‘Friendly’ bacteria protect from diabetes

Summaries of newsworthy papers include ‘Friendly’ bacteria protect from diabetes, Downward dog, When humans control fire, Survival strategies, Cortisone shakes up channels, Watching protein structures move in nanoseconds and Fish fingers point to origin of digits and All of p53

NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE

For papers that will be published online on 21 September 2008

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

This press release contains:

· Summaries of newsworthy papers:

Nature: ‘Friendly’ bacteria protect from diabetes

Genetics: Downward dog

Geoscience: When humans control fire

Immunology: Survival strategies

Chemical Biology: Cortisone shakes up channels

Methods: Watching protein structures move in nanoseconds

And finally… Nature: Fish fingers point to origin of digits

· 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.

Warning: This document, and the Nature journal papers to which it refers, may contain information that is price sensitive (as legally defined, for example, in the UK Criminal Justice Act 1993 Part V) with respect to publicly quoted companies. Anyone dealing in securities using information contained in this document, or in advance copies of a Nature journal’s content, may be guilty of insider trading under the US Securities Exchange Act of 1934.

PICTURES: To obtain artwork from any of the journals, you must first obtain permission from the copyright holder (if named) or author of the research paper in question (if not).

NOTE: Once a paper is published, the digital object identifier (DOI) number can be used to retrieve the abstract and full text from the journal web site (abstracts are available to everyone, full text is available only to subscribers). To do this, add the DOI to the following URL: http://dx.doi.org/ (For example, http://dx.doi.org/10.1038/ng730). For more information about DOIs and Advance Online Publication, see http://www.nature.com/ng/aop/.

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.

[1] Nature: ‘Friendly’ bacteria protect from diabetes
DOI: 10.1038/nature07336

‘Friendly’ bacteria help to stop the development of type 1 diabetes in mice, according to research published online this week in Nature. The findings could one day be used to develop bacteria-based treatments for patients, say the authors.

Type 1 diabetes is caused by destruction of the insulin-producing cells in the pancreas by the body’s own immune system. Alexander Chervonsky and colleagues studied the incidence of diabetes in genetically modified non-obese diabetic (NOD) mice that lack the part of the immune system that responds to bacteria. They found that NOD mice raised in a completely germ-free environment, and therefore lacking ‘friendly’ gut bacteria, developed severe diabetes. However, when they gave the mice back a cocktail of the usual bacteria found in the mammalian gut, the incidence of diabetes was significantly reduced.

The research indicates that the interaction between the immune system and our own ‘friendly’ bacteria could be a critical factor in modifying susceptibility to diabetes.

Author contact:
Alexander Chervonsky (University of Chicago, IL, USA)
Tel: +1 773 7021371; E-mail: [email protected]

[2] Genetics: Downward dog
DOI: 10.1038/ng.224

The mutation underlying the syndrome of exercise-induced collapse in Labrador retrievers has been identified, according to a study published online this week in Nature Genetics.

In the 1990s veterinarians characterized a newly observed syndrome affecting Labrador retrievers that were being trained for field trials. The dogs would develop a wobbly gait after 5–15 minutes of strenuous exercise, which would be accompanied by elevated body temperature, and finally a near-complete loss of control of the rear limbs. Most dogs would recover after 30 minutes, although occasional fatalities were reported.

Edward Patterson and colleagues carried out a genome scan of a group of affected Labrador retrievers, and identified a mutation in the gene DNM1. This gene encodes the protein dynamin 1, which is almost exclusively expressed in the brain and spinal cord, and has a key role in transmitting signals between neurons. The authors show that approximately 37% of Labrador retrievers carry one copy of the mutation, and its identification may allow the development of a genetic test that could be used to assist breeders.

Author contacts:
Edward Patterson (University of Minnesota, St. Paul, MN, USA)
Tel: +1 612 525 5799; E-mail: [email protected]

[3] Geoscience: When humans control fire (N&V)
DOI: 10.1038/ngeo313

Human activities since the industrial revolution have affected the amount of biomass burned in wildfires. A study published online this week in Nature Geoscience reports that biomass burning rose steadily after 1750, before declining abruptly around 1870.

