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This press release is copyright Nature.
VOL.452 NO.7184 DATED 13 MARCH 2008
This press release contains:
· Summaries of newsworthy papers:
Cancer: ‘Crime boss’ gene controls aggressive breast tumours
Climate science: Deep impact
Veterinary medicine: The worm turns
Ecology: Changing nitrate sinks
Cancer cells: Subverting a metabolic pathway for tumour growth
Immunity: Missing cells to blame in Job’s syndrome
Neuroscience: Neural coding of visual information
Biology: Partners in crime for neurodegenerative diseases
Biochemistry: Clever catalysis in a gut microorganism
And finally… DNA Lego
· Mention of papers to be published at the same time with the same embargo
· Geographical listing of authors
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[1] Cancer: ‘Crime boss’ gene controls aggressive breast tumours (pp 187-193)
Geneticists have identified a gene that promotes aggressive breast cancer by altering the behaviour of more than 1,000 other genes within tumour cells. What’s more, they find that knocking out this ‘kingpin’ gene causes the cancer cells to stop their runaway proliferation.
The gene, called SATB1, already known to be expressed in breast tumours, is a key factor in the process of metastasis — the spread of cancerous cells to other locations in the body — report Terumi Kohwi-Shigematsu and co-workers in this week’s Nature. In mouse models, they found that disrupting SATB1 stops cancer cells from dividing and spreading. Conversely, deliberately expressing this gene in cancer cells causes them to form very aggressive tumours.
This is consistent with SATB1’s normal role in the cell, as an ‘organizer’ of other genes, the researchers add. Aggressive tumours therefore form when this gene is overactivated, and the ‘mob’ of growth-promoting genes that it controls begins to run amok.
CONTACT
Terumi Kohwi-Shigematsu (Lawrence Berkeley Laboratory, University of California, Berkeley, CA, USA) Tel: +1 510 486 4983; E-mail: [email protected]
[2] Climate science: Deep impact (pp 206-209)
The Gulf Stream has a more extensive influence on atmospheric processes than previously thought, penetrating deep into the upper troposphere. A study in Nature this week elucidates details of this interaction, which also provides a possible pathway by which the Gulf Stream affects climate in remote regions — with implications for understanding the climatic response to changes in ocean circulation.
The Gulf Stream transports heat from the tropics northward across the Atlantic towards western Europe. It influences daily weather phenomena, such as cyclone and cloud formation, but its effect on longer-term climatic conditions is poorly understood.
Shoshiro Minobe and colleagues examine the influence of this ocean current on the atmosphere, using weather analyses, satellite data and an atmospheric circulation model. Their results show that the Gulf Stream anchors a rain band in which upward motion of air penetrates deep into the upper troposphere, well above the surface portion of the atmosphere. The results provide a mechanism by which the Gulf Stream can affect climate locally, and possibly in remote regions by forcing planetary waves.
The authors suggest that, as the Gulf Stream is expected to change in response to global warming, such interactions with the atmosphere will therefore play an important role in forming spatial patterns of future climate change.
CONTACT
Shoshiro Minobe (Hokkaido University, Sapporo, Japan)
Tel: +81 11 706 2644; Tel: [email protected]
[3] Veterinary medicine: The worm turns (pp 176-180; N&V)
Roundworms, or nematodes, can infect humans and domestic animals — the gastrointestinal blood-sucking Haemonchus contortus, for example, has a major negative impact on livestock production worldwide. Worse still, the parasites have developed resistance against all the major drugs, known collectively as anthelmintics. A paper in this week’s Nature describes a new chemical class of anthelmintics — dubbed amino-acetonitrile derivatives (AADs) — that works in quite a different way from the established drugs and should therefore by-pass the nematodes’ resistance mechanisms.
Ronald Kaminsky and colleagues have come up with the first novel candidate drug treatment in 25 years. They chemically synthesized AADs and then identified their mode of action, which is to target a protein specific to nematodes — making them well tolerated by the farm animals themselves. It is to be hoped that their findings might eventually find an application in infected humans as well.
