Obesity: Switching fat to lean

Summaries of newsworthy papers include Imaging of filaments from a giant galaxy, Oxidation strikes gold, Bacteria sacrifice themselves for the greater good, Ice clouds in the martian atmosphere, A potentially dangerous molecule on the loose and What a tangled web


This press release is copyright Nature.

VOL.454 NO.7207 DATED 21 AUGUST 2008

This press release contains:

· Summaries of newsworthy papers:

Obesity: Switching fat to lean

Hubble Space Telescope: Imaging of filaments from a giant galaxy

Catalysis: Oxidation strikes gold

Disease: Bacteria sacrifice themselves for the greater good

Planetary science: Ice clouds in the martian atmosphere

Tumour suppressors: A potentially dangerous molecule on the loose

And finally… What a tangled web

· Mention of papers to be published at the same time with the same embargo

· Geographical listing of authors

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[1] & [2] Obesity: Switching fat to lean (pp 1000-1004; 961-967; N&V)

Fat is more related to muscle than we realise, according to research published in Nature this week. In two related studies, scientists identify the factors that regulate fat formation. The research could help to develop new therapies to tackle obesity.

Although we all wish we had a little less of it, fat is essential for managing our energy balance and helping to regulate body temperature. There are two distinct types of fat tissue, with very different functions: white ‘bad’ fat acts as an energy store whereas brown ‘good’ fat helps in burning calories to generate body heat.

Yu-Hua Tseng and colleagues looked at the factors regulating fat tissue development and identified one factor — bone morphogenetic protein 7 (BMP7) — that uniquely promotes brown fat development. They showed that without BMP7 the stocks of brown fat in mouse embryos run low. When excess BMP7 was artificially introduced into mice, they observed a marked increase in brown fat whereas white fat remained normal.

Bruce Spiegelman and colleagues show that the two types of fat develop from distinct cell types in the early embryo. Following the fate of these cells, they observed brown fat to share a developmental pathway with muscle. PRDM16 is identified as the factor that regulates the switch between muscle and fat; in its absence, cells become muscle, but an excess pushes them to become brown, but not white, fat.

In a related News and Views article, Barbara Cannon comments that the research could “take us a step closer to the ultimate goal of promoting the brown fat lineage as a potential way of counteracting obesity”.

Yu-Hua Tseng (Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA) Author paper [1]
Tel: +1 617 735 1967; E-mail: [email protected]

Bruce Spiegelman (Dana-Farber Cancer Institute, Boston, MA, USA) Author paper [2]
Tel: +1 617 632 3567; E-mail: [email protected]

Barbara Cannon (The Wenner-Gren Institute, Stockholm University, Sweden) N&V author
Tel: +46 8 164 120; E-mail: [email protected]

[3] Hubble Space Telescope: Imaging of filaments from a giant galaxy (pp 968-970)

The giant elliptical galaxy NGC 1275 lies at the centre of a group of galaxies known as the Perseus cluster. It is surrounded by a huge glowing cloud of 100-million-year-old filaments. A paper in this week’s Nature describes the structure of these enormous filaments, obtained from Hubble Space Telescope images, and suggests how they might be stabilized in space.

Why NGC 1275’s filaments don’t break down and dissipate into the surrounding roasting hot gas has been a mystery until now. Andrew Fabian and colleagues analysed the telescope’s colour images of the filaments and found they were made up of long, narrow thread-like structures. They believe that magnetic fields in the threads, in pressure balance with the surrounding gas, stabilize the filaments.

Andrew Fabian (University of Cambridge, UK)
Tel: +44 1223 337509; E-mail: [email protected]

[4] Catalysis: Oxidation strikes gold (pp 981-983; N&V)

Gold is prized so highly because it is inert — it does not corrode or tarnish, and so retains its shine and lustre. But this all changes at the nanoscale, where minute gold particles start to show remarkable catalytic activity. A paper in this week’s Nature reports a particularly interesting example of this striking transformation in the metal’s behaviour.

Owain Vaughan and colleagues use 55-atom clusters to deposit 1.4-nanometre gold particles onto inert support materials. Despite the use of an inert support, and although the addition of initiators is avoided, the particles can catalyse the selective oxidation of styrene by molecular oxygen; in contrast, larger gold particles with diameters of 2 nm or larger have no effect. The researchers infer from these observations that the catalytic activity arises from the altered electronic structure that is intrinsic to small gold nanoparticles.

