Better digs benefit behavior: new neurons not required; Old drug finds a new target

Studies in recent years have shown that some brain regions continue to generate new neurons even during adulthood. Scientists have identified a new target for an old drug that has been used to treat tuberculosis for over 50 years.

NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE

For papers that will be published online on 30 April 2006. This press release is copyrighted to the Nature journals mentioned below.

This press release contains:

· Summaries of newsworthy papers:
Better digs benefit behavior: new neurons not required – Nature Neuroscience
Sensing bacterial infection – Nature Immunology
Old drug finds a new target – Nature Structural and Molecular Biology
· Mention of papers to be published at the same time with the same embargo
· Geographical listing of authors

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PLEASE CITE THE SPECIFIC NATURE JOURNAL AND WEBSITE AS THE SOURCE OF THE FOLLOWING ITEMS. IF PUBLISHING ONLINE, PLEASE CARRY A HYPERLINK TO THE APPROPRIATE JOURNAL’S WEBSITE.

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

[1] Better digs benefit behavior: new neurons not required
DOI: 10.1038/nn1696

Studies in recent years have shown that some brain regions continue to generate new neurons even during adulthood. The significance of these newborn cells for brain function remains unclear, as does the potential benefit of increasing their numbers. A new study in the June issue of Nature Neuroscience fails to find a causal relationship between behavioral improvements and increased neurogenesis in adult mice.

Laboratory mice housed in cages with extra room, toys and social interaction are less anxious and learn better than mice housed in typical cages, and they also generate more new neurons in the hippocampus, a brain area important for learning and memory. René Hen and colleagues blocked neurogenesis in the hippocampus of adult mice with x-ray radiation before housing them in enriched environments. After six weeks, irradiated mice showed the same improvement in learning and decrease in anxiety-like behavior as non-irradiated mice, suggesting that these behavioral effects were not due to an increase in new hippocampal neurons.

Author contact:
René Hen (Columbia University, New York, NY, USA)
Tel: +1 212 543 5328; E-mail: [email protected]

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

[2] Syndapin I is the phosphorylation-regulated dynamin I partner in synaptic vesicle endocytosis
DOI: 10.1038/nn1695

[3] Distinct timing in the activity of cannabinoid-sensitive and -insensitive basket cells
DOI: 10.1038/nn1688

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

[4], [5] & [6] Sensing bacterial infection
DOI: 10.1038/ni1336
DOI: 10.1038/ni1344
DOI: 10.1038/ni1346

New information on the complex interplay between host cells and bacteria during infection is reported in the June issue of Nature Immunology. Three studies provide a new understanding of the relationship between salmonella bacteria and the cells infected.

Host cells use special ‘sensors’ to detect unique components of invading bacteria and alert the rest of the body to the infection by triggering inflammation. Bacteria produce flagellin, a protein that bundles together to form the flagellum, a tail that allows bacteria to swim.

Teams led by Alan Aderem and Gabriel Nunez find that when salmonella bacteria infect a host cell, flagellin released from the bugs is detected by a sensor that triggers inflammation. In a complementary study, work from Ayub Qadri’s laboratory shows that host cells produce a lipid that ‘tricks’ salmonella into secreting flagellin so that the bugs can be detected by the host sensor, triggering an immune response. These studies provide exciting new details of how bacteria cause inflammation and how host cells are actively involved in that process.

Author contacts:
Ayub Qadri (National Institute of Immunology, New Delhi, India)
Tel: +91 11 26703733; E-mail: [email protected]

Alan Aderem (Institute for Systems Biology, Seattle, WA, USA)
Tel: +1 206 732 1203; E-mail: [email protected]

Gabriel Nunez (University of Michigan, Ann Arbor, MI, USA)
Tel: +1 734 764 8514; E-mail: [email protected]

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

[7] Quantitative proteomic analysis of B cell lipid rafts reveals that ezrin regulates antigen receptor–mediated lipid raft dynamics
DOI: 10.1038/ni1337

**************NATURE STRUCTURAL AND MOLECULAR BIOLOGY****************
(http://www.nature.com/natstructmolbiol)

[8] Old drug finds a new target
DOI: 10.1038/nsmb1089

Scientists have identified a new target for an old drug that has been used to treat tuberculosis for over 50 years. This finding, reported in the May issue of Nature Structural & Molecular Biology, should be useful for designing new antitubercular compounds.

Tuberculosis is a global health threat, and an estimated two million people die each year of the disease. The drug isoniazid is the first line of defense against the bacteria that cause the disease. It is processed by an enzyme in the microbe, and one of the resulting products interferes with the synthesis of the bacterial cell wall, thereby quickly killing the pathogen.

Blanchard and colleagues now find that isoniazid targets another process essential for the survival of the tubercular bacteria. They show that a different product from isoniazid processing inhibits an enzyme called DHFR, which is important for the synthesis of nucleic acid building blocks. The authors further demonstrate in detail how DHFR is inhibited by the isoniazid metabolite. These results may explain the emergence of some drug-resistant tubercular bacteria observed in the clinic and should provide a foundation for engineering new drugs for treating the disease.

