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Article Released Sun-4th-May-2008 17:27 GMT
Contact: Ruth Institution: Nature Publishing Group
 Natural genetic variant regulates yield potential in rice

Summaries of newsworthy papers include Evolution: New look at human family tree, Your number of fat cells stays constant in adulthood, Starting out on the road to maleness, Earth’s early magnetic field, Genetic susceptibility to obesity and Generating human autoimmune cells

NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE

For papers that will be published online on 04 May 2008

This press release is copyrighted to the Nature journals mentioned below.

This press release contains:

· Summaries of newsworthy papers:

Evolution: New look at human family tree – Nature

Obesity: Your number of fat cells stays constant in adulthood - Nature

Developmental genetics: Starting out on the road to maleness - Nature

Earth’s early magnetic field – Nature Geoscience

Genetic susceptibility to obesity – Nature Genetics

Natural genetic variant regulates yield potential in rice – Nature Genetics

Generating human autoimmune cells – Nature Immunology

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

· Geographical listing of authors


PDFs of all the papers mentioned on this release can be found in the relevant journal’s section of http://press.nature.com. Press contacts for the Nature journals are listed at the end of this release.

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****************************************************NATURE************************************************
(http://www.nature.com/nature)

[1] Evolution: New look at human family tree

DOI: 10.1038/nature06891

A new computer analysis of our immediate evolutionary family has refined our view of the relationships between different Homo species and related living and extinct hominid species. The study also supports the idea that the Neanderthals were indeed a distinct species from Homo sapiens.

The new method could help evolutionary analysts overcome some of the problems that arise when arbitrarily dividing species into distinct groups, say Rolando González-José and colleagues online in this week’s Nature. Many attempts to compile evolutionary trees are hampered by the fact that they try to divide human fossil skulls into categories such as ‘flat-faced’ or ‘protruding-faced’, when in reality these traits vary continuously rather than discretely.

Instead, the researchers used measurements from many human and ape fossil skulls, and condensed them into four parameters, reflecting variables such as skull roundness and jaw protrusion. When they analysed these variables, they found that the resulting evolutionary tree closely mirrors existing ones, suggesting that the method could be a valuable tool for evolutionary analyses. What’s more, the study supports the theory that all species currently assigned to the genus Homo are indeed a single family, with the 2-million-year-old Homo habilis at its root, and that, much more recently, H. sapiens and H. neanderthalensis were evolutionary cousins, rather than offshoots of the same species.

Author contact:

Rolando González-José (Centro Nacional Patagonico, Puerto Madryn, Argentina)
Tel: +54 2965 451 024; E-mail: rolando@cenpat.edu.ar


[2] Obesity: Your number of fat cells stays constant in adulthood

DOI: 10.1038/nature06902

The number of fat cells, or adipocytes, in your body remains more or less constant throughout adulthood, a new study online in this week’s Nature finds. The discovery suggests that the difference in the number of fat cells between lean and obese people is established in childhood, and then persists for life.

The number of fat cells remains constant even in formerly obese adults who have lost significant amounts of weight, report researchers led by Kirsty Spalding, who studied fat samples from liposuction and abdominal reconstruction surgery in lean and obese volunteers. This reflects the fact that the level of obesity is determined by a combination of the number and size of fat cells, which can grow or shrink as fat from food is deposited in them.

Although fat cell numbers remain constant during adulthood, this is a dynamic process of death and replenishment, Spalding and her colleagues report. Fat cells are replaced at the same rate that they die — roughly 10% every year. The researchers made their discovery by studying levels of radioactive isotopes in fat cells from people who had lived through the brief period of Cold War nuclear bomb testing from 1955 to 1963. People whose fat cells were deposited before the onset of testing nevertheless incorporated radioactive matter after, showing that their fat cells were being replenished.

The fact that fat cells are constantly dying and being replaced could potentially offer an opportunity to develop new anti-obesity therapies, the researchers suggest.

