Drug target for obesity?

A molecule that makes mammals feel full up has been identified, and drugs that target it may help to treat obesity. Other newsworthy papers include Vision: Bug eyes get a makeover - Nature, One step toward more efficient cloning - Nature Genetics, New strategy for controlling inflammation - Nature Immunology


For papers that will be published online on 01 October 2006

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

This press release contains:

* Summaries of newsworthy papers:

Neuroscience: Drug target for obesity? - Nature

Vision: Bug eyes get a makeover - Nature

One step toward more efficient cloning - Nature Genetics

New strategy for controlling inflammation - 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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[1] Neuroscience: Drug target for obesity?

DOI: 10.1038/nature05162

A molecule that makes mammals feel full up has been identified, and drugs that target it may help to treat obesity.

Appetite is regulated, at least in part, in a brain region called the hypothalamus. In a paper published online by Nature this week, Masatomo Mori and colleagues show that a fragment of the secreted protein NUCB2, dubbed nesfatin-1, is expressed in this control centre and induces a feeling of satiety.

When nesfatin-1is injected into the brain, rats eat less and begin to lose weight. When nesfatin-1 is blocked, animals eat more.

Author contact:
Masatomo Mori (Gunma University Graduate School of Medicine, Maebashi, Japan)
Tel: +81 27 220 8120; E-mail: [email protected] <mailto:[email protected]>

[2] Vision: Bug eyes get a makeover
DOI: 10.1038/nature05128

Altering the expression of a single gene dramatically alters the architecture of insect compound eyes, according to researchers in a report to be published online this week by Nature.

The protruding compound eyes of insects are made up of many tiny simplified eyes, each containing a number of rod-shaped, light-sensitive cells called rhabdomeres. In fruitfly and housefly eyes, the rhabdomeres are separated from each other and function independently - a so-called 'open system'. But in the 'closed system' of bees, and some mosquitoes and beetles, the rhabdomeres are fused together and function as a unit.

Charles S. Zuker and colleagues have identified three genes involved in rhabdomere assembly. The loss of one gene, called spacemaker, converts an open system to a closed one. Furthermore, introducing the same gene into the light-sensitive cells of a closed system transforms it to an open one.

Author contact:

Charles S Zuker (Howard Hughes Medical Institute & University of California-San Diego, La Jolla, CA, USA)
Tel: +1 858 534 7728; E-mail: [email protected]

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

[3] Bidirectional control of CNS capillary diameter by pericytes
DOI: 10.1038/nature05193

[4] Fast neurotransmitter release triggered by Ca influx through AMPA-type glutamate receptors
DOI: 10.1038/nature05123

[5] Role of Bax and Bak in mitochondrial morphogenesis
DOI: 10.1038/nature05111

*********************************NATURE GENETICS **************************

[6] One step toward more efficient cloning
DOI: 10.1038/ng1895

A one-step somatic cell nuclear transfer procedure using a differentiated cell as a nuclear donor is reported for the first time in a paper in the November issue of Nature Genetics. The study demonstrates that fully differentiated granulocytes - a specialized type of white blood cell - yield cloned mice with greater efficiency than undifferentiated blood stem cells.

Somatic cell nuclear transfer - SCNT - is the procedure by which cloned animals are typically produced and involves the injection of a nucleus from a donor cell into an egg whose nucleus has been removed. Previous studies report that cloned mice could only be generated with differentiated cells as nuclear donors using a two-step procedure, in which the early embryos generated by SCNT are first used to generate embryonic stem cells that are subsequently injected into another recipient embryo. Other studies also report that the cloning efficiency for embryonic stem cells is much higher than for other kinds of cells.

Yang and colleagues injected nuclei from blood cells at different stages of differentiation into donor eggs and report that the nuclei of granulocytes allow for more efficient production of cloned embryos than blood stem cells. They report that two live pups were born using this procedure, although these died shortly after birth. The authors believe that their findings - that a non-dividing, fully differentiated cell from an adult animal can be used to generate a live-born cloned mouse in a one-step SCNT procedure - contradict current assumptions concerning the efficiency of adult stem cells as donors in cloning.

Author contact:
Xiangzhong Yang (University of Connecticut, Storrs, CT, USA)
Tel: +1 860 486 8728; E-mail: [email protected]

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

[7] Regulation of primary cilia formation and left-right patterning in zebrafish by a noncanonical Wnt signaling mediator, duboraya

DOI: 10.1038/ng1892

[8] Differences in reactive oxygen species production explain the phenotypes associated with common mouse mitochondrial DNA variants

DOI: 10.1038/ng1897

[9] Mutations in FRMD7, a newly identified member of the FERM family, cause X-linked idiopathic congenital nystagmus
DOI: 10.1038/ng1893

[10] Genome-wide analysis of estrogen receptor binding sites
DOI: 10.1038/ng1901

*********************************NATURE IMMUNOLOGY *************************

[11] New strategy for controlling inflammation

DOI: 10.1038/ni1392

A previously unknown method of terminating immune responses is reported in a study to be published in the November issue of Nature Immunology.

