Protecting mothers from fetal immune recognition

Summaries of other newsworthy papers from Nature include Inducing connections between brain sites alters motor function - Nature, The bottom line for silk - Nature Materials, Bittersweet news for neural stem cell grafts - Nature Medicine, TAPping into mammalian interaction proteomics - Nature Methods


For papers that will be published online on 22 October 2006

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

This press release contains:

* Summaries of newsworthy papers:

Inducing connections between brain sites alters motor function - Nature

The bottom line for silk - Nature Materials

Bittersweet news for neural stem cell grafts - Nature Medicine

Protecting mothers from fetal immune recognition - Nature Immunology

TAPping into mammalian interaction proteomics - Nature Methods

* Mention of papers to be published at the same time with the same embargo
* Geographical listing of authors

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[1] Neuroscience: Inducing connections between brain sites alters motor function

DOI: 10.1038/nature05226

Artificially connecting the activity of two brain sites can alter the motor function of freely behaving monkeys, according to a study published online in Nature this week. Associative plasticity - the classic theory that the paired activity of neurons underlies learning and memory in the brain - has, until now, been difficult to demonstrate in behaving animals.

Eberhard Fetz and colleagues implanted a 'Neurochip' into the brains of two adult monkeys (Macaca nemestrina), in an area of the primary motor cortex that controls wrist movement. They mapped the motor output of two sites within this area by observing the different wrist movements elicited when each of the sites was stimulated. A conditioning stage was then undertaken during which nerve impulses recorded at one site - referred to as Nrec - were used to trigger the delivery of an electrical stimulus to the other site - referred to as Nstim. The authors report that this changed the motor output of the first brain site, such that stimulating Nrec resulted in wrist movements similar to those observed following stimulation of Nstim.

The authors propose that their findings show that functional reorganization can be induced using neural activity at one site to trigger stimulation at another, thus creating an artificial connection. This represents a novel development for the field of brain-computer interface technology, and may have practical implications for rehabilitation after brain injury.

Author contact:

Eberhard Fetz (University of Washington, Seattle, WA, USA)
Tel: +1 206 543 4839; E-mail: [email protected]

******************************* NATURE MATERIALS ***************************** (<>)

[2] The bottom line for silk

DOI: 10.1038/nmat1762

Remarkable similarities between the flow behaviour of silkworm and spider silks are revealed in a study to be published in the November issue of Nature Materials. This is surprising because these silks evolved to have different functions and their protein compositions and mechanical properties are quite distinct.

Fritz Vollrath and colleagues’ characterization study is the first to compare directly the native silk feedstock of two different animal species. The authors note that both feedstocks have the typical flow behaviour of a standard polymer melt, which is important because it means that the melt-flow theory developed for polymers also applies to silk.

Spider silk, in particular, has mechanical properties that outperform most industrial fibres but it defies all attempts at reproduction. Now this improved understanding of the flow characteristics of native silk feedstock may take us a step closer to translating natural spinning to artificial silk production.

Author contact:

Fritz Vollrath (University of Oxford, UK)
Tel: +44 1865 271216; E-mail [email protected]

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

[3] Lithographically patterned nanowire electrode position

DOI: 10.1038/nmat1759

[4] A gallium nitride single-photon source operating at 200K

DOI: 10.1038/nmat1763

[5] A predictive mechanism for dynamic strain ageing in aluminium-magnesium alloys

DOI: 10.1038/nmat1765

*****************************Nature MEDICINE**********************************

[6] Bittersweet news for neural stem cell grafts

DOI: 10.1038/nm1495

Using human embryonic stem - HES - cells directed to a neural fate to treat Parkinson’s disease might be more complicated than previously thought, according to an article to be published in the November issue of Nature Medicine. The study reports that when transplanted into rats, these cells demonstrate the potential to give rise to tumors.

Parkinson’s disease involves the degeneration of dopamine-releasing cells in a region of the brain known as the substantia nigra, leading to motor problems. Previous studies have attempted to coax stem cells into becoming dopamine-releasing, in the hope that they could be transplanted into the brain of people with the disease to replace the degenerated cells. One problem that researchers have encountered is the difficulty of obtaining enough cells to perform transplantation experiments in animal models.

