During the European summer Edinburgh, the Scottish capital, is famously the place to be at while it hosts its world-renowned Festival. But this year it is also the place where the European Zebrafish Meeting was celebrated. The efforts of the Local and International Organizing Committees of the 7^th European Zebrafish Meeting made this possible.

As a 2nd year PhD student, I was very keen to visit this exciting city and to take part in my first international meeting. The opening reception consisted of a cocktail in the Edinburgh International Conference Centre, which gave visiting researchers the chance to meet fellow scientists from other countries but also to have a look at the sponsors’ stands. It was a promising start that was then followed by four days of amazing talks and poster sessions.

The attendees had the opportunity to choose from a wide variety of sessions on subjects such as behavior, sensory systems, regeneration and stem cells, infection and immunity, organogenesis, muscle, skin and connective tissue, cancer and, of course, development. All of those I managed to attend had excellent speakers. In particular, I enjoyed Robert Reinhardt’s (Wittbrodt Lab) talk about vertebrate synexpression genes, where he showed that synexpression groups (composed of spatio-temporally co-expressed genes which act in the same biological process) share common cis-regulatory motifs. As my own project is on eye development I was also partial to the talk by Fabienne Poulain (University of Utah) who proposed a model to explain the trajectory of retinal axons in the optic tract. She explained how dorsal axons in the retina arrive to the lateral part of the tectum and how the others degenerate. This sorting is a heparan sulfate-dependent mechanism.

Florence Marlow´s talk (Solnika-Krezel lab) about the new cell polarity pathway component Gpr125 was also very interesting. This gene is involved in the stabilization of polarity within the plane of an epithelium. Finally, it’s certainly worth mentioning Florencia Cavodeassi´s talk (Stephen Wilson lab) about morphogenesis of the forebrain. She explained the important role that boundaries of Ephrin activity in the anterior neural plate have in the specification of the eye field and the subsequent morphogenesis of the forebrain.

During the poster sessions, students like myself shared our research and got helpful feedback from doubts with the wide variety of experts available, who were happy to discuss our queries.

At this meeting, PhD students like me had a great opportunity to expand our scientific knowledge. It doesn´t matter what you are working on, at the EZM you can learn a lot about what people are doing all over the world and about the latest techniques available. Hopefully, you can also discover new tools that might be useful for your own project and which you had not considered.

Once the talks had finished, the hosting committee organized a concert in St. Mary’s Cathedral, where we enjoyed listening to one of the most famous choirs in the world.

However, this was not the end of our cultural experience. We were yet to see the most emblematic place in Edinburgh. The visit to Edinburgh Castle during the last night of the Meeting was amazing.  The environment transported us back to the Middle Ages. We could breathe the power of many Scottish kings. We were treated to a cocktail in the courtyard, where we enjoyed a performance by a group of bagpipers: you have not experienced Scotland if you’ve not heard bagpipes.  It was all very exciting indeed.

Finally, Berta Alsina and the Spanish committee presented a brief overview of Barcelona (Spain) where the next European Zebrafish Meeting will take place in 2013.

If, like myself, you have fish as your experimental model, I encourage you to attend a zebrafish meeting at some point during your PhD because it opens up the possibilities of what your model can do for you, and you get to meet many people from the community. The Edinburgh Meeting was a great occasion to learn about cutting edge science and I am very glad I was part of it.

Enjoy the photos and feel free to share your comments.

(4 votes)

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The Cell: An Image Library

Help us reach our goal of 1000 members in our LinkedIn group. Join us at http://www.linkedin.com/groups?about=&gid=3733425.