CONTACT
Ronald Kaminsky (Novartis Animal Health, St Aubin, Switzerland)
Tel: +41 26 6791621; E-mail: [email protected]
Roger Prichard (McGill University, Quebec, Canada) N&V author
Tel: +1 514 398 7729; E-mail: [email protected]
[4] Ecology: Changing nitrate sinks (pp 202-205; N&V)
Terrestrial ecosystems are becoming steadily more saturated with nitrogen generated as a result of human activities, but only about a quarter of this ends up in the oceans — suggesting that nitrogen is being removed in ‘sinks’ along the way. A paper in this week’s Nature sheds new light on the crucial contribution by rivers and streams in this process.
Patrick Mulholland and colleagues undertook a huge field campaign to investigate nitrogen uptake and denitrification in 72 streams in the United States and Puerto Rico that drain watersheds of varying land-use types. They found that the efficiency of nitrogen removal by biological organisms in small streams deteriorates as nitrate concentrations increase in the water — a pattern that held across nitrate concentrations varying by up to six orders of magnitude and across eight ecological communities, or biomes.
The authors warn that large-scale land conversion to support the production of biofuels, for example, may generate higher nitrogen loads, potentially compromising their removal in stream networks and delivering more to estuaries and coastal oceans.
CONTACT
Patrick Mulholland (Oak Ridge National Laboratory, TN, USA)
Tel: +1 865 574 7304; E-mail: [email protected]
Sybil Seitzinger (Rutgers University, New Brunswick, NJ, USA) N&V author
Tel: +1 732 932 6555 (ext 342); E-mail: [email protected]
[5] & [6] Cancer cells: Subverting a metabolic pathway for tumour growth (pp 230-233; 181-186)
Tumour cells generally use altered metabolic pathways for energy production, in particular they display a switch in the way glucose is metabolized. Although this aberration was first noticed by Otto Warburg some 80 years ago, two papers in this week’s Nature shed further light on the mechanisms underlying this switch.
Lewis Cantley and colleagues looked at pyruvate kinase — an enzyme involved in glucose metabolism — which exists in some cancer cells in an embryonic form known as M2. By making the cells produce the adult (M1) form instead, the team were able to set cancer cells back on to their normal metabolic course and curb the cells’ tumour-forming capacity. In an accompanying paper, they reveal how M2 pyruvate kinase is subject to internal controls that do not affect M1, which may explain the different modes of glucose metabolism in cancer cells.
The discovery that M2 aids tumour growth demonstrates the importance of the specialized metabolism of cancer cells, say the authors.
CONTACT
Lewis Cantley (Beth Israel Deaconess Medical Center, Boston, MA, USA) Author papers [5] & [6]
Tel: +1 617 667 0947; E-mail: [email protected]
[7] Immunity: Missing cells to blame in Job’s syndrome (AOP)
DOI: 10.1038/nature06764
***This paper will be published electronically on Nature's website on 12 March at 1800 London time / 1400 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 13 March, but at a later date. ***
Immunologists have made a breakthrough in understanding a rare immune disease called Job’s syndrome — so called because its symptoms include recurring outbreaks of abscesses similar to the boils suffered by the eponymous Biblical character. The new research shows that sufferers lack a specific type of white blood cell, leaving them open to repeated attack by certain bacterial and fungal pathogens.
Writing online in this week’s Nature, a team led by Daniel Douek describes how sufferers of Job’s syndrome, more properly called hyper-IgE syndrome (HIES), are unable to produce cells called TH17 helper cells. These immune cells produce a protein called interleukin-17, and are crucial for protection against invading pathogens.
The discovery ties in with the fact that sufferers are known to have defects in a gene called stat3, which is involved in the differentiation of TH17 cells, a common type of white blood cell, into their various specific types. The lack of this particular component of the immune system explains why sufferers experience repeated infections by the same pathogens, particularly fungal infection and Staphylococcus bacteria.