Jennifer Marlon, Patrick Bartlein and colleagues compiled records of natural charcoal deposited in lakes and peat swamps for the past two millennia. They found that until 1750, global biomass burning patterns closely follow climate variations. However, beginning around the time of the industrial revolution, the amount of burning began to increase, which the researchers associate with increasing population and the use of slash and burn farming techniques. They link the subsequent decline with increased agriculture and livestock grazing, as well as active fire suppression. The changes since 1750 are generally not consistent with climate changes reported for the time, which the team considers as evidence for the increasing influence of human activities.

In an accompanying News and Views article, Andrew Scott writes that this work “is an important contribution to our understanding of the relationship between fire and climate”.

Author contacts:
Jennifer Marlon (University of Oregon, Eugene, OR, USA)
Tel: +1 203 507 2462; E-mail: [email protected]

Patrick Bartlein (University of Oregon, Eugene, OR, USA)
Tel: +1 541 346 4967; E-mail: [email protected]

News & Views author:
Andrew Scott (Royal Holloway University of London, UK)
Tel: +44 17 8444 3608; E-mail: [email protected]

[4] Immunology: Survival strategies
DOI:10.1038/ni.1653

Scientists have discovered a molecule that helps activated immune cells survive in the face of massive amounts of the antimicrobial signalling protein, interferon-gamma. A paper online this week in Nature Immunology suggests the molecule Irgm1 is critical to allow continued immune responses in the face of chronic infections, such as those seen in many parasitic diseases.

Interferons are antimicrobial compounds that help eradicate viruses and other intracellular pathogens. High concentrations of interferons are toxic to nearby cells. Hence it has always been a dilemma as to how those immune cells that make interferon-gamma in response to infection can themselves survive.

Carl Feng and colleagues identify a molecule called Irgm1 that plays a key role in this process – protecting immune cells that produce interferon-gamma from succumbing to its toxic effects. They show that immune cells from mice lacking Irgm1 fail to multiply and instead undergo a form of cellular suicide upon exposure to interferon-gamma. Fewer immune cells result in uncontrolled infections and all of the mice died from their infection. Mice lacking both Irgm1 and interferon-gamma survive infection, showing that Irgm1 protects these immune cells from the toxic effects of interferon-gamma.

Author contact:
Carl Feng (National Institute of Allergy and Infectious Diseases, Bethesda, MD, USA)
Tel: +1 301 594 2890; E-mail: [email protected]

[5] Chemical Biology: Cortisone shakes up channels
DOI: 10.1038/nchembio.114

Cortisone, a steroid hormone produced by the adrenal gland, can unexpectedly separate potassium channel subunits that aid membrane depolarization and coordinated muscle contraction. A study online this week in Nature Chemical Biology raises questions as to whether this type of control might have implications for human disease including ataxia and cardiac arrhythmia and simultaneously provides a chemical scaffold for future drug development.

The cell membrane separates intra and extracellular environments. After a change in the charge distribution across the membrane required for muscle contraction, potassium channels of the Shaker family open temporarily and relieve the charge imbalance by creating a pore that releases potassium ions.

Ming Zhou and colleagues performed both structural analyses and functional studies to demonstrate that the hormone binds between channel subunits, separating them, allowing the channel to remain open. Discovery of a hormone that dissociates channel subunits was surprising since few small molecules have been identified that disrupt other protein-protein interactions.

Author contact:
Ming Zhou (Columbia University College of Physicians and Surgeons, New York, NY, USA)
Tel: +1 212 342 3722, Email: [email protected]

[6] Methods: Watching protein structures move in nanoseconds
DOI: 10.1038/nmeth.1255

Viewing changes in protein structure with nanosecond-scale time resolution is now possible, with a new technique published online this week in Nature Methods.

Proteins are dynamic macromolecules. They carry out their biological functions by altering their structures¾with motions ranging from subtle to substantial and from slow to very fast. Some methods for monitoring these changes, such as optical spectroscopy, are very good at detecting fast changes but do not yield much information about the overall three-dimensional protein structure. Other methods, such as nuclear magnetic resonance (NMR) spectroscopy or X-ray crystallography, are very good for looking at three-dimensional structure, but have limited ability to detect very fast motions.