In the current study, Steven Goldman and colleagues cultured HES cells while exposed to particular proteins and in the presence of human fetal glial, or brain ‘support’, cells. This allowed them to obtain enough cells to transplant into and alleviate the motor deficits of rats. However, after some time, the grafts started to show areas that no longer consisted of dopamine-releasing neurons, but of dividing cells that had the potential to give rise to tumors. The authors believe that their findings mandate caution before moving the application of such stem cell-derived grafts to the clinic as a possible treatment for Parkinson’s disease.

Author contact:
Steven Goldman (University of Rochester Medical Center, NY, USA)
Tel: +1 585 275 9550; E-mail: [email protected]

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

[7] Genomic signatures to guide the use of chemotherapeutics
DOI: 10.1038/nm1491

[8] Humanized mice mount specific adaptive and innate immune responses to EBV and TSST-1
DOI: 10.1038/nm1431

[9] GTP cyclohydrolase and tetrahydrobiopterin regulate pain sensitivity and persistence
DOI: 10.1038/nm1490

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

[10] Protecting mothers from fetal immune recognition

DOI: 10.1038/ni1397

A protein expressed in developing embryos may protect mothers against immune-mediated attack by fetal cells, according to a study to be published in the December issue of Nature Immunology. This protein, called Zfp608, appears to function by switching off the expression of Rag genes, which are involved in the development and function of fetal immune cells.

Thomas Aune and colleagues identified Zfp608 by honing in on a genetic defect exhibited by a strain of mice called ZORI, which have a compromised immune system. These mice have reduced numbers of T lymphocytes, immune cells that develop in the thymus. Normally mice express Zfp608 during embryonic development but stop its expression soon after birth. In contrast, ZORI mice continue to express Zfp608 in their thymus well beyond birth; continued Zfp608 expression is therefore linked to lack of thymic immune cell development.

The authors show that Zfp608 inhibits Rag gene expression in thymic cells, which explains the defect in T lymphocyte development observed in ZORI mice. They speculate that the timing of Zfp608 expression in embryos might play a protective role by preventing the development of fetal immune cells that could potentially recognize and attack maternal tissues, thereby harming both mother and her unborn offspring.

Author contact:
Thomas M Aune (Vanderbilt University School of Medicine, Nashville, TN, USA)
Tel: +1 615 343 7353; E-mail: [email protected]

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

[11] Mutual activation of natural killer cells and monocytes mediated by NKp80-AICL interaction
DOI: 10.1038/ni1402

**********************************NATURE METHODS**************************

[12] TAPping into mammalian interaction proteomics

DOI: 10.1038/nmeth968

A new method enabling the efficient isolation of protein complexes from mammalian cells is described in an article published online by Nature Methods this week. The technique can identify the partners in protein interaction networks, known as the ‘interactome’, which will help researchers to understand how specific proteins interact and function together in the cell.

A widely used affinity purification technique, tandem affinity purification, or TAP, uses specially designed purification tags as hooks to fish out a protein of interest and its interaction partners under gentle, close-to-physiological conditions that preserve binding interactions. The protein's interactome can then be identified with the aid of mass spectrometry. However, the method was originally developed in yeast, and the tag constructs were never optimized for their direct application in mammalian cells.

Giulio Superti-Furga and colleagues now describe a TAP-tag variant optimized for use in mammalian cells. Though they constructed and tested several variants, the purification tag with the most efficient properties consisted of two protein G immunoglobulin-binding units and a streptavidin-binding protein separated by a tobacco etch virus (TEV) protease cleavage site. This tag can be appended recombinantly to a protein of interest and used to isolate the protein and its interaction partners from cells in a two-step procedure.

Although the overall procedure is very similar to the yeast TAP method, the new tags enable the purification of mammalian protein complexes from a relatively small amount of cells and in quantities an order of magnitude higher than by using the original TAP tag. With this method, the authors conclude that "Large-scale approaches to explore the human proteome and cellular machinery should become more feasible."