Author contact:

Kirsty Spalding (Karolinska Institute, Stockholm, Sweden)
Tel: +46 70 437 1542; E-mail: kirsty.spalding@cmb.ki.se


[3] Developmental genetics: Starting out on the road to maleness

DOI: 10.1038/nature06944

Growing up male is a genetic lifestyle decision — early in embryonic development, genes on the Y chromosome activate the development of specialized cells that ultimately become the testes. Without this ‘on switch’ for maleness, the developing gonads become ovaries by default and the embryo develops as a female.

A study of mice now shows how the developing gonads start out on this road to maleness. In a paper published online in Nature this week, geneticists Robin Lovell-Badge and Ryohei Sekido describe how a gene called Sry, carried on the Y chromosome, boosts another gene elsewhere in the genome that in turn governs the development of sperm-producing cells called Sertoli cells — a crucial component of the testes.

By studying gene expression patterns in developing mouse embryos, the researchers deduced that Sry produces a protein that combines with another protein, steroidogenic factor 1 (SF1). This complex then binds to a DNA region that boosts the expression of another gene, Sox9, which controls a host of genes involved in sperm development.

Elucidating this pathway not only reveals how maleness develops from the ‘default’ female developmental pathway; defects in this process may also explain how people who are genetically ‘male’ or ‘female’ end up developing the ‘wrong’ sexual anatomy.

Author contact:

Robin Lovell-Badge (National Institute for Medical Research, London, UK)
Tel: +44 20 8816 2126; E-mail: rlovell@nimr.mrc.ac.uk


Other papers from Nature to be published online at the same time and with the same embargo:

[4] Neural substrates of vocalization feedback monitoring in primate auditory cortex
DOI: 10.1038/nature06910

[5] Essential role for Nix in autophagic maturation of erythroid cells
DOI: 10.1038/nature07006

****************************************NATURE GEOSCIENCE******************************************
(http://www.nature.com/ngeo)

[6] Earth’s early magnetic field

DOI: 10.1038/ngeo181

The Earth’s magnetic field reversed less frequently on early Earth, reports a paper online this week in Nature Geoscience. The Earth’s magnetic field, and the location of the magnetic North Pole, wanders and even reverses over the course of millions of years.

Andrew Biggin and colleagues analysed palaeomagnetic data — records of the magnetic field recorded in minerals from volcanic rocks — for a period from 2.82 to 2.45 billion years ago. They found that, relative to the past 200 million years, reversals were far less common. The team suggests that the geodynamo, which generates the Earth’s magnetic field, was far more stable 2 billion years ago. They link this to the small size of the inner core on early Earth, which could have stabilized the field behaviour.

Author contact:
Andrew Biggin (Universiteit Utrecht, Netherlands)
Tel: +31 30 253 5246; E-mail: biggin@geo.uu.nl

***********************************************NATURE GENETICS **************************************
(http://www.nature.com/naturegenetics)

[7] & [8] Genetic susceptibility to obesity

DOI: 10.1038/ng.140
DOI: 10.1038/ng.156

Scientists have discovered genetic variants that increase the risk of obesity and insulin resistance in the general population, according to two studies published online this week in Nature Genetics. Until now only one locus (FTO) has been associated convincingly with increased risk of obesity.

A consortium of investigators led by Mark McCarthy, Ines Barroso and Nicholas Wareham analyzed the genomes of more than 90,000 individuals and found that a variant near MC4R, encoding the melanocortin-4 receptor, increases susceptibility to obesity. Previous studies had shown that the melanocortin-4 receptor is expressed in neurons in the hypothalamus and is a key regulator of food intake and energy expenditure. Although it is unclear how this variant affects MC4R expression or function, the fact that mutations in the gene are known to cause rare cases of severe childhood obesity lends confidence to the association.

In a separate study, Jaspal Kooner and colleagues carried out a genome-wide scan of several thousand individuals of Indian Asian or European ancestry, and identified a variant near MC4R as increasing risk of obesity and insulin resistance. The risk variant was more frequent in individuals of Indian Asian ancestry, which the authors suggest may account for the increased burden of obesity in Indian Asians.

