The “Nuit Blanche” in Paris. A city wide exposition of contemporary arts from dusk till dawn. Performances, light shows, dance, installations. Along the Canal Saint-Martin the visitors stroll from one exhibition to the next or sit down and take a break, chatting and drinking. A bit further up Boulevard Avenue Richerand the south-west entrance to the Hospital Saint Louis gives entry to a backyard. On the facade of the 17th century building, retinal pigmented epithelial cells perform their dance. Nothing but their cytoskeleton exposed in white before the dark building, magnified 10000-fold, accelerated 100-fold. One cell gets hold of a support beam, gradually spreading out over all its length. Loosing grip, rounding up and going into mitosis. Each daughter cell spreading out again. Other cells remain at one place, yet their cytoskeleton still moves, searching an exit from the confined space of a window.

When Manuel Thery came to me with the idea that we have to project cells onto a building – and cells which had been grown on micro-patterns in the shape of that same building – it was obvious that this idea simply had to be done. First, the general public has little access to all those beautiful images one takes when working with cells. Second, curiosity and “wanting to understand” needs to be promoted as a value by itself. Physics is not engineering, and biology is not R&D for pharmaceuticals. And the cytoskeleton with its appearing and disappearing regularities has the graphical power to draw you in and want you to grasp its function, without necessarily thinking about the benefit. Third, we try to find cues of how cells react to extracellular geometrical constraints in our day-to-day science, and we were curious ourselves, what we would see on these complex shapes. Fourth, as a structural scaffold for the cell (amongst other functions), the cytoskeleton shares some properties and constraints of engineering and architecture, and the metaphor has been made before. Fifth, simply, because we can.

The plan was simple:

1) take a photo of a public building
2) extract some interesting shapes from the building
3) produce micro-patterns of these shapes, the size of a single or several cells – micro-patterns are protein patterns for cell attachment on a substrate that otherwise repels cells
4) culture cells with fluorescently labeled cytoskeletal elements on these micro-patterns
5) do some live cell video microscopy
6) select the nicest videos and project the cells back on the original place of the pattern on the building, the size of the building, accelerated, for everyone to see.

Although that project may sound simple, it is by no means a one person, one weekend prep. At least, if you are a newbie to micro-patterning, live cell imaging, and your cell culture experience dates back more than a PhD’s time. Keep in mind that photo toxicity of the stain will kill the cells pretty quickly if you illuminate too strongly and frequently. On the other hand, if you want to play your time-lapse movies at a speed that people do not recognize it as a sequence of images, you need hundreds of frames for tens of seconds of footage, so you require days with an image every 5-10 min. And have cells survive under a microscope for 48h, on previously untested patterns of adhesive regions… is performing an experiment. And as such may just not work the first few times you try. Add the little pressure of a deadline (the day of the event that cannot be shifted).

But it gets even more involved with the work of the artists from the amazing Groupe Laps:

cut of the movie (the choreographies for the cells); giving the cells music to move to; correcting the image of the house for spherical aberration, so that the projection would align with the building; organizing the equipment for the projection; finding, in all those hundreds of movies, those that would be used;  organizing the permissions to project onto the building; sticking non-reflecting foil over the windows on the day of the event; aligning the images with the features of the building; …

For someone having been involved in any sort of larger scale artistic event, all this may sound evident, but I was amazed by just how complex the basic idea would get.

Another change is the mindset between me and the artist. For them a cool sequence of cells would do. For me it also had to reflect a typical cell on these patterns – while still yielding footage with good enough contrasted structures to allow the projection.

Only on the evening itself did I see how well the composition by Groupe Laps had worked. It was very different from what I had imagined on the outset, and much richer for the fact that it did not look like all the images you would see in a publication – if you cared to project them on a house, that is.