The surprising effectiveness of gold catalysts is important in industrial selective oxidation reactions. As the 1.4-nm particles are also robust and stable, the team’s cluster-based approach could offer a viable route to the synthesis of powerful gold catalysts suitable in practical applications.

Owain Vaughan (University of Cambridge, UK)
Tel: +44 20 7014 4045; E-mail: [email protected]

Owain Vaughan was involved in this research while at Cambridge University but is currently employed by Nature Nanotechnology.

Wayne Goodman (Texas A&M University, College Station TX, USA) N&V author
Tel: +1 979 845 0214; E-mail: [email protected]

[5] Disease: Bacteria sacrifice themselves for the greater good (pp 987-990)

Pathogenic bacteria such as Salmonella can evolve the ability to sacrifice themselves for the sake of their fellows, potentially resulting in stronger and more damaging infections, a new evolutionary analysis suggests.

The phenomenon, called self-destructive cooperation, can help bacterial infections gain a foothold in diseases such as Salmonella enterocolitis, which involves colonization of the gut. By studying mice infected with the bacterium, researchers led by Michael Doebeli demonstrate how some Salmonella cells split open and release inflammation-inducing molecules, laying down their lives in the process but giving their fellow cells the chance to thrive in the gut.

Doebeli and colleagues also describe a computer analysis showing how such behaviour can evolve in pathogen populations. If the population members all have the genes for this selfless behaviour, but only a subset of cells actually go through with this sacrificial activity, then those genes will persist in the population because of the benefit they confer to the survivors.

Michael Doebeli (University of British Columbia, Vancouver, BC, Canada)
Tel: +1 604 822 3326; E-mail: [email protected]

[6] Planetary science: Ice clouds in the martian atmosphere (pp 971-975)

Clouds of ice have an important role controlling the stability and composition of the martian atmosphere. Planetary scientists made the discovery by analysing fresh observations from the Mars-Express spacecraft that has been circling the ‘red planet’ since 2003.

Franck Lefèvre and colleagues report in this week’s Nature that the inclusion of chemical reactions occurring on ice clouds in their model study greatly improved the agreement between observed ozone levels and model simulations, in comparison with model simulations based on gas phase chemistry alone.

Mars’s ozone is degraded by reactions with destructive chemicals called hydrogen radicals on the surface of the ice clouds. The hydrogen radicals also initiate catalytic cycles that recycle carbon dioxide, the main component of the martian atmosphere. Ozone is therefore a sensitive tracer of the chemistry that regulates the atmosphere of Mars. The findings of Lefèvre and colleagues indicate that factoring in the chemistry on ice clouds gives a better account of the behaviour of the planet’s largely carbon-dioxide-based atmosphere.

Franck Lefèvre (Université Pierre et Marie Curie, Paris, France)
Tel: +33 1 44 27 47 73; E-mail: [email protected]

[7] Tumour suppressors: A potentially dangerous molecule on the loose (AOP)
DOI: 10.1038/nature07290

***This paper will be published electronically on Nature's website on 20 August at 1800 London time / 1300 US Eastern time (which is also when the embargo lifts) as part of our AOP (ahead of print) programme. Although we have included it on this release to avoid multiple mailings it will not appear in print on 21 August, but at a later date. ***

Ubiquitin is a small protein that is used to tag other proteins inside the cell — among other things, to earmark it for localization to a particular cellular compartment. A paper in this week’s Nature reveals how losing this tag can cause a protein called PTEN to break loose from the cell nucleus and stop it carrying out its normal function of nipping potential cancers in the bud.

Pier Paolo Pandolfi and colleagues show that an enzyme agent known as HAUSP is responsible for removing PTEN’s ubiquitin tag — if for any reason HAUSP becomes overactive, this deubiquitinylation will drive PTEN out of the cell nucleus and cause its important tumour-suppressing ability to be lost. Under these circumstances, human prostate cancer, for example, rapidly takes off.

The team found that another molecule in the nucleus, PML, normally keeps PTEN in place by curtailing HAUSP’s overactivity. PML is therefore also a tumour suppressor, and can give rise to an acute form of leukaemia if it mutates into a form with disrupted activity.

