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This press release is copyright Nature.
VOL.451 NO.7175 DATED 10 JANUARY 2008
This press release contains:
· Summaries of newsworthy papers:
Tropical disease: Plant hormone turns up in human parasite
Cancer: MicroRNAs that reduce metastasis
Space: Antimatter close to home
Cancer biology: Suppressing a leukaemia suppressor
Immunodeficiency: A shortage of oxygen to beat infection
Nanotechnology: Roughened silicon nanowires take the heat
And finally… The genetics of sex
· Mention of papers to be published at the same time with the same embargo
· Geographical listing of authors
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[1] Tropical disease: Plant hormone turns up in human parasite (pp 202-206)
As diseases caused by tropical parasites become more resistant to drugs, new treatments are urgently being sought. A paper in this week’s Nature reports the surprising discovery that the pathogenicity of a parasite known as Toxoplasma gondii is under the control of a hormone previously found only in plants and some primitive sea creatures — making it a potential target for an inhibiting drug that won’t affect the human host.
David Sibley and his colleagues compared plant and parasite genomes to discover a T. gondii metabolic pathway responsible for synthesizing the plant hormone abscisic acid, which turns out to be crucial for the parasite’s replication and development.
Accordingly, they tested the effect of the herbicide fluridone — which prevents the hormone from working in plants — on laboratory mice infected with T. gondii. Parasite burden in treated animals was significantly reduced.
The malaria parasite Plasmodium falciparum is related to T. gondii and also carries genes implicating abscisic acid in its development. Perhaps the ripples from this unexpected new discovery may extend to a better understanding of malaria infection.
CONTACT
David Sibley (Washington University School of Medicine, St Louis, MO, USA)
Tel: +1 314 362 8873; E-mail: [email protected]
[2] Cancer: MicroRNAs that reduce metastasis (pp 147-152)
Restoring the expression of certain microRNAs (miRNAs) that are lost as breast cancer starts to metastasize suppresses the spread of the cancer, reports a paper in this week’s Nature.
Joan Massagué and colleagues identify a set of miRNAs that stop being expressed as human breast cancer cells develop metastatic potential. They then demonstrate that restoring the expression of this miRNA set in malignant cells suppresses lung and bone metastasis.
One in particular, miR-126, reduces overall tumour growth when restored, and another, miR-335, regulates a set of genes that increase the risk of metastasis. The association with metastatic relapse suggests that these molecules could be used in better prognosis for patients.
CONTACT
Joan Massagué (Memorial Sloan-Kettering Cancer Center/Howard Hughes Medical Institute, New York, NY, USA)
Tel: +1 646 888 2044; E-mail: [email protected]
[3] Space: Antimatter close to home (pp 159-162)
The origin of positrons is explored in research in Nature this week. Astronomers know that antimatter is found in our own Galaxy, but until now questions have remained as to where it originates.
The existence of gamma-ray line radiation at 511 kiloelectron volts (keV) demonstrates that electrons are colliding with positrons, and therefore proves the existence of this antimatter. Such radiation has been known for 30 years to come from the general direction of the Galactic Centre, but now astronomers have the tools to work out the distribution of this emission.
Georg Weidenspointner and colleagues look at four years of spectroscopic data from the INTEGRAL satellite and reveal an unexpectedly asymmetrical distribution of the 511-keV gamma-ray emissions. Their findings suggest that positrons originate in binary stars containing black holes or neutron stars that produce particularly energetic emission.
CONTACT
Georg Weidenspointner (Max-Planck-Institut, Muenchen, Germany)
Tel: +49 89 83 94 00 72; E-mail: [email protected]
Please note the author is travelling until 06 January it may be easiest to arrange interview by email
Gerry Skinner (Goddard Space Flight Centre, Greenbelt, MD, USA) Co-author
Tel: +1 310 286 1350; E-mail: [email protected]
[4] Cancer biology: Suppressing a leukaemia suppressor (pp 202-206)
The expression of genes that help to limit the growth of normal cells can sometimes be turned down in cancer, causing cells to divide uncontrollably — hence their branding as ‘tumour suppressor’ genes. Previously, this ‘silencing’ of gene expression was shown to result from changes in a particular methylation modification of the DNA encoding tumour suppressor genes, but puzzlingly, no mutations had been found in the enzymes that carry out methylation. A paper in this week’s Nature resolves this conundrum by identifying an RNA agent inside the cell nucleus that is able to tamper with the expression of one such gene, p15, which is silenced in leukaemia and other cancers.
Andrew Feinberg and colleagues pinpointed the rogue RNA because of its ‘antisense’ pattern of bases, which are a match with those of p15’s DNA. They worked out a molecular mechanism to explain how this antisense RNA effectively manages to silence both copies of the gene present in the cell, leaving it stripped of its protection against unregulated growth. This seems to be a general mechanism, as many tumour suppressor genes are found to have nearby antisense RNAs. This seems to be a general mechanism, as many tumour suppressor genes are found to have nearby antisense RNAs.
CONTACT
Andrew Feinberg (Johns Hopkins University School of Medicine, Baltimore, MD, USA)
Tel: +1 410 614 3489; E-mail: [email protected]
[5] Immunodeficiency: A shortage of oxygen to beat infection (pp 211-215)
Chronic granulomatous disease (CGD) is a genetic affliction that undermines the ability of children to fight off bacterial and fungal infections, manifesting as suppurating abscesses (granulomas) on the skin or in the lung, liver or bone marrow. A paper in this week’s Nature offers new insight into the mechanisms contributing to this excessive inflammation.