The Cell: An Image Library http://www.cellimagelibrary.org

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Here are the research highlights from the current issue of Development:

Shaping up the Hippo pathway

The Hippo pathway, which regulates cell proliferation, is regulated by cell density: low cell density induces weak Hippo signalling, leading to nuclear accumulation of the transcriptional co-activator Yap and the promotion of proliferation, whereas high cell density prevents nuclear accumulation of Yap and suppresses proliferation. The mechanisms by which cells detect density, however, are unknown. Here, on p. 3907, Hiroshi Sasaki and colleagues show that cell morphology plays a key role in regulating the Hippo pathway. The researchers show that manipulation of NIH3T3 cell morphology, by culture on fabricated microdomains, regulates the subcellular localisation of Yap. These changes in cell morphology, they report, lead to changes in actin stress fiber quantities and the subsequent regulation of Yap phosphorylation and localisation. Finally, the researchers show that stress fibers regulate Yap upstream of, or at the level of, the protein kinase Lats. The researchers thus propose that a cell morphology-based mechanism, mediated by stress fibers, cooperates with a cell adhesion-based mechanism to achieve density-dependent control of cell proliferation.

Vreteno: a novel protein in germline piRNA biogenesis

In Drosophila, Piwi-interacting RNAs (piRNAs) preserve genome integrity in the germline by silencing mobile genetic elements, such as transposons. On p. 4039, Ruth Lehmann and co-workers report the identification of Vreteno, a novel gonad-specific protein that is essential for germline development and primary piRNA biogenesis in Drosophila. The researchers demonstrate that vreteno (vret), which was identified in a screen for maternal-effect mutations affecting oocyte polarity, is essential for germline development. They further show that Vret, which contains two Tudor domains, interacts with Piwi and Aubergine to regulate their stability and subcellular localisation. Using microarray analyses, they confirm that vret regulates transposon silencing in both the germline and somatic tissues of the Drosophila gonad. Finally, the authors report, in the absence of Vret, Piwi-bound piRNAs are lost, whereas piRNAs can engage in Aubergine- and Argonaute 3-dependent `ping-pong’ amplification. The authors thus suggest that Vreteno regulates transposon silencing by acting at the early stages of primary piRNA processing.

Joining forces: PCP and apical-basal polarity

Cell polarity can be defined in terms of the polarity of a cell with respect to others in the same plane (planar cell polarity; PCP), or in terms of polarity based on the subcellular localisation of cell structures, proteins or domains (apical-basal polarity; ABP). The extent to which these polarity pathways are linked, however, is unclear. Here, Janet Heasman and colleagues investigate interactions between the PCP protein Vangl2 and the ABP component aPKC in Xenopus oocytes (p. 3989). The researchers show that Vangl2 is enriched animally in subcortical islands, where it interacts with vesicle associated membrane protein 1 (VAMP1) and acetylated microtubules. The distribution of these islands and the microtubule cytoskeleton, they report, is dependent on aPKC. Importantly, the researchers show that both maternal Vangl2 and aPKC are required to establish asymmetries in the oocyte and early embryo. These data highlight important links between the PCP and ABP pathways, suggesting that Vangl2 and aPKC are part of a common network that influences oocyte and embryo patterning.

Snail enhancers step out of the shade

The expression of critical developmental genes can be regulated by multiple cis-regulatory modules (CRMs), and it has been suggested that remote CRMs are redundant to promoter proximal CRMs. But what is the function of these multiple CRMs and are they truly redundant? To answer this question, Angelike Stathopoulos and co-workers (p. 4075) examine two CRMs from the Drosophila snail gene locus and show that these CRMs interact in a non-additive manner to regulate snail expression. The researchers demonstrate that the CRMs drive distinct patterns of gene expression in early embryos. Furthermore, they report, the distal CRM acts to limit the expanded expression domain of the proximal CRM, whereas the proximal CRM serves to `dampen’ the levels of expression driven by the distal CRM. Importantly, the CRMs are not functionally equivalent; only the distal CRM is required in snail transgenes to rescue snail mutants. Thus, the authors propose, complex interactions between CRMs are required for fine-tuning the patterns and levels of snail expression during development.