CONTACT
Daniel Douek (National Institute of Health, Bethesda MD, USA)
Tel: +1 301 594 8484; E-mail: [email protected]
[8] Neuroscience: Neural coding of visual information (pp 220-224)
Our perception of the environment relies on neural networks being able to adapt rapidly to changes in incoming stimuli. A paper in this week’s Nature reveals how this adaptation improves coding accuracy across neuronal populations, which in turn may also optimize performance during viewing.
Diego Gutnisky and Valentin Dragoi focus on a brief form of adaptation — on the timescale of visual fixation — in the primary visual cortex of macaque monkeys. They find that this adaptation causes a decrease in the correlations that occur between pairs of monkey neurons, reorganizing their distribution across the entire network to potentially improve the accuracy of how visual cortex encodes information.
The authors hypothesize that the rapid sequence of fixations during natural viewing induces this adaptation, thereby maximizing image-discrimination performance in real time.
CONTACT
Valentin Dragoi (University of Texas-Houston Medical School, Houston, TX, USA)
Tel: +1 713 500 5710; E-mail: [email protected]
Diego Gutnisky (University of Texas-Houston Medical School, Houston, TX, USA) Co-author
Tel: +1 713 500 5821; E-mail: [email protected]
[9] Biology: Partners in crime for neurodegenerative diseases (AOP)
DOI: 10.1038/nature06731
***This paper will be published electronically on Nature's website on 12 March at 1800 London time / 1400 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 13 March, but at a later date. ***
Spinocerebellar ataxia type 1 (SCA1) is an inherited neurodegenerative disease caused by faulty insertion of stretches of glutamines in the so-called Ataxin1 protein. Precisely how stretches of glutamines confer toxicity to a protein is not clear — whether for SCA1, or for similar disorders such as Huntington’s disease. An article by Huda Zoghbi and colleagues online in Nature greatly enhances our understanding of the mechanism that underlies this type of disorder.
SCA1 is characterized by progressive loss of coordination, motor impairment and the degeneration cells in the cerebellum. The results in this study show that the glutamine stretch confers such toxicity because it can simultaneously cause both a gain and a loss of Ataxin1 function. Whether Ataxin1 gains or loses functionality depends entirely on the protein partners it is associated with.
The authors propose a model in which the enhanced function of one particular protein complex is combined with a simultaneous loss of function of other protein complexes. And, the authors argue, their model may well apply to other neurodegenerative diseases.
CONTACT
Huda Zoghbi (Baylor College of Medicine, Houston, TX, USA)
Tel: +1 713 798 6558; E-mail: [email protected]
[10] Biochemistry: Clever catalysis in a gut microorganism (pp 239-242; N&V)
The gut bacterium Clostridium difficile, an occasional scourge of hospital wards, uses a special enzyme known as a dehydratase to help it to ferment amino acids. A paper in this week’s Nature shows how this enzyme catalyses a chemically awkward reaction in the process — revealed by the discovery of an unusual intermediate compound that is formed from the substrate by the enzyme.
Antonio Pierik and colleagues identified this intermediate to be an allylic ketyl radical, an unusual type of radical known so far only from organic chemistry. The dehydratase can eliminate the elements of water from this intermediate — a reaction that other enzymes would find almost impossible. The absence of radical generators, such as oxygen, makes this class of enzymes unprecedented in biochemistry.
CONTACT
Antonio Pierik (University of Marburg, Germany)
Tel: +49 642 12 86 38 56; E-mail: [email protected]
Joseph Jarrett (University of Hawaii at Manoa, Honolulu, HI, USA) N&V author
Tel: +1 808 956 6721; E-mail: [email protected]
[11] And finally… DNA Lego (pp 198-201)
Scientists have created a versatile strategy for building three-dimensional structures on the nanometre scale. The strategy provides scientists with a simple method of coaxing strands of DNA to assemble spontaneously into complex structures.
The double-helix structure of DNA and its base pairing that enables recognition and highly selective binding of complementary DNA strands are well known. A variety of surface patterns and nanostructures have already been made from DNA, by producing DNA molecules that interact just in the way needed to form the desired pattern or structure. But large and more complex three-dimensional structures are difficult to make using existing fabrication methods, which would require the use of hundreds of unique DNA strands.