Since we could not assume that the public would grasp that the images showed live cells, we also provided two information boards to describe the project in a short text as you might expect in an exhibition. However, we were surprised by the number of people who were at the event, and because a 10m high projection of something moving draws more attention than 1m high panel of written text, only a minority took advantage. Therefore, the level of understanding ranged from fellow scientists “yay, z-stack of microtubules”, over raising curiosity with many, to some complete ignorance that this had anything to do with biology. On the other hand, many spectators were clearly drawn in by the videos, watching the installation several times over. And I like to believe there was a lot wider spectrum of interpretation and thought, specifically because there was no classroom-ready explanation available.

In the case that you plan an outreach activity with collaborators foreign to your field or even science, my main advise would be to make sure you take the time to collaborate closely; to get to know each other and mutually showing additional possibilities and clarifying impossibilities on either side takes some iterations. This may apply less to smaller events, or repeating ones, where you can learn on the job and grow the event slowly. But for larger scale one-offs this is paramount. In fact, the sole regret I have about my experience with the nuit blanche project is that – because of distance and safety regulations – I could never show the involved artists our laboratories, so my work still remains abstract to them, and that we did not have regular “lab”-meetings, as is the case with my research.

If you ask yourself whether you should get involved in some outreach activity of the sort, involving people foreign to science, and specifically if you are not familiar with their line of work: Do it! It broadens the horizon and experiencing some recognition from someone outside of ones usual line of work has a special quality for both sides.

This post is part of a series on science outreach. You can read the introduction to the series here and read other posts in this series here.

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The latest issue of Development includes a paper by Clare Blackburn and colleagues at the Medical Research Council Centre for Regenerative Medicine, University of Edinburgh, showing that the aged mouse thymus can be regenerated in vivo by the upregulation of a single transcription factor, FOXN1. This work has generated quite a lot of interest in the media, so we reproduce below the press release by the Medical Research Council. You can read the research article here.
 
 

Caroline Hendry, PhD
Stem Cells & Regeneration Reviews Editor at Development

Bredenkamp, N., Nowell, C., & Blackburn, C. (2014). Regeneration of the aged thymus by a single transcription factor Development, 141 (8), 1627-1637 DOI: 10.1242/dev.103614

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The pathological atrophy of skeletal muscle is a serious biomedical problem for which no effective treatment is currently available. Those most affected populations are the elderly diagnosed with sarcopenia and patients with cancer, AIDS, and other infectious diseases that develop cachexia.

A study by scientists at the Institute for Research in Biomedicine (IRB), headed by Antonio Zorzano, also full professor of the University of Barcelona, reveals a potential therapeutic target to tackle muscle wasting in these risk populations.

In the study published today in the Journal of Clinical Investigation (JCI), one of the journals with highest impact in experimental medicine, the researchers associate the activity of the DOR protein with muscle atrophy and point to DOR as a plausible target against which to develop a drug to prevent muscle deterioration in certain diseases.

DOR (Diabetes- and Obesity-regulated gene), also known as TP53INP2, is a protein involved in autophagy, a quality control process that ensures cells stay healthy. The researchers have found that increased DOR expression in the muscle of diabetic mice leads to enhanced autophagy, which in turn favours the loss of muscle mass in these animals.

The advantage of developing a DOR inhibitor is that autophagy, a process necessary to keep cells healthy, would not be completely blocked in the absence of this protein. DOR is not essential for autophagy, but acts more as an accelerator. Thus, the inhibition of DOR would only partially reduce autophagy as other molecules involved would exert their activity normally, thus maintaining the levels of autophagy in a beneficial range for cells.

“If we could treat patients with sarcopenia and cachexia, or people at risk of these conditions, using a drug to inhibitor DOR then we would be able to stop or prevent muscle wasting,” explains the expert in diabetes and obesity Zorzano, head of the “Heterogenic and Polygenic Diseases” lab at IRB.

“We are showing pharmaceutical researchers a new possible therapeutic target for two diseases that seriously impair the quality of lives of those who suffer from them,” says the scientist.

