Morphogenesis, the shaping of tissues and organs, is driven by a series of events that proceed in a coordinated manner, both spatially and temporally. Such events include changes in cell shape, cell adhesion, and cell migration, which happen at a precise developmental stage in single cells or cell collectives. The detailed study of morphogenetic processes relies upon the ability to perturb these localized changes in the otherwise intact organism, ideally with sub-cellular precision and on a time-scale of seconds. However, this is impossible to achieve with traditional genetic or chemical tools.

When, in 2011, I started my PhD in the De Renzis group at EMBL, optogenetics had just been elected “Method of the Year” by Nature Methods¹ and was included in Science’s “Breakthroughs of the Decade”². Since its early approaches at the beginning of 2000s^3-5, optogenetics has greatly facilitated the study of neuronal circuits in the brain. In these pioneering experiments, mice were made to express light-sensitive ion channels in selected populations of neurons, thus allowing control over brain activity with a pulse of laser light. By the end of 2000s, a few studies reported using optogenetics also in non-excitable cells^6-8. Despite these advances, being able to control morphogenetic movements with light still represented a challenge.

My longstanding interest in biotechnology led me to propose co-opting optogenetics to modulate cell behaviour during Drosophila morphogenesis. Data from our lab had shown that a particular plasma membrane lipid, phosphatidylinositol-4,5-bisphosphate (PI(4,5)P₂), is essential for cell morphogenesis in the Drosophila embryo⁹. Indeed, PI(4,5)P₂ is known to act as a molecular scaffold for actin-binding proteins, thereby regulating actin polymerization at the cell cortex. PI(4,5)P₂ depletion from the plasma membrane is mediated by a class of enzymes known as inositol-polyphosphate-5-phosphatases (5-phosphatases). I reasoned that by modulating PI(4,5)P₂ metabolism at the plasma membrane, I should be able to deplete actin from the cell cortex. Because cortical actin is key for many biological processes ranging from cell contractility to cell division, this tool would allow the control of a wide spectrum of morphogenetic events. The not-so-trivial question was how to do that using light.

Just a couple of years before I started my PhD, a few research groups had developed optogenetic approaches to specifically control protein-protein interaction in cell culture^10-12. After considering the functional features of these tools, I decided to use the Cry2-CIB1 system¹², as it can be rapidly activated with blue light and does not need the addition of an exogenous chromophore. The Cry2-CIB1 system is composed of two photosensitive modules: Cryptochrome 2 (Cry2) and CIB1, which interact only in the presence of blue light (458-488 nm). This system had already proved suitable to control phosphoinositide metabolism in cultured cells¹³. In the optogenetic approach I set up, a GFP-tagged CIB1 localizes to the cells’ plasma membrane, whereas the 5-phosphatase, which is fused to Cry2 and mCherry, stays in the cytosol. The fluorescent tags would allow me to monitor the protein location in vivo. To test whether I could use this system to modulate morphogenetic movements, I decided to focus on ventral furrow formation, the invagination of the Drosophila mesodermal tissue, as this process is highly dependent on actin dynamics and cell contractility. During ventral furrow formation, a stripe of ~1000 ventral cells constrict their apical surfaces and fold inwards as a tube. The core idea is that in the dark, the 5-phosphatase would remain cytosolic, and morphogenesis would proceed normally (Figure 1A). In the presence of blue light, the 5-phosphatase would relocate to the plasma membrane, where it would deplete PI(4,5)P₂ and, in turn, actin from the cell cortex. This should result in the inhibition of cell contractility and a blockade of ventral furrow formation (Figure 1B).

