Nanotechnology: Fresh water for less

Clinical promise for RNA interference; To catch a virus; The helping and hurting hands of microglia; Sugar assembly line in tuberculosis; Hemoglobin variants associated with malaria parasite transmission; Niche genetics influence leukaemia; Vitamin A biofortification in corn; Intense star formation in distant galaxies


For papers that will be published online on 21 March 2010

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

This press release contains:

· Summaries of newsworthy papers:

Nanotechnology: Fresh water for less

Nature: Clinical promise for RNA interference

Immunology: To catch a virus

Neuroscience: The helping and hurting hands of microglia

Chemical Biology: Sugar assembly line in tuberculosis

Genetics: Hemoglobin variants associated with malaria parasite transmission

Nature: Niche genetics influence leukaemia

Genetics: Vitamin A biofortification in corn

Nature: Intense star formation in distant galaxies

· 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 Press contacts for the Nature journals are listed at the end of this release.

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[1] Nanotechnology: Fresh water for less
DOI: 10.1038/nnano.2010.34

A device for converting sea water to fresh water that could be powered by a battery is reported online in Nature Nanotechnology this week. Established desalination methods require high power consumption or can only operate efficiently on a large scale, and are therefore difficult to use in disaster- or poverty-stricken areas.

Jongyoon Han and colleagues developed a device that uses a phenomenon known as ion-concentration polarization, which occurs when a current of ions travels through an ion-selective nanochannel. The nanochannel is situated between two microchannels containing streams of sea water. When a voltage is applied across the nanochannel, ions are enriched at one end of the nanochannel and depleted at the other. As a result, salt ions in the sea water that are near the nanochannel are repelled. By separating one of the microchannels into two channels near this repulsion zone, the saltier water can be pulled off and the desalted water, which has no charge, can pass through the charged region and into a separate freshwater channel.

The method allows both salts and larger particles — such as cells, viruses and microorganisms — to be removed at a power efficiency similar to state-of-the-art large-scale plants.

Author contact:
Jongyoon Han (Massachusetts Institute of Technology, Cambridge, MA, USA)
Tel: +1 617 253 2290; E-mail: [email protected]

[2] Nature: Clinical promise for RNA interference
DOI: 10.1038/nature08956

The first proof-of-principle study showing that the gene-silencing technique RNA interference (RNAi) can indeed lower levels of gene expression in humans is revealed in this week’s Nature. The study, in human tumour biopsies, marks an important step towards the possible therapeutic use of RNAi to target disease.

RNA interference, a naturally occurring form of gene regulation, can be induced experimentally by treatment with small interfering RNAs (siRNAs), double-stranded RNA molecules designed to interfere specifically with key genes. In this study, biopsies from three melanoma patients who had received siRNA infusions revealed dose-dependent reductions in the levels of target messenger RNA and protein.

The results form part of the first in-human phase I clinical trial of systemic siRNA treatment for patients with solid cancers using a targeted, nanoparticle delivery system — designed to help the siRNA get to where it needs to go. Mark E. Davis and colleagues show that the injected siRNA yields its effects by RNAi, a feat hitherto demonstrated in mouse and non-human primate models. Because RNAi is likely to be applicable to any gene, the study hints that targeted delivery of siRNA by nanoparticles may prove a useful way of controlling many previously unreachable drug targets.

Author contact:
Mark E. Davis (California Institute of Technology, Pasadena, CA, USA)
Tel: +1 626 395 4251; E-mail: [email protected]

[3] Immunology: To catch a virus
DOI: 10.1038/ni.1856

How immune cells quickly and efficiently capture influenza vaccines to trigger protective antibody responses is presented in a study published online this week in Nature Immunology.

Antigen-presenting dendritic cells (DCs) are immune cells that capture and process antigens—in this case the inactivated form of influenza used in vaccines—and present bits of these antigens to activate other immune cells, such as B cells.

Michael Carroll and Shannon Turley found that DCs in draining lymph nodes latch onto sugars present on the viral surface. This sugar recognition is achieved by a receptor called SIGN-R1. Blocking SIGN-R1 inhibited DC recognition of the influenza viruses, and more importantly blunted the ensuing antibody response by nearby B cells—the cells responsible for antibody production. The scientists also visualized live DC movement in the lymph nodes of mice immunized with the influenza virus. Prior to immunization, the lymph node DCs were immobile, but upon catching the inactive lymph-borne virus using their SIGN-R1 receptors, the DCs became motile and migrated toward follicular areas rich in B cells.