An answer to why type 2 diabetic patients lose less muscle than those with type 1

The study also solves a biomedical enigma related to diabetes. Physicians did not understand why patients with type 2 diabetes—who become resistance to insulin or have very low levels of this hormone—are able to maintain muscle mass or minimize muscle wasting compared to patients with type 1 diabetes—who do not produce insulin—who show a clear loss of muscle mass. The IRB researchers demonstrate that the repression of DOR in muscle cells of type 2 diabetic animals allows the maintenance of muscle mass.

“We interpret DOR repression, which occurs naturally, as an adaptation mechanism to preserve muscle mass and to maintain greater muscular strength in type 2 diabetics,” explains David Sala, first author of the study, who has recently started a post-doctoral training period at Sanford-Burnham Medical Research Institute, in La Jolla, California.

Besides working with mice, the scientists have performed experiments on biopsies from skeletal muscle of patients with diabetes and patients resistant to insulin, thanks to collaboration with clinicians from the Université Lyon 1, in France, and from the Medical University of Byalistok, Poland, also included among the authors.

The project developed in Dr. Zorzano’s lab at IRB has been funded by the Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas (CIBERDEM), the Spanish Ministry of Economy and Knowledge, and the European project DIOMED, part of the Interreg-SUDOE programme.

Reference article:

Sala D, Ivanova S, Plana N, Ribas V, Duran J, Bach D, Turkseven S, Laville M, Vidal H, Karczewska-Kupczewska M, Kowalska I, Straczkowski M, Testar X, Palacín M, Sandri M, Serrano AL, & Zorzano A (2014). Autophagy-regulating TP53INP2 mediates muscle wasting and is repressed in diabetes. The Journal of clinical investigation PMID: 24713655

This article was first published on the 9th of April 2014 in the news section of the IRBBarcelona website.

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We will be doing some maintenance work on the Node on Wednesday the 9th of April, and unfortunately there will be no access to the site during that period. You can expect the Node to be down from 7 p.m. (British Summer time) for approximately 4 hours. We are sorry for the disruption, especially for those Node readers in America and the early risers in the Pacific. We will be up and running again as soon as we can!

If you spot any problems and would like to get in touch our email address is the node [at] biologists.com

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6^th Young Embryologist Annual Meeting
Friday 27^th June 2014
JZ Young LT, Anatomy Building, University College London

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Here are the highlights from the current issue of Development:

Spine-tingling new role for Sall4

Wnt, Fgf and retinoic acid signalling play a key role in patterning the posterior neural plate to form the midbrain, hindbrain and spinal cord. Despite intense study of Wnt signalling and neural patterning, only a few target transcription factors that mediate spinal cord development have been identified and the mechanism remains unclear. In this issue (p. 1683), Richard Harland and colleagues reveal a role for Spalt-like 4 (Sall4) in promoting the differentiation of neural progenitor cells in Xenopus via the repression ofpou5f3 (oct4). Morpholino-induced knockdown of Sall4 results in defects in neural tube closure and neural differentiation in the embryo, while morpholino injection at the 4-cell stage reduces expression of spinal cord markers hoxb9, hoxc10 and hoxd10 without affecting pan-neuronal identity. The authors find that when Sall4 activity is disrupted, expression of pou5f3increases, while overexpression of pou5f3 disrupts the expression of key spinal cord identity genes. These data uncover a novel role for Sall4 in neural patterning, with a specific role in spinal cord differentiation.

Ageing thymus out-FOXed

The thymus is central to the adaptive immune system, but it is one of the first organs to undergo an age-related decline in function. Reduced expression of the thymic epithelial cell (TEC)-specific transcription factor FOXN1 has been associated with thymus degeneration, but whether restoration of FOXN1 expression can regenerate an aged thymus is unknown. Now, on p. 1627, Clare Blackburn and colleagues show that provision of FOXN1 in the thymus can reverse fully established age-related thymic degeneration. The authors use an elegant transgenic mouse model to induce the expression of FOXN1 exclusively in the TECs of aged mice, and show that the resulting rejuvenated thymus displays tissue architecture and gene expression similar to that of a much younger mouse. Importantly, the regenerated thymus can generate and export new T cells: a function that is crucial for its role in the adaptive immune system. This is the first report of the regeneration of a whole, aged organ by a single factor and has exciting implications for regenerative medicine.