When I started to test this optogenetic approach, I first looked at the effects of blue light illumination on the 5-phosphatase localization, and on PI(4,5)P₂ and actin levels. Upon a 1 s pulse of 488 nm light, the 5-phosphatase relocated to the plasma membrane. The relocalization of the 5-phosphatase resulted in a sharp reduction in PI(4,5)P₂ and cortical actin levels. I therefore went on to characterize the effects of PI(4,5)P₂ and actin depletion on cell contractility during ventral furrow formation. Illumination of the entire embryo with a 488 nm (single photon) laser resulted in the inhibition of both apical constriction and tissue folding. After this encouraging result, I sought to achieve spatial specificity in addition to temporal precision by photo-activating smaller groups of cells. However, light scattering within the tissue resulted in unwanted photo-activation of cells neighboring the illuminated areas, making the single photon approach impracticable. By discussing with in-house microscopy experts, I found out that this limitation could be overcome by using two-photon microscopy. Indeed, the requirement for near-simultaneous absorption of two photons makes it very likely that photo-activation remains limited to the area where the laser is focused. I therefore set up a protocol to achieve optimal levels of photo-activation with a two-photon laser (950 nm). To my delight, photo-activation could be achieved at the seconds time-scale and allowed high spatial precision, namely single cell resolution.

Having established this powerful approach, I tackled two interesting questions regarding ventral furrow formation. In particular, I tested whether apical constriction in ventral cells is required only to initiate the process of tissue bending, or whether it is necessary throughout the process to achieve complete folding of the tissue. By modulating apical constriction only in ventral cells, I could show that apical constriction is necessary not only to kick off, but also to sustain tissue folding.

Another open question concerned the way individual cells constrict during ventral furrow formation. When ventral cells reduce their apical surface, they do so in an asymmetric fashion: cells shrink along the embryo’s medial-lateral axis and remain elongated along the anterior-posterior (a-p) axis. This asymmetry in cell constriction, known as a-p anisotropy, is thought to be the result of higher tension along the a-p axis than along the medial-lateral axis. However, the origin of this tension was unknown. To address this question, I altered the geometry of the primordium by inhibiting cell contractility in two areas at the anterior and posterior end of the ventral furrow tissue. Then, I checked whether this resulted in any change in a-p anisotropy in cells that were left able to constrict (i.e. not illuminated with blue light). I could show that the degree of a-p anisotropy in non-illuminated cells was higher if the two illuminated areas were further apart than if they were close together along the a-p axis (Figure 2). In other words, if the rectangular geometry of the constricting tissue was preserved cells constricted in an asymmetric way. Instead, if the constricting patch of cells was squared-shaped, constriction was more symmetric, and resulted in roundish cells. This suggests that the geometry of the ventral furrow tissue impacts on the way individual cells constrict.

As I collected increasing amount of data, I needed to transform a lot of visual information into meaningful numbers, so I teamed up with Joseph Barry, who at that time was a postdoc in Wolfgang Huber’s group at EMBL. Joe did a great job of developing algorithms to quantify cell features, such as area and a-p anisotropy. For this project, I heavily relied on the EMBL Advanced Light Microscopy Facility, the state-of-the-art equipment available in the Developmental Biology Unit, and of course the valuable input of my supervisor Stefano De Renzis. Shortly after publication in Developmental Cell¹⁴, our optogenetic approach generated the interest of many research groups around the world, as apical constriction is a highly conserved cellular mechanism during morphogenesis. However, besides apical constriction, cell contractility drives a multitude of cell behaviors, from cytokinesis to cell migration. Therefore, I expect that our approach will be useful to the community for addressing intriguing questions about animal development.

In the meanwhile, optogenetics has enabled the modulation of many other cellular activities, including organelle transport, cell-cell signalling, apoptosis, and gene expression^15-20. The translation of these tools to living organisms will undoubtedly provide new insights into the mechanisms by which embryos grow and develop. As a developmental biologist and recent PhD graduate, I am very much looking forward to seeing where lights will guide us.