Ciliogenesis: arrested development at the node

The rotation of cilia on cells within the node of mammalian embryos generates a leftward fluid flow that establishes left-right asymmetry. But what regulates ciliogenesis at the node? Here (p. 3915), Yuji Mishina and colleagues show that cell cycle arrest, mediated by bone morphogenetic protein (BMP) signalling, is required in node cells to trigger nodal ciliogenesis in mice. The authors show that epiblast-specific deletion of Acvr1, which encodes a BMP type 1 receptor, results in abnormal left-right patterning in early embryos; the node forms in these mutants but nodal ciliogenesis is compromised. Using Acvr1-deficient mouse embryonic fibroblasts, they further demonstrate that BMP signalling through ACVR1 positively regulates p27^Kip1 stability and phosphorylation, which in turn maintains quiescence and allows the formation of primary cilia. Importantly, the researchers report, p27^Kip1 is present and phosphorylated in quiescent nodal cells, whereas the corresponding cells in Acvr1 mutants are proliferative and show reduced p27^Kip1 expression and phosphorylation. These studies provide valuable insight into the mechanisms by which primary cilia form at the node.

Distinct roles for Nodal and Cripto in stem cells

Extra-embryonic endoderm stem (XEN) cells can be derived from the mouse primitive endoderm, which gives rise to two extra-embryonic tissues: the visceral endoderm (VE) and the parietal endoderm. However, despite displaying many characteristics of primitive endoderm, XEN cells only contribute effectively to parietal endoderm in mouse chimeras. Here, Michael Shen and co-workers study the differentiation of XEN cells in response to Nodal, a member of the TGFβ superfamily, and Cripto, a Nodal co-receptor (p. 3885). Importantly, the researchers show that XEN cells treated with either Nodal or Cripto display an up-regulation of VE markers and contribute to VE in chimeric embryos. Notably, they report, the response of XEN cells to Nodal and Cripto differs: the response to Nodal is blocked by treatment with an Alk4/Alk5/Alk7 kinase inhibitor, whereas the response to Cripto is unaffected, suggesting that Cripto can act independently of these receptors’ activity. These findings provide key insights into visceral endoderm specification and define distinct pathways for Nodal and Cripto during cell differentiation.

Plus…

Mechanisms of thymus organogenesis and morphogenesis

The thymic microenvironment supports T cell development and regeneration and, as reviewed by Gordon and Manley, recent studies have made significant progress in identifying the mechanisms that control the specification, early organogenesis and morphogenesis of the thymus. See the Review article on p. 3865

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FGF and Retinoic Acid Signaling during development and regeneration

The inner ear is a highly complex sensory organ that allows us to communicate with the external world. Sensory information is captured by specialized sensory cells that emerge during development in a precise temporal and spatial order. This PhD project will address the question on how FGF and Retinoic Acid signals regulate the development and regeneration of sensory cells and how extrinsic signals are integrated at a molecular level. We use the zebrafish as model system to address these questions. You will be combining functional experiments through transgenic fish lines, in vivo imaging of progenitors and studies of regulatory regions by computational and ChIP experiments. The project provides multidisciplinary training using state-of-the-art techniques and you will therefore be well placed for a future career in biomedical sciences. The Department of Experimental Life Sciences at Universitat Pompeu Fabra is part a leading biomedical research center with an excellent international projection. The PRBB, located in front of the sea and highly international, will provide you with a young, dynamic and interacting atmosphere to ensure you opportunities to discuss and learn from experts in diverse fields. Applicants should have a BSc in biomedical science (or equivalent) and a MSc with strong academic record to apply to competitive PhD fellowships. Applicants should be highly motivated in the field of stem cell, developmental biology and regeneration and be familiar with developmental biology techniques. Basic knowledge of programming or zebrafish manipulation will be strongly encouraged. The position will be available from September-October 2011 for four years. Funding is available for the first year.