Muscling in on stem cell hierarchy

Muscle stem cells, called satellite cells, are responsible for muscle growth and repair throughout life. Different subsets of satellite cells have varying degrees of self-renewal and differentiation potential, but how and when these different subsets arise has not been addressed in vivo. Now, on p. 1649, Andrew Brack and colleagues analyse the precise timing of phenotypic and functional divergence of different satellite cell subpopulations in mouse muscle. The authors use a genetic approach to label satellite cells with an inducible reporter, which becomes diluted with every round of cell division. In this way, the authors identify label-retaining cells (LRCs) that possess greater self-renewal potential than non-LRCs, which are prone to differentiation. The LRCs emerge shortly after birth, become functionally distinct at later stages of postnatal muscle maturation, and are re-established after injury. By comparing slow and fast dividing cells, the authors identify the cell cycle inhibitor p27^kip1 as a novel regulator of LRCs, required to maintain their self-renewal potential.

Nucleolus precursor body makeover

Unlike somatic cells, the nucleus of the oocyte and very early embryo contains a morphologically distinct nucleolus called the nucleolus precursor body (NPB). Although this enigmatic structure has been shown to be essential for normal mammalian development, its precise function remains unclear. In this issue, Helena Fulka and Alena Langerova now demonstrate (p. 1694) a crucial role for the NPB in regulating major and minor satellite DNA sequences and chromosome dynamics in the mouse. Absence of the NPB during the first embryonic cell cycle causes a significant reduction in satellite DNA sequences, and the authors also observe extensive chromosome bridging of these sequences during the first embryonic mitosis. The authors further demonstrate that the NPB is unlikely to be involved in ribosomal gene activation and processing as previously believed, since this process can still occur in NPB-depleted early embryos. This study uncovers an interesting and novel role for the NPB in early embryogenesis.

Moss stem cells do it differently

The WUSCHEL (WUS) family of transcription factors is well known for its role in stem cell maintenance in seed plants. There are two paralogues of the WUS-RELATED HOMEOBOX 13 (WOX13) gene in the moss Physcomitrella patens, but their function is unknown. Now, on p. 1660, Mitsuyasu Hasebe, Thomas Laux and colleagues investigate the role of theWUX13L paralogues in moss and find that the two genes act redundantly to promote stem cell formation, but via a mechanism that differs from that of seed plants. Using a double knockout of the WOX13Lparalogues, the authors show that WOX13L activity is required to initiate the cell growth that is necessary for stem cell formation from detached leaves. Further transcriptome analysis of the double mutant compared with wild-type moss reveals that the WOX13L genes are required for the upregulation of cell wall-loosening genes, revealing a novel function of the WOX gene family.

Change of heart for RA signalling

Retinoic acid (RA) is essential for many developmental processes, but signalling levels must be tightly regulated since too much RA signalling can cause developmental defects. Cyp26 enzymes help to control this balance, metabolising RA and ensuring the correct specification of multiple different organs. Loss of Cyp26 activity can affect heart formation, and now (see p. 1638) Ariel Rydeen and Joshua Waxman reveal a mechanism that may underpin this. The authors show that Cyp26 activity in the zebrafish anterior lateral plate mesoderm (ALPM) is required for the correct specification of cardiac versus vascular lineages. Specifically, loss of Cyp26 activity in zebrafish embryos results in an accumulation of RA and a subsequent increase in the specification of atrial cells at the expense of endothelial progenitors. The authors propose that the Cyp26 enzymes can have non-cell-autonomous consequences through regulating the amount of RA in the local environment to promote vascular specification by defining the boundary between atrial and endothelial progenitor fields in the ALPM.