^{1. Method of the Year 2010. Nat Meth 8, 1-1, doi:10.1038/nmeth.f.321 (2011). ↩}

^{2. Insights of the decade. Stepping away from the trees for a look at the forest. Introduction. Science (New York, N.Y.) 330, 1612-1613, doi:10.1126/science.330.6011.1612 (2010). ↩}

^{3. Zemelman, B. V., Lee, G. A., Ng, M. & Miesenbock, G. Selective photostimulation of genetically chARGed neurons. Neuron 33, 15-22 (2002). ↩}

^{4. Banghart, M., Borges, K., Isacoff, E., Trauner, D. & Kramer, R. H. Light-activated ion channels for remote control of neuronal firing. Nat Neurosci 7, 1381-1386, doi:10.1038/nn1356 (2004). ↩}

^{5. Boyden, E. S., Zhang, F., Bamberg, E., Nagel, G. & Deisseroth, K. Millisecond-timescale, genetically targeted optical control of neural activity. Nat Neurosci 8, 1263-1268 (2005). ↩}

^{6. Wu, Y. I. et al. A genetically encoded photoactivatable Rac controls the motility of living cells. Nature 461, 104-108, doi:10.1038/nature08241 (2009). ↩}

^{7. Wang, X., He, L., Wu, Y. I., Hahn, K. M. & Montell, D. J. Light-mediated activation reveals a key role for Rac in collective guidance of cell movement in vivo. Nature cell biology 12, 591-597, doi:10.1038/ncb2061 (2010). ↩}

^{8. Toettcher, J. E., Gong, D., Lim, W. A. & Weiner, O. D. Light-based feedback for controlling intracellular signaling dynamics. Nature methods 8, 837-839, doi:10.1038/nmeth.1700 (2011). ↩}

^{9. Reversi, A., Loeser, E., Subramanian, D., Schultz, C. & De Renzis, S. Plasma membrane phosphoinositide balance regulates cell shape during Drosophila embryo morphogenesis. The Journal of cell biology 205, 395-408, doi:10.1083/jcb.201309079 (2014). ↩}

^{10. Levskaya, A., Weiner, O. D., Lim, W. A. & Voigt, C. A. Spatiotemporal control of cell signalling using a light-switchable protein interaction. Nature 461, 997-1001, doi:10.1038/nature08446 (2009).↩}

^{11. Yazawa, M., Sadaghiani, A. M., Hsueh, B. & Dolmetsch, R. E. Induction of protein-protein interactions in live cells using light. Nature biotechnology 27, 941-945, doi:10.1038/nbt.1569 (2009).↩}

^{12. Kennedy, M. J. et al. Rapid blue-light-mediated induction of protein interactions in living cells. Nature methods 7, 973-975, doi:10.1038/nmeth.1524 (2010).↩}

^{13. Idevall-Hagren, O., Dickson, E. J., Hille, B., Toomre, D. K. & De Camilli, P. Optogenetic control of phosphoinositide metabolism. Proceedings of the National Academy of Sciences of the United States of America 109, E2316-2323, doi:10.1073/pnas.1211305109 (2012).↩}

^{14. Guglielmi, G., Barry, J. D., Huber, W. & De Renzis, S. An Optogenetic Method to Modulate Cell Contractility during Tissue Morphogenesis. Developmental cell, doi:10.1016/j.devcel.2015.10.020 (2015).↩}

^{15. Mills, E., Chen, X., Pham, E., Wong, S. & Truong, K. Engineering a photoactivated caspase-7 for rapid induction of apoptosis. ACS synthetic biology 1, 75-82, doi:10.1021/sb200008j (2012). ↩}

^{16. Liu, H., Gomez, G., Lin, S., Lin, S. & Lin, C. Optogenetic control of transcription in zebrafish. PloS one 7, e50738, doi:10.1371/journal.pone.0050738 (2012).↩}

^{17. Toettcher, J. E., Weiner, O. D. & Lim, W. A. Using optogenetics to interrogate the dynamic control of signal transmission by the Ras/Erk module. Cell 155, 1422-1434, doi:10.1016/j.cell.2013.11.004 (2013).↩}