If interested please send your application (including CV and Master, BSc academic record) by e-mail to:

Berta Alsina, PhD
Laboratory Developmental Biology
Universitat Pompeu Fabra-PRBB
Dr. Aiguader 88, 08003 Barcelona
Phone: 34-93-3160837
berta.alsina@upf.edu
http://www.upf.edu/devbiol/projectes/Alsina_lab.html

(1 votes)

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Do your ears perk up when you hear about embryonic stem cells?  We all have heard and/or participated in the controversy surrounding the use of them, yet there is no debate over their biological importance and medical potential.  A paper in Journal of Cell Science describes the newly-indentified role for Banf1 in ESC self-renewal.

Embryonic stem cells (ESCs) maintain their pluripotent state through a complicated process called self-renewal.  Self-renewal of ESCs is dependent on three main regulators—Sox2, Oct4, and Nanog.  Recently, Cox and colleagues conducted a proteomic screen to find proteins that associate with Sox2, and identified the DNA-binding protein Banf1.  Banf1 was already known to play important roles in worm and fly development, yet its role in mammalian development was unclear.  Cox and colleagues found that Banf1 is required for mouse and human ESC self-renewal.  The use of RNAi to reduce Banf1 levels led to differentiation of mouse ESCs into mesoderm and trophectoderm cell lineages.  As seen in the images above, Banf1 knockdown (middle and right columns) caused cell to no longer have the characteristic pluripotent ESC morphology (left column).  Banf1-reduced cells were more flattened, had more membrane processes, and showed less staining for the pluripotent stem cell marker alkaline phosphatase (red, bottom row).  When investigating the specific mechanism likely affected by Banf1 knockdown, Cox and colleagues found that cell cycle distribution was altered in mouse and human ESCs – Banf1 knockdown resulted in a higher portion of cells in G2-M phase, and fewer cells in S-phase.

For a more general description of this image, see my imaging blog within EuroStemCell, the European stem cell portal.

Cox JL, Mallanna SK, Ormsbee BD, Desler M, Wiebe MS, & Rizzino A (2011). Banf1 is required to maintain the self-renewal of both mouse and human embryonic stem cells. Journal of cell science, 124 (Pt 15), 2654-65 PMID: 21750191

(4 votes)

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At the ISSCR meeting in Toronto in June I noticed this display at the top of the escalators:

These fabrics with patterns related to stem cells are part of an ongoing exhibition at Toronto’s Ontario Science Centre (OSC). In collaboration with the Stem Cell Network, the “Super Cells: The Wonder of Stem Cells” exhibit displays stem cell-inspired work by students from art schools across the city of Toronto.

At the museum itself, this is one of the works on display:

(Image by Ricardipus on Flickr, used with permission. Click image for more info.)

The fashion aspect of the exhibit reminds me a bit of Primitive Streak, but Super Cells covers other art forms as well.

From the press release:

“This year marks the 50th anniversary of the discovery of stem cells by Canadian scientists Drs. James Till and Ernest McCulloch. “Till and McCulloch’s discovery in 1961 was unparalleled at the time and their findings continue to influence the field of stem cell research to this day,” said Drew Lyall, Executive Director of the Stem Cell Network. “This exhibition is a fitting tribute to their work, which took place here in Toronto.” “

In addition to the exhibit, the museum also organised Skype chats with stem cell researchers during the ISSCR meeting. Visitors to the science centre could ask delegates of the ISSCR meeting about their research via Skype. I didn’t get a chance to see this at the conference (so I don’t know who was interviewed), but the chats will hopefully be posted on the science centre’s YouTube channel.

Super Cells is at the Ontario Science Centre until October 2nd, 2011. If you’re in Toronto before then, take a look. The rest of the museum is really great as well!