Marco Cammarata, Hyotcherl Ihee and colleagues report new developments in the technique of time-resolved wide-angle X-ray scattering (TR-WAXS) that allow them to monitor very fast, nanosecond-scale protein movements in the context of the overall three-dimensional structure. They use TR-WAXS to gain insights into the rapid structural changes that occur in the well-known oxygen-transport protein haemoglobin.

The method can be applied for studying a wide range of protein motions with very fast time resolution.

Author contacts:
Marco Cammarata (European Synchrotron Radiation Facility, Grenoble, France)
Tel: +33 4 76 88 29 37; E-mail: [email protected]

Hyotcherl Ihee (Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea)
Tel: +82 42 350 2844; E-mail: [email protected]

[7] And finally… Nature: Fish fingers point to origin of digits
DOI: 10.1038/nature07339

Finger-like divisions in the fins of ancient fish are the predecessors of our fingers and toes, according to research published online in Nature this week. The discovery comes from a re-examination of an ancient fish fossil — Panderichthys — that is evolutionarily related to land vertebrates.

The idea that digits of land vertebrates were derived from fin radials fell out of favour largely based on early studies of Panderichthys, which appeared to lack digit-like fin radials. Catherine Boisvert and colleagues present a new CT study of this ancient fossil showing that the old interpretation was in error — in fact Panderichthys did indeed have finger-like divisions in its fins.

Author contact:
Catherine Boisvert (Uppsala University, Sweden)
Tel: +46 18 471 6223; E-mail: [email protected]

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

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

[8] Sae2, Exo1 and Sgs1 collaborate in DNA double-strand break processing
DOI: 10.1038/nature07312

[9] Paracrine Wingless signalling controls self-renewal of Drosophila intestinal stem cells
DOI: 10.1038/nature07329

NATURE BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)

[10] Small-molecule inhibition of HIV-1 Vif
DOI: 10.1038/nbt.1496

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

[11] Proof-by-synthesis of the transcriptional logic of mammalian circadian clocks
DOI: 10.1038/ncb1775

[12] Targeting of the F-actin-binding protein drebrin by the microtubule plus-tip protein EB3 is required for neuritogenesis
DOI: 10.1038/ncb1778

[13] Jade-1 inhibits Wnt signalling by ubiquitylating beta-catenin and mediates Wnt pathway inhibition by pVHL
DOI: 10.1038/ncb1781

NATURE GENETICS (http://www.nature.com/naturegenetics)

[14] Insights from retinitis pigmentosa into the roles of isocitrate dehydrogenases in the Krebs cycle
DOI: 10.1038/ng.223

[15] The Pristionchus pacificus genome provides a unique perspective on nematode lifestyle and parasitism
DOI: 10.1038/ng.227

NATURE GEOSCIENCE (http://www.nature.com/ngeo)

[16] The role of surface heat fluxes in tropical intraseasonal oscillations
DOI: 10.1038/ngeo312

[17] Antarctic temperature at orbital timescales controlled by local summer duration
DOI: 10.1038/ngeo311

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

[18] Cyclophilin D deficiency attenuates mitochondrial and neuronal perturbation and ameliorates learning and memory in Alzheimer’s disease
DOI: 10.1038/nm.1868

[19] Inhibition of lipoprotein-associated phospholipase A2 reduces complex coronary atherosclerotic plaque development
DOI: 10.1038/nm.1870

NATURE METHODS (http://www.nature.com/nmeth)

[20] Imaging individual mRNA molecules using multiple singly labeled probes
DOI: 10.1038/nmeth.1253

[21] Building consensus spectral libraries for peptide identification in proteomics
DOI: 10.1038/nmeth.1254

NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)

[22] Current saturation in zero-bandgap, top-gated graphene field-effect transistors
DOI: 10.1038/nnano.2008.268

[23] Designing artificial cells to harness the biological ion concentration gradient
DOI: 10.1038/nnano.2008.274