^{18. Grusch, M. et al. Spatio-temporally precise activation of engineered receptor tyrosine kinases by light. The EMBO journal 33, 1713-1726, doi:10.15252/embj.201387695 (2014).↩}

^{19. Motta-Mena, L. B. et al. An optogenetic gene expression system with rapid activation and deactivation kinetics. Nature chemical biology 10, 196-202, doi:10.1038/nchembio.1430 (2014).↩}

^{20. van Bergeijk, P., Adrian, M., Hoogenraad, C. C. & Kapitein, L. C. Optogenetic control of organelle transport and positioning. Nature 518, 111-114, doi:10.1038/nature14128 (2015).↩}

(5 votes)

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Last week saw ASAPbio, a meeting that discussed the role that preprints can play in the life sciences (for a an introduction to preprints check out this video or this wikipedia page).  Those of you on twitter will have followed the #ASAPbio discussion with interest,  and the footage of the conference is now available online. What is your experience: have you deposited your manuscript on a preprint service like bioRxiv? If not, have you considered doing so, and what would persuade/deter you? This month we are asking:

What is the value of preprint servers in Biology?

Share your thoughts by leaving a comment below! You can comment anonymously if you prefer. We are also collating answers on social media via this Storify. And if you have any ideas for future questions please drop us an email!

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In 2014, Development organised a very successful meeting on how the use of stem cell technologies can inform our understanding of human development (you can read about it here or watch the movie below). The next edition of this meeting will take place in the USA this September and applications are now open! The deadline for applications is the 15th of June, but we encourage you to apply early to avoid disappointment. Just click the image above or follow this link.

(1 votes)

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ISBN 9789814678537 – 28USD/18GBP

The idea of human germline genetic modification is too close for comfort right now. However, society in general does not seem to realise the proximity of this threat or the technical basis of this threat, making the publishing of Paul’s book ‘GMO Sapiens – The Life-Changing Science of Designer Babies’ timely. This book is 250 pages of a digestible history of genetic modification and technologies and opinions that are leading to the very real and urgent threat of heritable human genetic modification.

In reading this book it should be noted from the start that while the validation of many that modification of the human germline would be useful for eliminating human disease, in the light of existing, safer and more efficient PGD (pre-implantation genetic diagnosis ) technologies (Chapter 5), this argument seems to front a human desire for modifications towards predicted ‘improvement’ of humans, Human+ if you want to go for the transhumanist view (Chapter 7). Personally, I do not believe there is a valid argument for genetic modification of the nuclear genome in the human germline (in light of PGD). To hide ‘positive eugenics’ (Chapter 7) behind a veil of ‘eliminating human disease’ is frankly wrong. Expert interviews in this book from renowned scientists shamelessly expressing their desire to ‘improve’ humans is scary. However, it was mentioned early that creating panic or scaring people is not the goal of this book, but rather to inform and energize people to become part of the discussion about this new inevitable reality. Reading this book is going to catch you up with the best of the best.

If we stick to arguments and perspectives on the heritable genetic ‘improvement’ of humans, Paul provides a thorough and balanced view. Who should choose what is better? Do we know enough about the human genome to safely predict ‘better’? Will better be for the individual or for society as a whole? All of these views and more are discussed in the book giving time to both sides. There are however a lot of question marks, which reasonable people will approach with caution. But it is not the reasonable who will be pioneering clinical germline modification. It is a fact that someone will heritably modify the human genome (someone has – Chapter 4 and Chapter 9) and use this to enhance perceived positive traits. How will we react to this? How will we manage the unseen consequences.

However, once the mistakes have been made, the technology refined and the benefits become clear, would I say no? Paul presents a story where you have yourself wondering what choices you would make if presented with a list of options; Should I choose that my children are resistant to diseases? Should I choose that my children have reasonably sizes physical features so they do not get teased at school? In a society where these options were available as a reproductive shopping list, what parent would not choose what is ‘best’ for their child? Are we aiming towards human agriculture?

