­dy, pub­lished in the Jan­u­ary is­sue of the jour­nal Ar­chives of Gen­er­al Psy­chi­a­try. The cer­e­bral cor­tex is a lay­er of brain cells cov­er­ing the sur­face of the brain and linked to ad­vanced think­ing func­tions.

High-reac­tive in­fants are char­ac­ter­ized at age four months by vig­or­ous ac­ti­vity and cry­ing in re­sponse to un­fa­mil­iar stim­u­li, ac­cord­ing to the au­thors, Carl Schwartz, di­rec­tor of the hos­pi­tal’s De­vel­op­men­tal Neuroim­ag­ing and Psy­cho­pa­thol&sh Re­search Lab­o­r­a­to­ry, and col­leagues. Low-reac­tive in­fants by con­trast stay more still and cry less in re­spose to the same situa­t­ions.

High-reac­tive in­fants tend to be­come be­hav­iorally in­hib­ited in the sec­ond year of life, while low-reac­tive in­fants tend the op­po­site way, the au­thors added.