This efficient DC capture of virus and delivery to B cells ensures rapid antibody responses can occur, which is necessary to combat fast-replicating pathogens such as live influenza virus.

Authors contact:
Michael C. Carroll (Harvard Medical School, Boston, MA, USA)
Tel: +1 617 713 8700; E-mail: [email protected]

Shannon J. Turley (Dana Farber Cancer Institute, Boston, MA, USA)
Tel: +1 617 632 4990; E-mail: [email protected]

[4] Neuroscience: The helping and hurting hands of microglia
DOI: 10.1038/nn.2511

By monitoring the movement of microglia—immune cells of the brain—in a mouse model of Alzheimer’s disease (AD), scientists report that neuronal loss in the disease model is mitigated if the microglia’s abilities to recognize and move towards neurons are disrupted. These results, published online this week in Nature Neuroscience, could be important in finding new targets for the development of therapeutic strategies to combat neuron loss in AD.

Progressive neuronal loss is a hallmark of AD, though the exact role of immune response in the disease progression is unclear. For example, microglia can eliminate amyloid beta aggregation, a common protein build-up found in AD brains. However, microglia are also known to be neurotoxic in the rodent models of Parkinson’s disease and amyotrophic lateral sclerosis (ALS). Little is known about neurotoxic functionality of microglia in AD.

In order to better understand if microglia is involved in AD-related neuronal death, Jochen Herms and colleagues used in vivo imaging to simultaneously visualized neurons and microglia in the brains of mice in a rodent model of Alzheimer’s disease. By imaging these cells in the same live animals up to four weeks, the scientists found that microglia are locally recruited to neurons before, but not after, cells begin to die and be eliminated. However, when the same in vivo imaging was conducted on mice lacking Cx3cr1—a gene for a microglial receptor crucial in neuron-microglia communication—neuron loss in the mouse model of AD was prevented. These findings also suggest that microglia can be either beneficial or detrimental to neuronal death that is context-dependent on the type of neurodegeneration.

Author contact:
Jochen Herms (Ludwig Maximilians University, Munich, Germany)
Tel: +49 89 2180 78010, E-mail: [email protected]

[5] Chemical Biology: Sugar assembly line in tuberculosis
DOI: 10.1038/nchembio.340

A key enzyme in the tuberculosis bacterial pathogen Mycobacterium tuberculosis is involved in a previously unknown pathway for building polysaccharides. The results, published this week in Nature Chemical Biology, offer a potential new drug target against tuberculosis.

The gene glgE was previously demonstrated to be essential in M. tuberculosis; however the biological function of the corresponding enzyme, GlgE, was unknown. Using genetic and biochemical approaches, William Jacobs and colleagues identified four enzymes involved in a pathway that converts a naturally-occurring sugar compound into polysaccharides called alpha-glucans. The scientists found that inactivating one of these enzymes, TreS, was not lethal to the bacteria, indicating that this pathway is not required for growth. However, inactivating GlgE was lethal, causing the buildup of toxic levels of the enzyme’s sugar substrate, maltose-1-phosphate. In addition, the scientists found that the combined inactivation of TreS and an enzyme for an alternate alpha-glucan biosynthetic pathway was lethal, highlighting the important roles of alpha-glucan’s in M. tuberculosis growth.

Though the biological role of the GlgE pathway remains to be elucidated, GlgE and the alpha-glucan pathways more generally, are possible drug targets that can now be tested in in vivo models of tuberculosis infection.

Author contact:
William Jacobs Jr. (Albert Einstein College of Medicine, Bronx, NY, USA)
Tel: +1 718 678 1075; E-mail: [email protected]

[6] Genetics: Hemoglobin variants associated with malaria parasite transmission
DOI: 10.1038/ng.554

Hemoglobins C and S (HbC and HbS, respectively) are associated with an increase in malaria parasite transmission from the human host to the mosquito, according to a study published online this week in Nature Genetics. These results suggest that the host’s genetic variations can affect transmission rates of malaria.