There may be someone in the world right now miscarrying or having an abortion from a defective genetically modified human embryo. This urgency and a thread of caution is present throughout the book. But what I find troubling, exciting but scary, is that I find myself agreeing with an undertone, I do not support human germline genetic modification but with all the new information and perspectives available to me I have found myself questioning my own views and will be watching any developments with a fascinated interest I would rather not admit to.

(2 votes)

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https://www.jobs.manchester.ac.uk/displayjob.aspx?jobid=10973

We are seeking an enthusiastic and outstanding postdoctoral researcher to join a multidisciplinary team led by Prof. Chris Thompson.  This project aims to address the role and regulation of heterogeneity in development using Dictyostelium discoideum as a model system. Dictyosteliumpermits a uniquely powerful combination of approaches to be applied (e.g. imaging, informatics, genetics) and thus provides an opportunity and generate the first integrative ‘top to bottom’ understanding of how heterogeneity, stochastic differentiation and cell sorting result in robust developmental patterning.

You will address the fundamental biological questions regarding the role and regulation of heterogeneity in development you will use Dictyostelium discoideum as a model system. Dictyosteliumpermits a uniquely powerful combination of approaches to be applied.  Firstly, developmental patterning in Dictyostelium is based on ‘salt and pepper’ differentiation followed by sorting out, and therefore heterogeneity has been proposed to play a pivotal role.  Secondly, Dictyostelium is amenable to forward and reverse genetic manipulation, is easily and rapidly grown in the lab to biochemical scales, whilst its relatively small number of defined cell types can be tracked in vivo by live cell imaging during development. Dictyostelium therefore provides an opportunity and generate the first integrative ‘top to bottom’ understanding of how heterogeneity, stochastic differentiation and cell sorting result in robust developmental patterning.

You will use your extensive experience in bioinformatics, computational biology, molecular biology, genetics, cell biology or live cell imaging techniques to determine the molecular basis and gene networks that regulate heterogeneity. These different approaches are highly complementary and your ability to integrate these approaches is crucial. Consequently, multidisciplinary training (especially in computational and wet lab skills) is essential. You should currently hold or be about to obtain a PhD in a relevant field.

Although you will be based in Manchester, several short visits to collaborators will be required for data analysis and project development.

The post funded by the Wellcome Trust and is available for up to 3 years.

Successful candidates will be subject to pre-employment screening carried out on our behalf by a third party. The offer of employment will be dependent on the successful candidate passing that screening. Whilst you will be required to provide express consent at a later stage, by continuing with your application now you acknowledge that you are aware that such screening will take place, and agree to take part in the process.

The School of Life Sciences is committed to promoting equality and diversity, including the Athena SWAN charter for promoting women’s careers in STEMM subjects (science, technology, engineering, mathematics and medicine) in higher education. The School received a Silver Award in 2009 for their commitment to the representation of women in the workplace and we particularly welcome applications from women for this post. Appointment will always be made on merit. For further information, please visit: http://www.wils.ls.manchester.ac.uk/athenaswanawards/

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Researchers at IRB Barcelona and CSIC discover a mechanism through which the cells of an organism interact with their extracellular matrix

The cells of an organism interact not only with each other but with the extracellular matrix that surrounds them. Increasing evidence is unveiling the relevance of this structure—which is secreted by the cells themselves— for the correct function of the organism and also for the development of various diseases.

A new study published in eLife and headed by Jordi Casanova and Sofía J. Araújo, both scientists at the Institute for Research in Biomedicine (IRB Barcelona) and the Instituto de Biología Molecular de Barcelona (IBMB-CSIC), describes a cell communication mechanism that allows the organisation of the extracellular matrix and how this structure affects cells through a feedback system.