PLUS…

The evolution and conservation of left-right patterning mechanisms

Morphological asymmetry is a common feature of animal body plans, from shell coiling in snails to organ placement in humans. Many vertebrates use cilia for breaking symmetry during development: rotating cilia produce a leftward flow of extracellular fluids that induces asymmetric expression of the signaling protein Nodal. By contrast, Nodal asymmetry can be induced flow-independently in invertebrates. Here, Martin Blum et al ask when and why flow evolved, and propose that flow was present at the base of the deuterostomes and that it is required to maintain organ asymmetry in otherwise perfectly bilaterally symmetrical vertebrates. See the Hypothesis on p. 1603

The Hippo pathway effectors TAZ and YAP in development, homeostasis and disease

Over the past 20 years, diverse roles for the Hippo pathway have emerged, the majority of which in vertebrates are determined by the transcriptional regulators TAZ and YAP.  Accurate control of the levels and localization of these factors is thus essential for early developmental events, as well as for tissue homeostasis, repair and regeneration. Here, Bob Varelas provides an overview of the processes and pathways modulated by TAZ and YAP and outlines how TAZ and YAP contribute to organ homeostasis and regeneration. See the Review on p. 1614

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The Australia and New Zealand Society for cell and developmental biology (ANZSCDB) supports several local state meetings held each year for members of the society to come together to present their work.  The emphasis is on giving early career researchers a chance to present their research, to meet with group heads and for everyone to develop a greater appreciation for the diversity for science carried out in the disciplines of developmental and cell biology.  I was delighted to be invited as one of the 3 plenary speakers for this years New South Wales (NSW) state meeting held on the 31^st of March at the Lowy Cancer Centre, University of NSW, Sydney.  This years meeting attracted over 150 registrants, the largest number of participants for a state meeting in NSW.

The plenary speakers, from left: Prof. Denise Montell (UCSB), Dr Megan Wilson (Otago) and Prof. Freddy Radtke (EPFL)

The meeting started with an exciting plenary talk by Prof. Freddy Radtke (EPFL, Switzerland) on the role of Notch as a lineage specifier, stem cell gatekeeper and additionally how Notch functions in cancer. He presented data on the function of the Notch pathway in pigmented tissues such as the skin/melanocytes and eye.  Notch is required for controlling cell fate during cornea wound healing, in the absence of Notch signaling the corneal epithelium adopts a more skin like cell fate during repair (cue some hairy eye ball pictures!).  Persistent inflammation in the absence of Notch appears to be partly responsible for this response, which leads to blindness in mice.  The second plenary speaker Denise Montell (from UCSB) spoke about her work on Drosophila oogenesis to study collective cell migration and included many beautiful images and movies  (check them out on her laboratories website –  https://labs.mcdb.ucsb.edu/montell/denise/videos).  Her group found that the border cells required E-cadherin for collective directional migration through the nurse cell cluster to arrive near the anterior pole of the oocyte.    This is surprising as E-cadherin down regulation is considered a main requirement for epithelial to mesenchyme transition and subsequent cell migration in many other systems.

Dr Guy Barry (Post-doc at Garvan Institute) spoke about identifying non-coding RNA upregulated during neurogenesis using a human iPS-derived neuronal cell culture model.   PhD student Pei Yan Lui (UNSW,CCIA) is researching the role of a long ncRNA associated with the MYCN oncogene that is also expressed in neuroblastoma tissue along with MYCN.  High levels of this ncRNA also correlate with poor survival in an animal model.   Omesha Perena (PhD student from CMRI, University of Sydney) in investigating the  mechanisms between hTert activation and replicative immortality, one of the hallmarks of a cancer cell.  Dr Sophie Pageon a post-doctoral researcher at the UNSW described her research using new imaging methods to track the spatial organization and dynamics of cell receptors at the immune synapse.  Helen Bellchamber (PhD student at ANU) is studying the impact post-translational modification (sumoylation) has on the function of the Zic5 transcription factor.