(3 votes)

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Since I was an undergraduate student at the Veterinary School in Milan, and throughout the rest of my scientific career, I have been fascinated with the complexities of mammalian preimplantation development. That’s why the publication of our recent paper “Waves of early transcriptional activation and pluripotency program initiation during human preimplantation development” feels like the natural conclusion of a long journey that started with buckets of cow ovaries in Italy, and ended with a collective effort shared by our team in the Stem Cell Bank at the Center for Regenerative Medicine in Barcelona (CMR[B]), under the direction of Drs Izpisua Belmonte and Veiga.

In just hours, the newly formed mammalian embryo terminates the program of the two gametes that formed it, escapes apoptosis, remodels its chromatin to a functional state, starts dividing, and turns on its genome while using up the reserves of protein and RNA inherited from mum (and dad, a little). This last process, termed embryonic genome activation (EGA), represents one of the first signs of “independent life” of a new individual.

As much as the researchers at the CMR[B] are used to manipulating embryos and work with tiny amount of material, studying preimplantation processes in general, and EGA in particular, is a great challenge in our species, as embryos are very scarce, heterogeneous in quality, and RNA amplification methods almost invariably introduce a very significant bias in downstream data quality. An incredible opportunity to look into details of this process came as the CMR[B] established a collaboration with Herbert Auer of the University of Barcelona. His facility just recently validated a method to amplify very small amount of RNA without bias, and we proceeded to apply this “pico-profiling” to a very detailed time course of single human embryos.

Among the many complex interactions that our study has unveiled, one certainly stands out: the human embryo starts EGA one full day before we thought since seminal works were published more than 30 years ago (Braude et al, 1988). Using a combination of extremely reliable transcriptional profiling and de novo transcription inhibition by amanitin treatment, we have been able to show that the human embryo transcribes from its own genome as early as the 2-cell stage (about 30hr after fertilization).

In order to make our data genome-wide expression data easily available to the scientific community at large we have prepared a free online database, HuMER (Human Embryo Resource; http://intranet.cmrb.eu/Human_embryos/home.html). It is our hope and desire that this resource would help us improve our ability to draw interdisciplinary connections between biological events and, in the process, increase our understanding of preimplantation development.

Written by first author of the paper, Dr. Rita Vassena.

Vassena, R., Boue, S., Gonzalez-Roca, E., Aran, B., Auer, H., Veiga, A., & Belmonte, J. (2011). Waves of early transcriptional activation and pluripotency program initiation during human preimplantation development Development, 138 (17), 3699-3709 DOI: 10.1242/dev.064741

(9 votes)

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Here are the highlights from the current issue of Development:

Human embryos make an early transcriptional start

Human preimplantation development is a highly dynamic process that lasts about 6 days. During this time, the embryo must complete a complex program that includes activation of embryonic genome transcription and initiation of the pluripotency program. Here, Juan Carlos Izpisua Belmonte and co-workers use pico-profiling (an accurate transcriptome amplification method) to reveal the timing of sequential waves of transcriptional activation in single human oocytes and embryos (see p. 3699). The researchers (who have developed HumER, a free, searchable database of their gene expression data) report that initiation of transcriptional activity in human embryos starts at the 2-cell stage rather than at the 4- to 8-cell stage as previously reported. They also identify distinct patterns of activation of pluripotency-associated genes and show that many of these genes are expressed around the time of embryonic genome activation. These results link human embryonic genome activation with the initiation of the pluripotency program and pave the way for the identification of factors to improve epigenetic somatic cell reprogramming.

See the post written by the first author of this paper for more information

Worming into organ regeneration

Planarian flatworms have amazing regenerative abilities. Tissue fragments from almost anywhere in their anatomically complex bodies can regenerate into complete, perfectly proportioned animals, a feat that makes planarians ideal for the study of regenerative organogenesis. Now, on p. 3769, Alejandro Sánchez Alvarado and colleagues provide the first detailed description of the excretory system of Schmidtea mediterranea, which consists of internal protonephridial tubules composed of specialised epithelial cells. Using α-tubulin antibodies to stain cilia in the planarian’s excretory system and screens of gene expression patterns in whole mounts, the researchers show that protonephridial tubules form a complex branching structure that has a stereotyped succession of cell types along its length. Organ regeneration originates from a precursor structure that undergoes extensive branching morphogenesis, they report. Moreover, in an RNAi screen of signalling molecules, they identify EGF signalling as a crucial regulator of branching morphogenesis. Overall, these results establish the planarian protonephridia as a model system in which to study the regeneration and evolution of epithelial organs.