Malaria is a life-threatening disease caused by the Plasmodium parasites and transmitted to humans via infected mosquitoes. It is known that genetic variants in two types of hemoglobin, HbC and HbS, protect against malaria.

David Modiano and colleagues investigated whether HbC and HbS also affect the transmission of the malaria parasite from human to mosquito. The scientists conducted a large survey of close to 4000 individuals in rural West Africa and observed higher levels of infectious parasites in HbC genetic variant carriers. Next, the scientists performed transmission experiments involving over 6000 mosquitoes that received genotype-controlled blood meals. They observed that transmission of the malaria parasite from human blood to mosquito is enhanced when the blood meal came from individuals carrying HbC.

Author contact:
David Modiano (University of Rome ‘La Sapienza’, Italy)
Tel: +39 3470 013734; E-mail: [email protected]

[7] Nature: Niche genetics influence leukaemia
DOI: 10.1038/nature08851

Certain blood cancers can be triggered by genetic changes in the blood cells’ microenvironment, a new mouse model of cancer indicates. The finding may have implications for our understanding and treatment of leukaemia.

Deletion in bone progenitor cells of Dicer1, a gene involved in microRNA processing, disrupts normal blood cell production and can lead to leukaemia, David Scadden and colleagues report in this week's Nature. The progenitor cells, which form part of the ‘niche’ surrounding blood cells, have lower levels of Sbds, the gene mutated in Schwachman–Bodian–Diamond syndrome — a human bone marrow failure that predisposes to leukaemia.

The team envisage a ‘niche-based’ model of oncogenesis in which a change in a specific microenvironmental cell acts as the primary moment in a multi-step process towards malignancy of a supported, but distinct cell type. Signals generated by the microenvironment may therefore represent possible therapeutic targets for treatment and prevention strategies.

Author contact:
David Scadden (Massachusetts General Hospital, Boston, MA, USA)
Tel: +1 617 726 5615; E-mail: [email protected]

[8] Genetics: Vitamin A biofortification in corn
DOI: 10.1038/ng.551

Naturally occurring genetic variants at the crtRB1 gene—involved in synthesis of beta-carotene, a precursor of vitamin A—are associated with increased levels of beta-carotene in maize, according to a report published online this week in Nature Genetics. These favorable variants are presently being bred into tropical maize grown in developing countries where vitamin A is needed to improve health.

In developing countries, vitamin A deficiency (VAD) leads to blindness in several hundred thousand children each year, half of whom die from VAD-related problems. Vitamin A biofortification of crops using naturally occurring genetic variants is one solution in combating VAD and other micronutrient malnutrition.

Using maize, Torbert Rocheford and colleagues surveyed naturally occurring variants of beta-carotene hydroxylases—enzymes known to be involved in the synthesis of beta-carotene. The scientists identified a combination of genetic variants at crtRB1 that led to an average increase of beta-carotene in maize from a baseline level of 0.5 micrograms/gram to approximately 9 micrograms/gram.

Author contact:
Torbert Rocheford (Purdue University, West Lafayette, IN, USA)
Tel: +1 217 417 5093; E-mail: [email protected]

[9] Nature: Intense star formation in distant galaxies
DOI: 10.1038/nature08880

A high-resolution view of conditions occurring within the star-forming regions of a galaxy during the period of peak galaxy formation is published in Nature this week. The study suggests that the underlying physics of star formation is similar to that of local galaxies, just writ large.

Massive galaxies in the early Universe have been shown to be forming stars at surprisingly high rates — at about a thousand solar masses per year. Most telescopes however, are unable to probe individual star-forming regions within these galaxies, because their spatial resolution is not yet high enough.

Mark Swinbank and colleagues take advantage of a cosmic lens and also use high-resolution imaging to investigate the physical properties of these star-forming regions. They find a distant galaxy that has been magnified by a galaxy cluster along the line of sight, known as a gravitational lens. They find that the star-formation regions are a hundred times bigger, and ten million times more luminous, than the dense cores of giant molecular clouds.