Cesar Canales (PhD student from UNSW) is studying GTF21RD1 a novel transcription factor associated with Williams-Beuren Syndrome.  He is characterizing the phenotype of the mouse mutant for this factor, which has a very similar facial syndrome including overgrowth of epidermal tissues of the face (including the lips).  Dr Hongjun Shi (VCCRI) presented his work studying the effect of hypoxia on the developing embryonic heart, nice work to understand how environment and genetics influences susceptibility to developmental disease in this case, congenital heart disease.  They have found short-term hypoxia exposure resulted in an increase in embryos with outflow tract heart defects and he is currently investigating the molecular mechanisms underlying the interaction between hypoxia and heart development.  Dr Wendy van Zuijlen (UNSW) is studying how cytomeglalovirus (CMV) can easily pass through the placenta to the infant since around 2000 infants are born each year with CMV infections and this virus can also cause developmental defects.

Dr Thomas Owens accepting the Post-doc speaker prize from Prof. Sally Dunwoodie (ANZSCDB, president-elect)

Two prizes were offered for best speakers.  The Post-doctoral speaker prize went to Dr Tomas Owens (Post-doc at University of Sydney working with Dr Matthew Naylor).  He spoke about the role of Runx2 as a cell fate regulator during mammary gland development.  Knockout of Runx2 specifically in developing mammary tissue resulted in a delay in mammary gland development during pregnancy.  Additionally, he has also been investigating the role of high RUNX2 levels in basal-like breast cancers by using mouse models of breast cancer.

Clarissa Rios-Rojas (UQ) winner of the student speaker with Prof Nicholas Hawkins (HoS School of MEDICAL SCIENCES, UNSW)

The PhD speaker prize was awarded to Clarissa Rios (PhD student with Peter Koopman, UQ Brisbane).  To determine the consequences of germ cell loss on gonad development, she has been using OPT 3D to model testicular cord formation in the presence or absence of germ cells. Clarissa is also looking at how the absence of germ cells effects the  number and specification of cell types in the developing testis.

With over 70 posters to visit, deciding on the poster prizes were a hard call for the judges.  The best poster from a Post-doc went to Dr Gonzalo del Monte Nieto (VCCRI) for his work on heart chamber development and the role of biomechanical forces and the extracellular matrix.   Anne-Marie Mooney (University of Sydney) was the PhD poster winner for her poster on CBFbeta transcriptional co-activator factors in mammary gland development, function and its role in carcinogenesis and metastasis.

My plenary completed the meeting with a bit of EvoDevo (evolution and development) work on the evolution of developmental pathways (using honeybee and sea squirt models) and the evolution of whole body regeneration in a chordate model.   I would like to thank NSW scientists Annemiek Beverdam (UNSW), Matt Naylor (USyd/Bosch), Caroline Ford (UNSW), Nicolas Fossat (CMRI) and Will Hughes (Garven) for their hard work at putting together a fantastic meeting.

 The organisers of the meeting: from left. Dr Matthew Naylor, Dr Nicolas Fossat, Dr Caroline Ford and Dr Annemiek Beverdam

For more details on the ANZSCDB please see http://www.anzscdb.org/

Dr Megan Wilson

Department of Anatomy,

University of Otago,

New Zealand

(2 votes)

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Postdoctoral Position

We invite applications for a postdoctoral research fellow to join the lab of “Imaging and Regulation of Morphogenesis in Higher Vertebrates” at the Pasteur Institute in Paris, France. Our lab is interested in understanding morphogenesis of developing structures, at a cellular level. Using avian models we combine state-of-the-art live imaging microscopy, quantitative analyses, biophysical, cellular and molecular biology approaches to access the cellular dynamics of development.