In this week’s Nature, Chengde Mao and colleagues overcome this problem by programming DNA to fold first into a basic structural unit. Depending on the reaction conditions, four, twenty or sixty of these units then bind to each other and assemble into either tetrahedra, dodecahedra or ‘buckyballs’ (football-shaped structures). Other complex structures should also be accessible using this strategy. The authors suggest that the complexity of these polyhedra, combined with the simplicity of their fabrication, should make them attractive for use in materials science and nanotechnology.
CONTACT
Chengde Mao (Purdue University, West Lafayette, IN, USA)
Tel: +1 765 494 0498; E-mail: [email protected]
ALSO IN THIS ISSUE…
[12] Genetic basis of fitness differences in natural populations (pp 169-175)
[13] Reflected light from sand grains in the terrestrial zone of a protoplanetary disk (pp 194-197)
[14] Diversity and productivity peak at intermediate dispersal rate in evolving metacommunities (pp 210-214)
ADVANCE ONLINE PUBLICATION
***These papers will be published electronically on Nature's website on 12 March at 1800 London time / 1400 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 13 March, but at a later date. ***
[15] SIRT6 is a histone H3 lysine 9 deacetylase that modulates telomeric chromatin
DOI: 10.1038/nature06736
[16] Functional metagenomic profiling of nine biomes
DOI: 10.1038/nature06810
[17] SAR11 marine bacteria require exogenous reduced sulphur for growth
DOI: 10.1038/nature06776
[18] Sophisticated particle-feeding in a large Early Cambrian crustacean
DOI: 10.1038/nature06724
GEOGRAPHICAL LISTING OF AUTHORS…
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.
AUSTRALIA
Adelaide: 16
COTE D’IVOIRE
Lanada: 3
FRANCE
Marseille: 16
Montpellier: 14
GERMANY
Heidelberg: 13
Marburg: 10
JAPAN
Hokkaido: 2
Sapporo: 2
Yokohama: 2
SINGAPORE
Singapore: 16
SWEDEN
Uppsala: 12
SWITZERLAND
Basel: 3
Bern: 3
St Aubin: 3
UNITED KINGDOM
Ascot: 14
Bath: 10
Cambridge: 18
Liverpool: 14
Oxford: 12, 14
UNITED STATES OF AMERICA
California
Berkeley: 1
Palo Alto: 15
San Diego: 16
Santa Barbara: 16
Stanford: 15
Connecticut
Middletown: 13
Florida
St Petersburg: 16
Georgia
Athens: 4, 16
Tucker: 4
Hawaii
Honolulu: 2
Illinois
Argonne: 16
Urbana: 16
Indiana
Muncie: 4
Notre Dame: 4
West Lafayette: 11
Kansas
Manhattan: 4
Maryland
Baltimore: 15
Bethesda: 7, 15
Rockville: 16
Massachusetts
Boston: 5
Cambridge: 3, 5, 6, 9, 13, 15
Woods Hole: 4, 17
Michigan
Hickory Corners: 4
Minnesota
Minneapolis: 9
New Hampshire
Durham: 4
New Mexico
Albuquerque: 4
New York
Mill Brook: 4
Ohio
Cincinnati: 4
Oregon
Corvallis: 4, 17
Pennsylvania
Carlisle: 13
Philadelphia: 1
Tennessee
Knoxville: 4
Nashville: 7, 9
Oak Ridge: 4
Texas
Houston: 8, 9, 13
Virginia
Blacksburg: 4
Washington
Tacoma: 4
Vancouver: 4
Wyoming
Laramie: 4
UZBEKISTAN
Tashkent: 13
PRESS CONTACTS…
For North America and Canada
Katie McGoldrick, Nature Washington
Tel: +1 202 737 2355; E-mail: [email protected]
For Japan, Korea, China, Singapore and Taiwan
Mika Nakano, Nature Tokyo
Tel: +81 3 3267 8751; E-mail: [email protected]
For the UK/Europe/other countries not listed above
Katherine Anderson, Nature London
Tel: +44 20 7843 4502; E-mail [email protected]
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