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

[24] FMRFamide neuropeptides and acetylcholine synergistically inhibit egg laying by C. elegans
DOI: 10.1038/nn.2186

[25] Improved visual sensitivity during smooth pursuit eye movements
DOI: 10.1038/nn.2194

[26] Links from complex spikes to local plasticity and motor learning in the cerebellum of awake-behaving monkeys
DOI: 10.1038/nn.2197

NATURE PHOTONICS (http://www.nature.com/nphoton)

[27] Fast focusing using a pinned-contact oscillating liquid lens
DOI: 10.1038/nphoton.2008.198

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

[28] The role of magnetic anisotropy in the Kondo effect
DOI: 10.1038/nphys1072

[29] Optical nanotomography of anisotropic fluids
DOI: 10.1038/nphys1077

[30] Coherent generation of non-classical light on a chip via photon-induced tunneling and blockade
DOI: 10.1038/nphys1078

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

[31] Structural model for strain-dependent microtubule activation of Mg-ADP release from kinesin
DOI: 10.1038/nsmb.1487

[32] A torque component present in mitotic kinesin Eg5 revealed by three-dimensional tracking
DOI: 10.1038/nsmb.1491

[33] Mapping a molecular link between allosteric inhibition and activation of the glycine receptor
DOI: 10.1038/nsmb.1492

[34] Crystal structures of the SAM-III/SMK riboswitch reveal the SAM-dependent translation inhibition mechanism
DOI:10.1038/nsmb.1494

***************************************************************************************************************
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.

CANADA:
Saskatoon: 2

CHINA
Beijing: 9

DENMARK
Copenhagen: 6

ESTONIA
Talinn: 7

FRANCE
Grenoble: 6
Montpellier: 3

GERMANY
Giessen: 25
Hamburg: 28
Tubingen: 15

ITALY
Palermo: 6
Rende: 29

JAPAN
Hyogo: 11
Tokyo: 31, 32

KOREA
Daejon: 6

MEXICO
Jalisco: 27

NETHERLANDS
Groningen: 14
Leiden: 28

ROMANIA
Bucharest: 29

SINGAPORE
Singapore: 22

SWEDEN
Uppsala: 7

SWITZERLAND
Bern: 3
Geneva: 25
Lausanne: 28
Zurich: 21

UNITED KINGDOM
Bristol: 1, 3
London: 12, 28, 33
Plymouth: 12
Southampton: 19
St. Andrews: 18

UNITED STATES OF AMERICA

California
Berkeley: 28
La Jolla: 2, 10
San Francisco: 1, 26
San Jose: 28
Santa Barbara: 30
Stanford: 30

Colorado
Fort Collins: 16

Connecticut
New Haven: 1, 23

Delaware
Newark: 14

Illinois
Argonne: 34
Chicago: 1

Maine
Bar Harbor: 1
Orono: 17

Maryland
Bethesda: 4, 6
Gaithersburg: 21, 23

Massachusetts
Boston: 13, 14
Cambridge: 17, 20, 24
Worcester: 10

Minnesota
St. Paul: 2, 29

Missouri
St Louis: 1, 15

Montana
Bozeman: 3

New York
Ithaca: 1, 34
New York: 5, 8, 16, 18, 22
Troy: 27

Ohio
Cleveland: 29
Cincinnati: 18
Columbus: 34

Oregon
Eugene: 3

Pennsylvania
King of Prussia: 19
Philadelphia: 19, 26

Texas
Dallas: 4

Utah
Salt Lake City: 3

Washington
Seattle: 16, 19, 21

PRESS CONTACTS…

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]

Katherine Anderson (Nature New York)
Tel: +1 212 726 9231; E-mail: [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)
Peter Hare
Tel: +1 212 726 9284; E-mail: [email protected]

Nature Cell Biology (London)
Bernd Pulverer
Tel: +44 20 7843 4892; E-mail: [email protected]

Nature Chemical Biology (Boston)
Andrea Garvey
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 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)
Alison Stoddart
Tel: +44 20 7843 4593; 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)
Michelle Montoya
Tel: +1 212 726 9326; E-mail: [email protected]

About Nature Publishing Group

Nature Publishing Group (NPG) is a division of Macmillan Publishers Ltd, dedicated to serving the academic, professional scientific and medical communities. NPG's flagship title, Nature, was first published in 1869. Other publications include Nature research journals, Nature Reviews, Nature Clinical Practice and a range of prestigious academic journals including society-owned publications. NPG also provides news content through [email protected]. Scientific career information and free job postings are offered on Naturejobs.