This specific project aims at elucidating the cellular events underlying the initiation of limb bud formation and how such cell events are dynamically regulated at the molecular level, using the generation of transgenic avian lines. For more information about projects and the lab please visit: www.jgroslab.com.

The position is a 4-year postdoctoral position funded by the ERC (European Research Council), available immediately, although the starting date is flexible. We are seeking highly motivated candidates with expertise in developmental and/or cellular biology. Experience in imaging and chick development will be positively considered.

The Pasteur Institute, located in the vibrant city of Paris, has a longstanding history of excellence in developmental biology and in science in general, with access to excellent core facilities.

Applicants should send a cover letter (describing briefly research interests), a C.V and contact information for up to 3 academic references to jgros@pasteur.fr.

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The Wellcome Trust – Medical Research Council Cambridge Stem Cell Institute is founded on the belief that deep understanding of stem cell biology will be transformative for future healthcare http://www.stemcells.cam.ac.uk

The Institute is seeking clinician scientists at both junior and senior level to complement our existing programmes and contribute to translating ground-breaking developments in stem cell science into better management of malignancies and new regenerative medicines. Applications in any area of medicine are welcome, although we are particularly interested in expanding our translational programmes in haematology, neurology, orthopaedics, cardiovascular medicine and oncology.

Junior candidates will have a PhD and preferably a minimum of 1 year post-doctoral experience, original research achievements, and an exceptional project proposal.  Senior candidates should have an established track record as an independent group leader engaged in high quality science and have an outstanding and well-founded research proposal.

The Institute offers a collegiate environment with both excellent core facilities for laboratory-based studies (stem cell culture, transgenesis, flow cytometry, complex microscopy and bioinformatics) and extensive opportunities to pursue patient based studies. Successful candidates will be supported to obtain external personal fellowship and grant support within 1-2 years. Start-up packages are available according to circumstances.

Your salary will be dependent on your honorary clinical contract status with the relevant NHS Trust and seniority. Salary range £31,301-£101,451.

Applications should be submitted using the University’s web page: http://www.jobs.cam.ac.uk/job/3613/.

Applicants should upload a CHRIS 6 (http://www.admin.cam.ac.uk/offices/hr/forms/chris6/), with a full curriculum vitae, contact details of 3 referees, and 1-2 page outline of research interests, by Wednesday 4^th June 2014.

The University values diversity and is committed to equality of opportunity.

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The Wellcome Trust – Medical Research Council Cambridge Stem Cell Institute is founded on the concept that deep understanding of stem cell biology will contribute to transforming future healthcare.

The Institute is seeking new Group Leaders at both junior and senior level to complement our existing programmes and contribute to ground-breaking discoveries in stem cell science. Applications in any area of mammalian stem cell biology are welcome and we are particularly interested in interfaces with:

(i)            mathematical, physical or chemical biology;

(ii)          bioengineering;

(iii)         malignancy

(iv)         regenerative medicine

Junior group leader candidates will have minimum of 3 years post-doctoral experience, distinctive research achievements, and an original project proposal.

Senior group leader candidate will be internationally recognised for independent high quality science and have an exceptional and well-founded research proposal.

The Institute offers a collegiate environment with excellent core facilities for stem cell culture, transgenesis, flow cytometry, complex microscopy and bioinformatics http://www.stemcells.cam.ac.uk. Successful candidates will be supported to obtain external personal fellowship and grant support within 1-2 years.  An interim start-up package is available. Depending on experience, you can expect remuneration between £37,756 – £64,170.

Applications should be submitted using the University’s recruitment web page: http://www.jobs.cam.ac.uk/job/2186/.

Applicants should upload a CHRIS 6 (http://www.admin.cam.ac.uk/offices/hr/forms/chris6/), a full curriculum vitae with contact details of 3 referees, and 1-2 page outline research proposal, by Wednesday 4^th June 2014.

The University values diversity and is committed to equality of opportunity.

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