Author contact:
Giulio Superti-Furga (Research Center for Molecular Medicine, Vienna, Austria)
Tel: +43 1 40160 70011; E-mail: [email protected]

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

[13] Two-chamber AFM: probing membrane proteins separating two aqueous compartments
DOI: 10.1038/nmeth965


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


[14] Using substrate engineering to harness enzymatic promiscuity and expand biological catalysis

DOI: 10.1038/nchembio828

Nature PHYSICS ( <>)

[15] Dispersionless slow light using gap solitons
DOI: 10.1038/nphys438

[16] Snapshots of laser wakefields
DOI: 10.1038/nphys442


[17] Complete genome of the mutualistic, N2-fixing grass endophyte Azoarcus sp. strain BH72
DOI: 10.1038/nbt1243

[18] Redirection of cytosolic or plastidic isoprenoid precursors elevates terpene production in plants
DOI: 10.1038/nbt1251


[19] A worldwide survey of haplotype variation and linkage disequilibrium in the human genome DOI: 10.1038/ng1911

[20] Transferability of tag SNPs in genetic association studies in multiple populations
DOI: 10.1038/ng1899

[21] SATB1 packages densely looped, transcriptionally active chromatin for coordinated expression of cytokine genes
DOI: 10.1038/ng1913


[22] IGF-I specifically enhances axon outgrowth of corticospinal motor neurons
DOI: 10.1038/nn1789

[23] Bayesian inference with probabilistic population codes
DOI: 10.1038/nn1790

[24] Optimal decoding of correlated neural population responses in the primate visual cortex
DOI: 10.1038/nn1792


[25] Par6-aPKC uncouples ErbB2 induced disruption of polarized epithelial organization from proliferation control
DOI: 10.1038/ncb1485

[26] VEGF controls endothelial-cell permeability by promoting the beta-arrestin-dependent endocytosis of VE-cadherin
DOI: 10.1038/ncb1486

[27] CD28 interaction with filamin-A controls lipid raft accumulation at the T-cell immunological synapse
DOI: 10.1038/ncb1492


[28] The FtsK gamma domain directs oriented DNA translocation by interacting with KOPS
DOI: 10.1038/nsmb1158

[29] Solution structures of the adhesion molecule DdCAD-1 reveal new insights into Ca2+-dependent cell-cell adhesion
DOI: 10.1038/nsmb1162

[30] Structural basis for ubiquitin recognition by the human ESCRT-II EAP45 GLUE domain
DOI: 10.1038/nsmb1160

[31] Structural basis of ubiquitin recognition by mammalian Eap45 GLUE domain
DOI: 10.1038/nsmb1163


[32] Direct growth of aligned carbon nanotubes on bulk metals
DOI: 10.1038/nnano.2006.56



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: 15

Vienna: 12

Ottawa: 14
Toronto: 25, 29
Vancouver: 14

Helsinki: 20

Orsay: 13
Paris: 13

Bielefeld: 17
Bremen: 17
Frankfurt am Main: 9
Halle/Saale: 17
Marburg: 17
Tubingen: 11

Padua: 27
Rome: 27
Rozzano: 27

Sayo: 31
Tokyo: 4
Tsukuba: 31
Yamaguchi: 4

Oslo: 31

Singapore: 29

Madrid: 27

Malmo: 20

Geneva: 18
Zurich: 4

Bath: 14
Cambridge: 28
Didcot: 2
London: 23
Oxford: 2, 28

Berkeley: 21
Irvine: 3
Los Angeles: 19, 20
Palo Alto: 4
San Diego: 8
Stanford: 4
Gainesville: 9
Tampa: 7
Honolulu: 20
Chicago: 19
Maywood: 20
Urbana: 18
Lexington: 18
Bethesda: 9, 26
Rockville: 9
Belmont: 9
Boston: 9, 20, 22
Cambridge: 20
Charlestown: 9
Ann Arbor: 16, 19
Warren: 5
Minneapolis: 8
New Mexico
Alberquerque: 5
New York
Cold Spring Harbor: 25
New York: 6
Rochester: 6, 23
Stony Brook: 25
Troy: 32
Upton: 30
Yorktown Heights: 17
North Carolina
Chapel Hill: 9
Durham: 7
Rhode Island
Providence: 5
Nashville: 10
Austin: 16, 24
Dallas: 8
Salt Lake City: 30
Seattle: 1


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

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

Ruth Francis (Senior Press Officer, 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 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)
Michelle Montoya
Tel: +1 212 726 9326; E-mail: [email protected]

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

Nature Methods (New York)
Allison Doerr
Tel: +1 212 726 9393; E-mail: [email protected]

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Published: 22 Oct 2006

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