NPG is a global company with principal offices in London and New York and offices in Basingstoke, Boston, Buenos Aires, Delhi, Hong Kong, Madrid, Melbourne, Munich, Paris, San Francisco, Tokyo and Washington DC. For more information, please go to www.nature.com.

-------------------------------------------------------------------------------------------------------

PRESS RELEASE FROM CANCER GENE THERAPY
(www.nature.com/cgt/)

This press release is copyrighted to Cancer Gene Therapy.

A PDF of the paper mentioned on this release can be found in the Academic Journal’s section of http://press.nature.com. Press contacts for the Nature journals are listed at the end of this release.

Warning: This document, and the NPG Academic Journals paper to which it refers, may contain information that is price sensitive (as legally defined, for example, in the UK Criminal Justice Act 1993 Part V) with respect to publicly quoted companies. Anyone dealing in securities using information contained in this document or in advanced copies of Nature’s content may be guilty of insider trading under the US Securities Exchange Act of 1934.

PLEASE CITE CANCER GENE THERAPY AND THE CANCER GENE THERAPY WEBSITE AS THE SOURCE OF THE FOLLOWING ITEM. IF PUBLISHING ONLINE, PLEASE CARRY A HYPERLINK TO www.nature.com/cgt/

All of p53

The fight against cancer takes a step forward this week with the online publication of a 50 page review on p53 in Cancer Gene Therapy. This offers the most up-to-date and comprehensive analysis of cutting-edge research into this fundamental molecule involved in almost all cancers.

p53 is an important protein that regulates cell proliferation and, in its mutated form, has been found in almost all types of cancers. Magali Olivier, Pierre Hainaut and their colleagues consider 78 papers on the subject*. The review examines how the different parts of the p53 molecule contribute to its overall activity and its role in upstream and downstream regulatory pathways critical to maintain normal tumour suppressor function. The role of specific p53 mutations and mechanisms of p53 inhibition which result in cancer pathogenesis and treatment resistance are also considered.

The extensive integration of this knowledge highlights possible applications of the research that will be of direct benefit to cancer patients, by improving detection, prognosis, prevention and therapy.

Author contact:
Magali Olivier (International Agency for Research Against Cancer, Lyon, France)
Tel: +33 4 7273 8669; E-mail: [email protected]

Media contacts:
Jen Middleton (Nature London)
Tel: +44 20 7843 4502; E-mail: [email protected]

Katherine Anderson (Nature New York)
Tel : +1 212 726 9231; E-mail : [email protected]

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

* The papers summarize the major findings presented at the 3rd International Workshop on Mutant p53 held at the International Agency for Research Against Cancer (IARC).

About Nature Publishing Group

Nature Publishing Group (NPG) is a division of Macmillan Publishers Ltd, dedicated to serving the academic, professional scientific and medical communities. NPG's flagship title, Nature, was first published in 1869. Other publications include Nature research journals, Nature Reviews, Nature Clinical Practice and a range of prestigious academic journals including society-owned publications. NPG also provides news content through [email protected] and scientific career information through Naturejobs.

NPG is a global company with principal offices in London and New York and offices in Basingstoke, Boston, Buenos Aires, Delhi, Hong Kong, Madrid, Melbourne, Munich, Paris, San Francisco, Tokyo and Washington DC. For more information, please go to www.nature.com.

Published: 21 Sep 2008

Contact details:

The Macmillan Building, 4 Crinan Street
London
N1 9XW
United Kingdom

+44 20 7833 4000
Country: 
Journal:
News topics: 
Content type: 
Websites: 
Reference: 

Nature and Nature Research Journals

Gut

Macromolecules

Medicine