Dissecting this network and discovering how it can go wrong in aggressive cancers raises the possibility of designing drugs to prevent the rogue relocation of PTEN and keep a humdrum housekeeping process from going haywire.

Pier Paolo Pandolfi (Beth Israel Deaconess Medical Center, Boston, MA, USA)
Tel: +1 617 667 3289; E-mail: [email protected]

[8] And finally… What a tangled web (AOP)
DOI: 10.1038/nature07235

***This paper will be published electronically on Nature's website on 20 August at 1800 London time / 1300 US Eastern time (which is also when the embargo lifts) as part of our AOP (ahead of print) programme. Although we have included it on this release to avoid multiple mailings it will not appear in print on 21 August, but at a later date. ***

The carbon/nutrient balance of the ocean’s microbial food web may have unexpected effects on the global carbon cycle, a study in this week’s Nature suggests.

The fate of carbon in the ocean is determined by the marine food web, so it is important to understand species interactions and how they are affected by nutrient supply to predict the dynamics of the carbon cycle. Frede Thingstad and colleagues altered the organic carbon/nutrient balance in special tanks housing phytoplankton, designed to mimic the Arctic ecosystem. They then added degradable organic carbon, with very unexpected results.

When bacterial growth was limited by mineral nutrients, extra organic carbon accumulated in the system. However, when bacteria were limited by organic carbon, addition of dissolved organic carbon reduced phytoplankton biomass and activity, and also the rate at which total organic carbon accumulated. The study highlights how the fate and effects of added degradable organic carbon depend critically on the state of the microbial food web.

Frede Thingstad (University of Bergen, Norway)
Tel: +47 55 58 26 83; E-mail: [email protected]


[9] The Trichoplax genome and the nature of placozoans (pp 955-960)

[10] Doping a semiconductor to create an unconventional metal (pp 976-980; N&V)

[11] Effect of phase transitions on compressional-wave velocities in the Earth’s mantle (pp 984-986)


***These papers will be published electronically on Nature's website on 20 August at 1800 London time / 1300 US Eastern time (which is also when the embargo lifts) as part of our AOP (ahead of print) programme. Although we have included them on this release to avoid multiple mailings they will not appear in print on 21 August, but at a later date. ***

[12] CDK targets Sae2 to control DNA-end resection and homologous recombination
DOI: 10.1038/nature07215

[13] ATP drives lamina propria TH17 cell differentiation
DOI: 10.1038/nature07240

[14] Structural insights into the evolutionary paths of oxylipin biosynthetic enzymes
DOI: 10.1038/nature07307


The following list of places refers to the whereabouts of authors on the papers numbered in this release. For example, London: 4 - this means that on paper number four, there will be at least one author affiliated to an institute or company in London. The listing may be for an author's main affiliation, or for a place where they are working temporarily. Please see the PDF of the paper for full details.

Ottawa: 2
Vancouver: 5

Bagneux : 6
Marseille: 8
Paris: 6, 14
Verrières-le-Buisson: 6

Hannover: 9

Rome: 7

Aoba-ku: 13
Okinawa: 9
Osaka: 13
Tokyo: 13

Maseru: 10

Christchurch: 4

Bergen: 8

Seville: 12

Stockholm: 14

Zurich: 5, 12

Cambridge: 3, 4, 12
Leicester: 13
London: 10
Nottingham: 3


Berkeley: 9
Stanford: 9
Walnut Creek: 9

Boulder: 6

New Haven: 9

Evanston: 1

Iowa City: 1

Baton Rouge: 10

Greenbelt: 6

Boston: 1, 2, 7

New Jersey
Murray Hill: 10

New York
New York: 2, 7
Stony Brook: 11

Houston: 9, 14

Madison: 3


From North America and Canada
Katherine Anderson, Nature New York
Tel: +1 212 726 9231; E-mail: [email protected]

Katie McGoldrick, Nature Washington
Tel: +1 202 737 2355; E-mail: [email protected]

From Japan, Korea, China, Singapore and Taiwan
Mika Nakano, Nature Tokyo
Tel: +81 3 3267 8751; E-mail: [email protected]

From the UK/Europe/other countries not listed above
Jen Middleton, Nature London
Tel: +44 20 7843 4502; E-mail [email protected]

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Published: 20 Aug 2008

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