Author contacts:
Mark McCarthy (University of Oxford, UK) Author paper [7]
Tel: +44 1865 857 298; E-mail: mark.mccarthy@drl.ox.ac.uk

Inês Barroso (Wellcome Trust Sanger Institute, Hinxton, UK) Co-author paper [7]
Tel: +44 1223 495 341; E-mail: ib1@sanger.ac.uk

Nicholas Wareham (Addenbrooke’s Hospital, Cambridge, UK) Co-author paper [7]
Tel: +44 1223 330 315; E-mail: nick.wareham@mrc-epid.cam.ac.uk

Jaspal Kooner (Imperial College London, UK) Author paper [8]
Tel: +44 20 8383 4751; E-mail: j.kooner@imperial.ac.uk


[9] Natural genetic variant regulates yield potential in rice

DOI: 10.1038/ng.143

Researchers have identified a gene that has significant effects on yield potential in rice, as well as adaptability of rice to temperate climates. The study, published online this week in Nature Genetics, has implications for rice productivity.

The productivity of many crop plants, including rice, is determined by yield potential, plant height and flowering time. Previous studies have identified a region on chromosome 7 that affected all three traits, but the specific gene involved has not yet been pinpointed.

Qifa Zhang and colleagues found that rice plants that are shorter, have fewer grains per cluster of flowers, and flower earlier—all traits that reduce yield—have a complete deletion of the gene Ghd7. The restoration of Ghd7 expression in plants with the deletion had considerable effects on yield-related traits, including a doubling of the time to flowering and a 67% increase in height.

The authors also determined the status of Ghd7 in 19 rice varieties from rice growing in a wide geographic range in Asia. Five different versions of Ghd7 were found. The most highly active versions were present in warmer regions, allowing rice plants to fully exploit light and temperature by delaying flowering and increasing yield. Less active or inactive versions were found in cooler regions, enabling rice to be cultivated in areas where the growing season is shorter.

Author contact:
Qifa Zhang (Huazhong Agricultural University, Wuhan, China)
Tel: +86 27 8728 2429; E-mail: qifazh@mail.hzau.edu.cn

Other papers from Nature Genetics to be published online at the same time and with the same embargo:

[10] The mouse X chromosome is enriched for multicopy testis genes showing postmeiotic expression
DOI: 10.1038/ng.126


*******************************************NATURE IMMUNOLOGY ************************************
(http://www.nature.com/natureimmunology)

[11] & [12] Generating human autoimmune cells

DOI: 10.1038/ni.1610
DOI: 10.1038/ni.1613

The essential ‘ingredients’ for producing a type of human immune cell involved in both mucosal immunity and autoimmunity are reported online this week in Nature Immunology. The findings address a controversy surrounding the requirements for producing this unique type of immune cell in humans and in mice.

Dan Littman and colleagues, and Vassili Soumelis and colleagues, set out to test whether specific immune signaling molecules previously shown to be required for producing mouse ‘T helper 17 cells’ — or ‘TH17 cells’ — were also required for producing human TH17 cells. An underlying issue in these studies was the usefulness of mouse models to study the causes and treatment of human disease: if mouse and human TH17 cells have fundamentally different developmental requirements, the use of mouse models might be called into question.

Both teams demonstrated that the key immune signaling molecule known as transforming growth factor-beta (TGF-beta) and one or more inflammation-producing cytokine(s), such as interleukin 6 (IL-6), are required for producing human and mouse TH17 cells. These studies are important not only because they help to define what is necessary for producing human TH17 cells, but they also calm concerns about studying human autoimmunity and mucosal diseases such as Crohn’s disease, inflammatory bowel disease and multiple sclerosis in mouse models.