For this study, the team of researchers used the fruit fly Drosophila melanogaster—a particular useful model for biomedical research. The study focused on the tracheal system, tubes that are analogous to the function of the human respiratory apparatus. This system has an extracellular matrix that covers the inside of the trachea, forming a structure that is comparable to the hose of a vacuum cleaner. Until now, it was believed that this matrix served only a structural purpose, preventing the tube from collapsing, but the team of scientists has demonstrated that it also regulates the cells that form it.

In 1929, the Canadian biologist W. R. Thompson published a study describing the tracheal system and its structure. Although he was able to describe it, he was unable to explain how it formed. This new study now provides an explanation of this 80-year enigma.

“The biological context of these cells modifies not only their behaviour but also their internal structure,” comments Casanova. “When we modify only the extracellular matrix, the cytoskeleton is also altered.”

“It is a two-fold mechanism,” says Sofía Araújo. “First actin filaments, a very important component of the cytoskeleton, serve as a mould for the deposition of the chitin of the matrix. Next, the matrix itself stabilises the cytoskeleton, anchoring actin in place.” The scientists propose that Src42A—a protein that belongs to the family of kinases that regulates the structure of the actin filament—is one of the main contributors to this system.

Casanova considers that the study explains one of the many mechanisms that allow communication between the extracellular matrix and cells. “The way in which cells communicate has been conserved over evolution: we are sure that this process will be discovered in other organisms. In our lab, we address how such communication allows cells to arrange themselves in such a way as to form tissues.”

The interaction between the cell and its extracellular matrix is also very important in inflammatory and cancer processes. “Tumour cells often take advantage of existing mechanisms, such as the one we have described, to cause havoc. The unravelling of these mechanisms may provide us with new tools to study diseases,” concludes Casanova.

Reference article:

A feedback mechanism converts individual cell features into a supracellular ECM structure in Drosophila trachea

Arzu Öztürk-Çolak, Bernard Moussian, Sofia J. Araújo and Jordi Casanova

eLife (2016): doi: 10.7554/eLife.09373.001

This article was first published on the 22nd of February 2016 in the news section of the IRB Barcelona website

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Here is some developmental biology related content from other journals published by The Company of Biologists.

Using the developmental biology toolkit to study cancer

Aiello and Stanger review the similarities between embryogenesis and cancer progression and discuss how the concepts and techniques of developmental biology are being applied to provide insight into all aspects of tumorigenesis. Read the review here [OPEN ACCESS].

A new gestational diabetes mellitus model

He and colleagues successfully establish a new chick embryo model to study the molecular mechanism of hyperglycemia-induced eye malformation. Read the paper here [OPEN ACCESS].

Cathepsin D sorting in neurons

Jadot and colleagues show that SEZ6L2 can serve as a receptor to mediate the sorting of cathepsin D to endosomes, and that this sorting process might contribute to neuronal development. Read the paper here.

Demethylase activity in ESC differentiation

Becker and colleagues show that KDM6-specific H3K27me3 demethylase activity is crucially involved in the DNA damage response and survival of differentiating murine ESCs. Read the paper here.

Hic-5 in angiogenesis and myofibroblast differentiation

Two studies investigate the role of focal adhesion protein Hic-5. Bayless and colleagues examine whether Hic-5 regulates endothelial sprouting in three dimensions (here), while Van De Water and co-workers report a crucial role for this protein in myofibroblast differentiation in response to TGF-β (here).

A role for miR-20a in endothelial-mesenchymal transition

Krenning and colleagues show that FGF2 induces the expression of miR-20a, a non-coding microRNA identified in a previous screen, which targets the TGFβ receptor complex and abolishes endothelial–mesenchymal transition. Read the paper here.