CGD results from a flaw in the seek-and-destroy machinery deployed by the white blood cells known as phagocytes to zap bacterial invaders; normally, the alien is engulfed and then bombarded with lethal oxygen radicals. Using genetically engineered mice as a model for CGD, Paolo Puccetti and colleagues find that failure to produce one of the most potent of these radicals, superoxide, not only cripples the phagocytes’ killing facility but also accounts for the microbes’ ability to set up sites of hyperinflammation.
The team scrutinized a metabolic pathway that produces immunoregulators known as kynurenines and discovered that without superoxide it can’t work properly, explaining why immune responses in CGD patients are messed up. However, the authors demonstrate that the block in this pathway can in principle be offset by a tricky replacement therapy involving a natural kynurenine.
CONTACT
Paolo Puccetti (University of Perugia, Italy)
Tel: +39 075 585 7463; E-mail: [email protected]
[6] & [7] Nanotechnology: Roughened silicon nanowires take the heat (pp 163-167 & 168-171; N&V)
Good thermoelectric materials are scarce — which is a pity, because theoretically they could be used to scavenge heat wasted from burning fossil fuels and convert it into electricity. Two papers in this week’s Nature describe how silicon devices could in principle be adapted and possibly scaled up for this purpose.
Bulk silicon is an inexpensive and widespread material with a well established processing infrastructure, but has poor thermoelectric properties. Peidong Yang and colleagues show how these can be markedly improved by electrochemical synthesis of arrays of roughened silicon nanowires. The roughening introduces defects that substantially reduce the nanowires’ thermal conductivity, holding promise for thermoelectric applications. In a related paper, James R. Heath and colleagues also demonstrate an improvement in the thermoelectric performance of silicon nanowires, this time by controlling the size of the nanowires and by doping them. They believe their approach could be applied to other classes of semiconductor nanomaterials.
The best thermoelectric material available is a compound of bismuth and tellurium, but that would be much more costly to scale up than silicon for salvaging heat waste.
CONTACT
Peidong Yang (University of California, Berkeley, CA, USA) Author paper [6]
Tel: +1 510 643 1545; E-mail: [email protected]
James R. Heath (California Institute of Technology, Pasadena, CA, USA) Author paper [7]
Tel: +1 626 395 6079; E-mail: [email protected]
Cronin B Vining (ZT Services, Auburn, AL, USA) N&V author
Tel: +1 334 887 2404; E-mail: [email protected]
[8] And finally… The genetics of sex (pp 183-196)
A simple fungus is presented as a model for sex determination in a paper in Nature this week. Although best known as a light-sensing model, Phycomyces blakesleeanus is now helping researchers understand the origin of sex and mating types at a much earlier evolutionary time.
As in other fungi, sex determination in P. blakesleeanus is not controlled by a whole chromosome, but by a small region of the genome, the sex locus. Using bioinformatics and genetic mapping, Joseph Heitman and colleagues identify two sex alleles, plus and minus, that play a vital role in sex determination. As with the SRY protein that is a master regulator of sexual differentiation in humans, the alleles encode transcription factors. Although further work is needed, these results provide a crucial step towards understanding the evolutionary trajectory of this sex-determining region in the fungal kingdom.
CONTACT
Joseph Heitman (Duke University, Durham, NC, USA)
Tel: +1 919 684 2824; E-mail: [email protected]
ALSO IN THIS ISSUE…
[9] Direct measurement of critical Casimir forces (pp 172-175; N&V)
[10] Seismic identification of along-axis hydrothermal flow on the East Pacific Rise (pp 181-184)
[11] Machaeridians are Palaeozoic armoured annelids (pp 185-188; N&V)
[12] The coevolution of choosiness and cooperation (pp 189-192)
[13] Ultra-fine frequency tuning revealed in single neurons of human auditory cortex (pp 197-201)
ADVANCE ONLINE PUBLICATION
***These papers will be published electronically on Nature's website on 09 January 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 10 January, but at a later date.***
[14] Lethargus is a Caenorhabditis elegans sleep-like state
DOI: 10.1038/nature06535
[15] Histone H2AX-dependent GABAA receptor regulation of stem cell proliferation
DOI: 10.1038/nature06488
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.
BELGIUM
Ghent: 11
CZECH REPUBLIC
Brno: 15
FRANCE
Gif-sur-Yvette: 3
Nouzilly: 1
Paris: 15
Toulouse: 3
GERMANY
Garching: 3
Munich: 3
Stuttgart: 9
IRELAND
Dublin: 11
ISRAEL
Jerusalem: 13
Rehovot: 13
Tel Aviv: 13
ITALY
Perugia: 5
JAPAN
Osaka: 1
NETHERLANDS
Noordwijk: 3
SWEDEN
Stockholm: 15
UNITED KINGDOM
Bristol: 12
London: 15
UNITED STATES OF AMERICA
California
Berkeley: 6
Los Angeles: 13
Pasadena: 7
Connecticut
New Haven: 11
New York
Buffalo: 5
New York: 2
Palisades: 10
Maryland
Baltimore: 4
Bethesda: 4
Greenbelt: 3
Minnesota
Rochester: 4
Missouri
Kansas City: 8
St Louis: 1
North Carolina
Durham: 8
Raleigh: 10
Pennsylvania
Philadelphia: 14
Texas
Dallas: 14
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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
Ruth Francis, Nature London
Tel: +44 20 7843 4562; E-mail [email protected]
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