Author contacts:
Dan Littman (New York University School of Medicine, New York, NY, USA) Author paper [11]
Tel: +1 212 263 7579; E-mail: littman@saturn.med.nyu.edu

Vassili Soumelis (Institut Curie, Paris, France) Author paper [12]
Tel: +33 1 44 32 42 27; E-mail: vassili.soumelis@curie.net

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Items from other Nature journals to be published online at the same time and with the same embargo:

NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)

[13] Gene expression signatures and small-molecule compounds link a protein kinase to Plasmodium falciparum motility
DOI: 10.1038/nchembio.87

[14] Metal swap between Zn7-metallothionein-3 and amyloid-beta–Cu protects against amyloid-beta toxicity
DOI: 10.1038/nchembio.89

Nature PHYSICS (http://www.nature.com/naturephysics)

[15] Coherent control of attosecond emission from aligned molecules
DOI: 10.1038/nphys964

[16] Oscillations and interactions of dark and dark–bright solitons in Bose–Einstein condensates
DOI: 10.1038/nphys962


NATURE MATERIALS (http://www.nature.com/naturematerials)

[17] Non-volatile ferroelectric control of ferromagnetism in (Ga,Mn)As
DOI: 10.1038/nmat2185

[18] Optical gain by a simple photoisomerization process
DOI: 10.1038/nmat2186

NATURE BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)

[19] Genome sequencing and analysis of the biomass-degrading fungus Trichoderma reesei (syn. Hypocrea jecorina)
DOI: 10.1038/nbt1403


NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)

[20] Improved nanofabrication through guided transient liquefaction
DOI: 10.1038/nnano.2008.95

[21] Self-regulation of photoinduced electron transfer by a molecular nonlinear transducer
DOI: 10.1038/nnano.2008.97

[22] Integrated three-dimensional microelectromechanical devices from processable carbon nanotube wafers
DOI: 10.1038/nnano.2008.98

[23] Photochemistry: Let there be light — but not too much
DOI: 10.1038/nnano.2008.124

Nature MEDICINE (http://www.nature.com/naturemedicine)

[24] Activation of c-Kit in dendritic cells regulates T helper cell differentiation and allergic asthma
DOI: 10.1038/nm1766

[25] Functional roles for C5a receptors in sepsis
DOI: 10.1038/nm1753

Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)

[26] MicroRNA-9 directs late organizer activity of the midbrain-hindbrain boundary
DOI: 10.1038/nn.2115

[27] Single-neuron labeling with inducible Cre-mediated knockout in transgenic mice
DOI: 10.1038/nn.2118


NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)

[28] Regulation of autophagy by cytoplasmic p53
DOI: 10.1038/ncb1730

[29] p53-Driven apoptosis limits centrosome amplification and genomic instability downstream of NPM1 phosphorylation
DOI: 10.1038/ncb1735

[30] Nanog and Oct4 associate with unique transcriptional repression complexes in embryonic stem cells
DOI: 10.1038/ncb1736


Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)

[31] Membrane-dependent signal integration by the Ras activator Son of sevenless
DOI: 10.1038/nsmb.1418

[32] The structural basis for cap binding by influenza virus polymerase subunit PB2
DOI: 10.1038/nsmb.1421


NATURE METHODS (http://www.nature.com/nmeth)

[33] Improving the photostability of bright monomeric orange and red fluorescent proteins
DOI: 10.1038/nmeth.1209

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GEOGRAPHICAL LISTING OF AUTHORS

The following list of places refers to the whereabouts of authors on the papers numbered in this release. 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.

ARGENTINA
La Plata: 1
Puerto Madryn: 1
Trelew: 1

AUSTRALIA
Darlinghurst: 25

AUSTRIA
Graz: 28
Vienna: 19

BRAZIL
Sao Paulo: 1

CANADA:
Quebec: 25

CHILE
Santiago: 19

CHINA
Shanghai: 30
Wuhan: 9

CZECH REPUBLIC
Prague: 17

FINLAND
Espoo: 19
Helsinki: 7
Oulu: 7
Seinajoki: 7

FRANCE
Chatenay-Malabry: 28
Fontainebleau: 12
Gif-sur-Yvette: 15
Grenoble: 32
Lille: 7, 8
Marseille: 19
Paris: 12, 15, 28
Toulouse: 14
Villejuif: 28

GERMANY
Berlin: 2
Cologne: 18
Erlangen: 23
Essen: 7
Hamburg: 16
Heidelberg: 32
Lubeck: 25
Munich: 7
Neuherberg: 26
Tubingen: 26
Ulm: 25