Author contact:
Mark Swinbank (Institute for Computational Cosmology, Durham, UK)
Tel: +44 191 334 3786; E-mail: [email protected]

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

Nature (

[10] Molecular mechanism of multivesicular body biogenesis by ESCRT complexes
DOI: 10.1038/nature08849

[11] Identification of two evolutionarily conserved genes regulating processing of engulfed apoptotic cells
DOI: 10.1038/nature08853


[12] Gain of miR-151 on chromosome 8q24.3 facilitates tumour cell migration and spreading through downregulating RhoGDIA
DOI: 10.1038/ncb2039

[13] Coupling between hydrodynamic forces and planar cell polarity orients mammalian motile cilia
DOI: 10.1038/ncb2040

[14] Vangl2 directs the posterior tilting and asymmetric localization of motile primary cilia
DOI: 10.1038/ncb2042


[15] Glycopeptide specific monoclonal antibodies suggest new roles for O-GlcNAc
DOI: 10.1038/nchembio.338


[16] High-spin ground states via electron delocalization in mixed-valence imidazolate-bridged divanadium complexes
DOI: 10.1038/nchem.585

[17] Million-fold activation of the [Fe2([mu]-O)2] diamond core for C–H bond cleavage
DOI: 10.1038/nchem.586

[18] Self-assembly and optically triggered disassembly of hierarchical dendron–virus complexes
DOI: 10.1038/nchem.592

[19] A ‘Texas-sized’ molecular box that forms an anion-induced supramolecular necklace
DOI: 10.1038/nchem.597


[20] Fragmentation of active continental plate margins owing to the buoyancy of the mantle wedge
DOI: 10.1038/ngeo825

[21] Heterogeneous nucleation of ice particles on glassy aerosols under cirrus conditions
DOI: 10.1038/ngeo817


[22] Irreversible nanogel formation in surfactant solutions by microporous flow
DOI: 10.1038/nmat2724

[23] Spatially homogeneous ferromagnetism of (Ga, Mn)As
DOI: 10.1038/nmat2715


[24] Pleiotrophin regulates the expansion and regeneration of hematopoietic stem cells
DOI: 10.1038/nm.2119

[25] Myeloperoxidase acts as a profibrotic mediator for atrial fibrillation
DOI: 10.1038/nm.2124

[26] The Mycobacterium tuberculosis protein LdtMt2 is a nonclassical transpeptidase required for virulence and resistance to amoxicillin
DOI: 10.1038/nm.2120


[27] Direct determination of molecular haplotypes by chromosome microdissection
DOI: 10.1038/nmeth.1443


[28] Identifying single nucleotides by tunnelling current
DOI: 10.1038/nnano.2010.42


[29] Presynaptic GABAA receptors enhance glutamatergic transmission and facilitate LTP induction at hippocampal mossy fiber synapses
DOI: 10.1038/nn.2512

[30] Control of sexual differentiation and behavior by the doublesex gene in Drosophila melanogaster
DOI: 10.1038/nn.2515

[31] Monitoring neural activity with bioluminescence during natural behavior
DOI: 10.1038/nn.2518


[32] Soliton–similariton fibre laser
DOI: 10.1038/nphoton.2010.33

Nature PHYSICS (

[33] Observation of a one-dimensional spin–orbit gap in a quantum wire
DOI: 10.1038/nphys1626

[34] Mott physics and band topology in materials with strong spin–orbit interaction
DOI: 10.1038/nphys1606

[35] Optimal matrix rigidity for stress-fibre polarization in stem cells
DOI: 10.1038/nphys1613

[36] Interplay between superconductivity and ferromagnetism in crystalline nanowires
DOI: 10.1038/nphys1621


[37] Structures of ClpP in complex with acyldepsipeptide antibiotics reveal its activation mechanism
DOI: 10.1038/nsmb.1787

[38] Spinophilin directs protein phosphatase 1 specificity by blocking substrate binding sites
DOI: 10.1038/nsmb.1786

[39] Structure of monoubiquitinated PCNA and implications for translesion synthesis and DNA polymerase exchange
DOI: 10.1038/nsmb.1776

[40] Conformational dynamics of single pre-mRNA molecules during in vitro splicing
DOI: 10.1038/nsmb.1767


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.