Characterising the fourth WASP

Wiskott–Aldrich syndrome proteins (WASPs) are nucleation-promoting factors that differentially control the Arp2/3 complex. Here, Bogdan and colleagues characterized WHAMY, the fourth Drosophila WASP family member, and show that it plays a role in myoblast fusion, macrophage cell motility and sensory organ development in Drosophila. Read the paper here.

Loss of PPARγ leads to impaired angiogenesis

Loss of PPARγ in mice leads to osteopetrosis and pulmonary arterial hypertension in mice, and is associated with vascular disease. Alastalo and colleagues now report  a novel mechanism by which  PPARγ can regulate endothelial cell homeostasis and angiogenesis. Read the paper here.

The embryos of Austrofundulus limnaeus, a killifish that resides in ephemeral ponds, routinely enter diapause II, a reversible developmental arrest promoted by endogenous cues rather than environmental stress. Toni and Padilla use A. limnaeus to examine epigenetic features associated with embryonic arrest. Read the paper here.

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Department/Location: Wellcome Trust – Medical Research Council Cambridge Stem Cell Institute, University of Cambridge

Salary: £28,982-£29,847

Reference: PS08402

Closing date: 20 March 2016

Fixed-term: The funds for this post are available for 2 years in the first instance.

The Wellcome Trust – Medical Research Council Stem Cell Institute at the University of Cambridge provides outstanding scientists with the opportunity and resources to undertake ground-breaking research into the fundamental properties of mammalian stem cells (http://www.stemcells.cam.ac.uk/).

Transcriptional control of lineage decisions in embryonic stem cells.

Applications are invited for a postdoctoral position to investigate the molecular control of embryonic stem cell lineage commitment and differentiation. The successful applicant will be part of an interdisciplinary collaboration between The Cambridge Stem Cell Institute and Microsoft Research to understand how information is processed by individual stem cells to bring about cell fate decisions.

For this position demonstrated experience in the analysis of transcriptional mechanisms will be required. The candidate is expected to have considerable expertise in molecular biological and biochemical techniques, basic mammalian cell culture, and to be familiar with basic programming and computational methods. Previous experience in higher-level programming, mammalian stem cell biology, and/or chromatin biochemistry is highly desired. The position will be based in the Hendrich laboratory and is available immediately.

You should have been awarded a PhD degree or equivalent and have several years laboratory experience.

To apply online for this vacancy and to view further information about the role, please visit: http://www.jobs.cam.ac.uk/job/9561. This will take you to the role on the University’s Job Opportunities pages. There you will need to click on the ‘Apply online’ button and register an account with the University’s Web Recruitment System (if you have not already) and log in before completing the online application form.

The closing date for all applications is the Sunday 20 March 2016.

Please upload your Curriculum Vitae (CV) and a covering letter in the Upload section of the online application to supplement your application. If you upload any additional documents which have not been requested, we will not be able to consider these as part of your application.

Informal enquiries are also welcome via email to: Dr Brian Hendrich Brian.Hendrich@cscr.cam.ac.uk, Dr Sara-Jane Dunn Sara-Jane.Dunn@microsoft.com or to jobs@stemcells.cam.ac.uk.

Interviews will be held on Monday 04 April 2016. If you have not been invited for interview by 01 April 2016, you have not been successful on this occasion.

Please quote reference PS08402 on your application and in any correspondence about this vacancy.

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

The University has a responsibility to ensure that all employees are eligible to live and work in the UK.

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Cat Vicente, who many of you will know as the Node’s Community Manager, is moving on to exciting new ventures. We’re really sorry to see her go – I’m sure you’ll agree that Cat has done a fantastic job running the Node over the past few years and she’ll be sorely missed, but we wish her all the best for the future.

And this means that her job is up for grabs – would you like to be the next Community Manager of the Node?

You can find full details of the position here, including more information on what the job actually entails, what kind of person we’re looking for, and the timeline for application.

Informal queries can be directed to our HR department, or feel free to drop me an email if you want to know more.

(4 votes)

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