Immune responses defend against invading pathogens and eliminate dangerous tumor cells, for example, but once the threat has been destroyed, the immune responses must come to an end. If left uncontrolled, immune activity can cause autoimmune conditions in which the immune system attacks healthy tissues of the body.

The immune system uses many strategies to shut down immune responses, one of which is signaling cells to die. Charles Serhan and colleagues demonstrate that in mice and humans, dying immune cells express a surface protein that allows them to act as ‘sponges’ to effectively ‘soak up’ and thus remove factors that would otherwise promote inflammation. These findings highlight a previously unappreciated role of dying immune cells, and identify a new method for controlling or terminating potentially harmful immune responses. The new findings potentially offer a strategy for dampening chronic inflammatory conditions by tricking the immune response to cease and desist.

Author contact:
Charles Serhan (Harvard Medical School, Boston, MA, USA)
Tel: +1 617 732 8822; E-mail: [email protected]

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

[12] Individual stem cells with highly variable proliferation and self-renewal properties comprise the human hematopoietic stem cell compartment

DOI: 10.1038/ni1393

[13] A thymic pathway of mouse natural killer cell development characterized by expression of GATA-3 and CD127
DOI: 10.1038/ni1395

[14] A pathway regulated by cell cycle inhibitor p27Kip1 and checkpoint inhibitor Smad3 is involved in the induction of T cell tolerance

DOI: 10.1038/ni1398


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 <http://www.nature.com/natureneuroscience>)

[15] Quantitative analysis of the activation mechanism of the multicomponent growth-factor receptor Ret

DOI: 10.1038/nchembio823

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

[16] Dynamic modeling of imatinib-treated chronic myeloid leukemia: functional insights and clinical implications
DOI: 10.1038/nm1487

[17] In vivo imaging of lymph node metastasis with telomerase-specific replication-selective adenovirus
DOI: 10.1038/nm1404

[18] Quantifying viable virus-specific T cells without a priori knowledge of fine epitope specificity
DOI: 10.1038/nm1413

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

[19] Protein chip fabrication by capture of nascent polypeptides
DOI: 10.1038/nbt1249

[20] Analyzing proteome topology and function by automated multidimensional fluorescence microscopy
DOI: 10.1038/nbt1250

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

[21] Capacity for 5-HT1A-mediated autoregulation predicts amygdala reactivity
DOI: 10.1038/nn1780

[22] Dynamic shifts in the owl’s auditory space map predict moving sound location
DOI: 10.1038/nn1781

[23] Local potassium signaling couples neuronal activity to vasodilation in the brain
DOI: 10.1038/nn1779

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

[24] Control of Rad52 recombination activity by double-strand break-induced SUMO modification
DOI: 10.1038/ncb1488

[25] Molecular mechanisms of coupled monoubiquitination
DOI: 10.1038/ncb1484

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

[26] Single-molecule observations of the neck linker conformational changes in the kinesin motor protein
DOI: 10.1038/nsmb1151

[27] Rad4-Rad23 interaction with SWI/SNF links ATP-dependent chromatin remodeling with nucleotide excision repair
DOI: 10.1038/nsmb1152

[28] Structural analysis of kasugamycin inhibition of translation
DOI: 10.1038/nsmb1150



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.

Graz: 9

Toronto: 12

Beijing: 6
Shanghai: 20

Paris: 13

Dresden: 24
Frankfurt/Main: 9
Freiburg: 9
Giessen: 9
Leipzig: 16, 20
Mannheim: 16
Magdeburg: 20
Munich: 20

Ioannina: 9

Milan: 25

Asahigaoka: 1
Ibaraki: 17
Kanazawa: 17
Okayama: 17
Saitama: 1
Showa-Machi: 1
Tokyo: 17, 26

Suwon: 5

Barcelona: 7
Madrid: 8
Zaragoza: 8

Cambridge: 9
Leeds: 9
Leicester: 9
London: 3, 9
Newcastle: 9
Nottingham: 9
Preston: 9
South Mimms: 24, 28

Little Rock: 9
Berkeley: 28, 29
La Jolla: 2, 7
San Francisco: 26, 28
Santa Clara: 10
Stanford: 22, 23
New Haven: 6
Storrs: 6
Athens: 28
Atlanta: 21
Chicago: 4
Baltimore: 5, 19, 23
Bethesda: 4, 5
Boston: 9, 10, 11, 14
Cambridge: 15
Charlestown: 11
Cincinnati: 23
Oxford: 28
Beaverton: 18
Philadelphia: 9
Pittsburgh: 6, 9, 20
Rhode Island
Providence: 10, 28
Austin: 23
Burlington: 23
Charlottesville: 10
Pullman: 27


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Tel: +44 20 7843 4658; E-mail: [email protected]

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

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Bernd Pulverer
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Nature Chemical Biology (Boston)
Andrea Garvey
Tel: +1 617 475 9241, E-mail: [email protected]

Nature Genetics (New York)
Alan Packer
Tel: +1 212 726 9277; E-mail: [email protected]

Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; 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 Structural & Molecular Biology (New York)
Michelle Montoya
Tel: +1 212 726 9326; E-mail: [email protected]

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Published: 01 Oct 2006

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