Sydney: 20

Bobo Dioulasso: 6

Yaounde: 6

Calgary: 30
London: 7, 29
Toronto: 7, 14
Vancouver: 23

Cassilla: 9

Jiangsu: 12
Shanghai: 12

Aarhus: 3

Cairo: 15

Bordeaux: 13
Gif-sur-Yvette: 40
Marseille: 13
Orsay: 33
Paris: 13, 26
Saint-Martin-d’Heres: 9

Bonn: 25
Braunschweig: 21
Dusseldorf: 5, 37
Goettingen: 25, 35
Hamburg: 25
Heidelberg: 21
Munich: 4, 9, 23
Postfach: 21
Tuebingen: 25
Wessling: 21
Wuppertal: 37

Pecs: 15

Jerusalem: 35
Rehovot: 33, 35

Rome: 6

Nagoya: 13
Osaka: 28
Saitama: 28
Sendai: 23
Tokyo: 23

Hyojadong: 1
Seoul: 28, 37

Texcoco: 8

Enschede: 18
Nijmegen: 18

Alicante: 29

Villigen: 23

Ankara: 32

Birmingham: 5
Bristol: 18
Durham: 9
Edinburgh: 9
Glasgow: 30
Leeds: 21
Norwich: 5
Nottingham: 3
Oxford: 3, 30


Birmingham: 15, 27

Berkeley: 16
Duarte: 2
Irvine: 4
Los Angeles: 2
Pasadena: 2, 9, 31
Riverside: 36
San Diego: 16
San Francisco: 13, 40
Santa Barbara: 34
Santa Clara: 40
Stanford: 33

New Haven: 38
Stamford: 22

Athens: 15
Atlanta: 27
Leesburg: 8

Urbana: 8, 33

West Lafayette: 8

Ames: 8
Iowa City: 39

Pittsburg: 25

Baltimore: 26
Bethesda: 10
College Park: 9

Boston: 3, 7
Cambridge: 1, 2, 7, 9, 31

Ann Arbor: 40
East Lansing: 8

Minneapolis: 17

Starkville: 8

Columbia: 40
St Louis: 22

Bozeman: 3

New Hampshire
Durham: 24

New Jersey
Murray Hill: 33
Piscataway: 9
Princeton: 9, 33

New York
Bronx: 5
Ithaca: 8, 40
New York: 7, 23
Syracuse: 22

Cleveland: 25

Hillsboro: 36

Philadelphia: 35
Pittsburgh: 17
University Park: 36

Rhode Island
Providence: 38

Knoxville: 22
Nashville: 27

Austin: 19, 34
College Station: 5
San Antonio: 2

Charlottesville: 11

Seattle: 22, 34


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

Rachel Twinn (Nature London)
Tel: +44 20 7843 4658; E-mail: [email protected]

Neda Afsarmanesh (Nature New York)
Tel: +1 212 726 9231; E-mail: n.afsarm[email protected]

Ruth Francis (Head of Press, Nature, London)
Tel: +44 20 7843 4562; E-mail: [email protected]

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

Nature Biotechnology (New York)
Michael Francisco
Tel: +1 212 726 9288; E-mail: [email protected]

Nature Cell Biology (London)
Sowmya Swaminathan
Tel: +44 20 7843 4656; E-mail: [email protected]

Nature Chemical Biology (Boston)
Sarah Daniels
Tel: +1 617 475 9241, E-mail: [email protected]

Nature Chemistry (London)
Stuart Cantrill
Tel: +44 20 7014 4018; E-mail: [email protected]

Nature Genetics (New York)
Myles Axton
Tel: +1 212 726 9324; E-mail: [email protected]

Nature Geoscience (London)
Heike Langenberg
Tel: +44 20 7843 4042; E-mail: [email protected]

Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: [email protected]

Nature Materials (London)
Vincent Dusastre
Tel: +44 20 7843 4531; E-mail: [email protected]

Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]

Nature Methods (New York)
Hugh Ash
Tel: +1 212 726 9627; E-mail: [email protected]

Nature Nanotechnology (London)
Peter Rodgers
Tel: +44 20 7014 4019; Email: [email protected]

Nature Neuroscience (New York)
Kalyani Narasimhan
Tel: +1 212 726 9319; E-mail: [email protected]

Nature Photonics (Tokyo)
Oliver Graydon
Tel: +81 3 3267 8776; E-mail: [email protected]

Nature Physics (London)
Alison Wright
Tel: +44 20 7843 4555; E-mail: [email protected]

Nature Structural & Molecular Biology (New York)
Sabbi Lall
Tel: +1 212 726 9326; E-mail: [email protected]

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Published: 21 Mar 2010

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