Author contact:
John Blanchard (Albert Einstein College of Medicine, Bronx, NY, USA)
Tel: +1 718 430 3096; E-mail: [email protected]

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

[9] Peptide bond formation does not involve acid-base catalysis by ribosomal residues
DOI: 10.1038/nsmb1091

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

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

[10] Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells
DOI: 10.1038/nature04753

[11] Transforming growth factor-beta induces development of the TH17 lineage
DOI: 10.1038/nature04754

[12] GTP-dependent twisting of dynamin implicates constriction and tension in membrane fission
DOI: 10.1038/nature04718

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

[13] A toolbox for lattice-spin models with polar molecules
DOI: 10.1038/nphys287

[14] Attosecond electron wave packet interferometry
DOI: 10.1038/nphys290

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

[15] Long-range resonantly enhanced triplet formation in luminescent polymers doped with iridium complexes
DOI: 10.1038/nmat1630

[16] Ultrasonic metamaterials with negative modulus
DOI: 10.1038/nmat1644

NATURE MEDICINE (www.nature.com/naturemedicine)

[17] Cytokine-mediated deployment of SDF-1 induces revascularization through recruitment of CXCR4+ hemangiocytes
DOI: 10.1038/nm1400

[18] Mig6 is a negative regulator of EGF receptor–mediated skin morphogenesis and tumor formation
DOI: 10.1038/nm1401

Nature BIOTECHNOLOGY (http://www.nature.com/naturebiotechnolgy)

[19] A structural basis for discriminating between self and nonself double-stranded RNAs in mammalian cells
DOI: 10.1038/nbt1205

[20] Stable expression of shRNAs in human CD34+ progenitor cells can avoid induction of interferon responses to siRNAs in vitro
DOI: 10.1038/nbt1206

[21] A fluorescent variant of a protein from the stony coral Montipora facilitates dual-color single-laser fluorescence cross-correlation spectroscopy
DOI: 10.1038/nbt1207

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

[22] Drosophila Pins-binding protein Mud regulates spindle-polarity coupling and centrosome organization
DOI: 10.1038/ncb1409

[23] Early mitotic degradation of Nek2A depends on Cdc20-independent interaction with the APC/C
DOI: 10.1038/ncb1410

[24] An interaction between integrin and the talin FERM domain mediates integrin activation but not linkage to the cytoskeleton
DOI: 10.1038/ncb1411

[25] The NuMA-related Mud protein binds Pins and regulates spindle orientation in Drosophila neuroblasts
DOI: 10.1038/ncb1412

NATURE GENETICS

[26] A common genetic variant in the NOS1 regulator NOS1AP modulates cardiac repolarization
DOI: 10.1038/ng1790

[27] Mutations in the gene encoding the PML nuclear body protein Sp110 are associated with immunodeficiency and hepatic veno-occlusive disease
DOI: 10.1038/ng1780

***Please note this is the only item on this press release for release on the 28th April 1800 London time (BST). All other items remain embargoed until Sunday 30 April 1800 London Time (BST)***

[28] Genome-wide analysis of mammalian promoter architecture and evolution
DOI: 10.1038/ng1789

*******************************************************************

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.

AUSTRALIA
Brisbane: 28
Melbourne: 19
Queensland: 28
Sydney: 27
Victoria: 17
Wentworthville: 2
Westmead: 27

AUSTRIA
Innsbruck: 12
Vienna: 18

BELGIUM
Ghent: 6

CANADA
British Columbia: 20
Vancouver: 17

DENMARK
Aarhus: 19

FINLAND
Helsinki: 28

FRANCE
Palaiseau Cedex: 14
Paris: 1

GERMANY
Freiburg: 27
Heidelberg: 9
Martinsried: 18
Munich: 9, 26
Neuherberg: 26
Witten: 9
Wuerzburg: 22

INDIA
New Delhi: 4

ITALY
Napoli: 28
Trieste: 28

JAPAN
Ibaraki: 28
Kanagawa: 28
Kobe: 22
Kyoto: 19
Nagoya City: 21
Saitama: 21, 28
Sapporo: 21
Tokyo: 21, 28
Yokohama: 28

MEXICO
Mexico: 5

THE NETHERLANDS
Amsterdam: 14

NORWAY
Bergen: 28

SINGAPORE
Singapore: 28

SOUTH AFRICA
Bellville: 28

SWEDEN
Lund: 14
Stockholm: 28

SWITZERLAND
Zurich: 7

UNITED KINGDOM
Cambridge: 23, 24
Durham: 15
Edinburgh: 2, 28
Leicester: 23
Oxford: 28
Surrey: 23

UNITED STATES OF AMERICA
Alabama
Birmingham: 11
California
Berkeley: 14
Duarte: 20
San Diego: 3, 28
San Francisco: 7, 17
Connecticut
New Haven: 12
Oregon
Eugene: 25
Florida
Jupiter: 28
Iowa
Coralville: 19, 20
Louisiana
Baton Rouge: 14
Maryland
Baltimore: 26
Bethesda: 11
Gaithersburg: 6
Massachusetts
Boston: 10, 26, 27
Cambridge: 6, 10
Michigan
Ann Arbor: 6
New York
Bronx: 8
Brooklyn: 8
New York: 1, 17
Ohio
Cleveland: 19
Washington
Seattle: 5, 7, 27

PRESS CONTACTS…

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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:

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Nature Cell Biology (London)

Bernd Pulverer
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Nature Chemical Biology (Boston)

Beatrice Chrystall
Tel: +1 617 475 9241, E-mail: [email protected]

Nature Genetics (New York)

Orli Bahcall
Tel: +1 212 726 9311; E-mail: [email protected]

Nature Immunology (New York)

Laurie Dempsey
Tel: +1 212 726 9372; E-mail: [email protected]

Nature Materials (London)

Maria Bellantone
Tel: +44 20 7843 4556; E-mail: [email protected]

Nature Medicine (New York)

Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]

Nature Neuroscience (New York)

Sandra Aamodt (based in California)
Tel: +1 530 795 3256; E-mail: [email protected]

Nature Physics (London)

Alison Wright
Tel: +44 20 7843 4555; E-mail: [email protected]

Nature Structural & Molecular Biology (New York)

Ed Feng
Tel: +1 212 726 9351; E-mail: [email protected]

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Published: 30 Apr 2006

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