GREECE
Crete: 2, 28

IRELAND
Cork: 27

ITALY
Cagliari: 7
Ferrara: 28
Naples: 28
Rome: 28

JAPAN
Tsukuba: 22

NETHERLANDS
Utrecht: 6

NEW ZEALAND
Wellington: 17

POLAND
Krakow: 15

SPAIN
Alicante: 18
Madrid: 18, 32
Tenerife: 19

SWEDEN
Gothenburg: 28
Malmo: 7
Stockholm: 2

SWITZERLAND
Lausanne: 7, 17
Zurich: 14

UNITED KINGDOM
Birmingham: 16
Bristol: 7
Cambridge: 7
Dundee: 7, 29
Exeter: 7
Glasgow: 7
Leeds: 7
Leicester: 7
London: 3, 7, 8, 10, 15, 24, 28, 29
Nottingham: 17
Oxford: 7
Reading: 15
Southampton: 7

UNITED STATES OF AMERICA

Arizona
Tempe: 21

California
Berkeley: 31
Davis: 19
La Jolla: 13, 33
Palo Alto: 19
San Diego: 13
Walnut Creek: 19

Florida
Tallahassee: 33

Maryland
Baltimore: 4, 7
Bethesda: 7
Gaithersburg: 7

Massachusetts
Boston: 7, 10, 25
Cambridge: 10

Michigan
Ann Arbor: 7, 8, 25

Nevada
Reno: 13

New Jersey
Princeton: 20

New Mexico
Albuquerque: 19
Los Alamos: 19

New York
Ithaca: 31
New York: 10, 11, 13, 31
Stony Brook: 28

North Carolina
Chapel Hill: 7
Durham: 27

Ohio
Cincinnati: 25

Oregon
Corvallis: 19

Pennsylvania
King of Prussia: 7
Pittsburgh: 24

Texas
Houston: 5, 30

Utah
Provo: 22
Salt Lake City: 5

Vermont
Burlington: 13

Washington
Richland: 19

Wisconsin
Madison: 19

PRESS CONTACTS…

For media inquiries relating to embargo policy for all the Nature Research Journals:

Rachel Twinn (Nature London)
Tel: +44 20 7843 4658; E-mail: r.twinn@nature.com

Katherine Anderson (Nature New York)
Tel: +1 212 726 9231; E-mail: k.anderson@natureny.com

Ruth Francis (Head of Press, Nature, London)
Tel: +44 20 7843 4562; E-mail: r.francis@nature.com

For media inquiries relating to editorial content/policy for the Nature Research Journals, please contact the journals individually:

Nature Biotechnology (New York)
Peter Hare
Tel: +1 212 726 9284; E-mail: biotech@natureny.com

Nature Cell Biology (London)
Bernd Pulverer
Tel: +44 20 7843 4892; E-mail: cellbio@nature.com

Nature Chemical Biology (Boston)
Andrea Garvey
Tel: +1 617 475 9241, E-mail: chembio@boston.nature.com

Nature Genetics (New York)
Orli Bahcall
Tel: +1 212 726 9311; E-mail: natgen@natureny.com

Nature Geoscience (London)
Heike Langenberg
Tel: +44 20 7843 4042; E-mail: h.langenberg@nature.com

Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: immunology@natureny.com

Nature Materials (London)
Alison Stoddart
Tel: +44 20 7843 4593; E-mail: materials@nature.com

Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: medicine@natureny.com

Nature Methods (New York)
Hugh Ash
Tel: +1 212 726 9627; E-mail: methods@natureny.com

Nature Nanotechnology (London)
Peter Rodgers
Tel: +44 20 7014 4019; Email: p.rodgers@nature.com

Nature Neuroscience (New York)
Sandra Aamodt (based in California)
Tel: +1 530 795 3256; E-mail: neurosci@natureny.com

Nature Physics (London)
Alison Wright
Tel: +44 20 7843 4555; E-mail: a.wright@nature.com

Nature Structural & Molecular Biology (New York)
Michelle Montoya
Tel: +1 212 726 9326; E-mail: nsmb@natureny.com

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Keywords associated to this article: Evolution, Obesity, Developmental genetics, Geoscience, Genetics, Immunology
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