Axons lead, lymphatics follow

Given the similar anatomies of vertebrate nerves, blood vessels and lymphatics, it is not surprising that guidance cues such as the netrins, which were discovered as molecules involved in axon pathfinding, also guide vessels. But do nerves and vessels share patterning mechanisms or do axons provide guidance for vessels? The laboratories of Dean Li, Chi-Bin Chien and Brant Weinstein now report that zebrafish motoneurons are essential for vascular pathfinding (see p. 3847). Netrin 1a is required for the development of the parachordal chain (PAC), a string of endothelial cells that are precursors of the main zebrafish lymphatic vessel. Here, the researchers identify muscle pioneers at the horizontal myoseptum (HMS) as the source of Netrin 1a for PAC formation. netrin 1a and dcc (which encodes the Netrin receptor) are required for the sprouting of the rostral primary axons and neighbouring axons along the HMS, they report, and genetic removal or laser ablation of these motoneurons prevents PAC formation. Together, these results reveal a direct requirement for axons in vascular guidance.

Satellite cells: stem cells for regenerating muscle?

Adult vertebrate skeletal muscle has a remarkable capacity for regeneration after injury and for hypertrophy and regrowth after atrophy. In 1961, Alexander Mauro suggested that satellite cells, which lie between the sarcolemma and basement membrane of myofibres, could be adult skeletal muscle stem cells. Subsequent cell transplantation and lineage-tracing studies have shown that satellite cells, which express the Pax7 transcription factor, can repair damaged muscle tissue, but are these cells essential for muscle regeneration and other aspects of muscle adaptability? In this issue, four papers investigate this long-standing question.

On p. 3639, Chen-Ming Fan and colleagues report that genetic ablation of Pax7⁺ cells in mice completely blocks regenerative myogenesis after cardiotoxin-induced muscle injury and after transplantation of ablated muscle into a normal muscle bed. Because Pax7 is specifically expressed in satellite cells, the researchers conclude that satellite cells are essential for acute injury-induced muscle regeneration but note that other stem cells might be involved in muscle regeneration in other pathological conditions.

Anne Galy, Shahragim Tajbakhsh and colleagues reach a similar conclusion on p. 3647. They report that local depletion of satellite cells in a different mouse model leads to marked loss of muscle tissue and failure to regenerate skeletal muscle after myotoxin- or exercise-induced muscle injury. Other endogenous cell types do not compensate for the loss of Pax7⁺ cells, they report, but muscle regeneration can be rescued by transplantation of adult Pax7⁺ satellite cells alone, which suggests that Pax7⁺ cells are the only endogenous adult muscle stem cells that act autonomously.

On p. 3625, Gabrielle Kardon and colleagues confirm the essential role of satellite cells in muscle regeneration in yet another mouse model. They show that satellite cell ablation results in complete loss of regenerated muscle, misregulation of fibroblasts and a large increase in connective tissue after injury. In addition, they report that ablation of muscle connective tissue (MCT) fibroblasts leads to premature satellite cell differentiation, satellite cell depletion and smaller regenerated myofibres after injury. Thus, they conclude, MCT fibroblasts are a vital component of the satellite cell niche.

Finally, on p. 3657, Charlotte Peterson and colleagues investigate satellite cell involvement in muscle hypertrophy. By removing the gastrocnemius and soleus muscles in the lower limb of mice, the researchers expose the plantaris muscle to mechanical overload, which induces muscle hypertrophy. After two weeks of overload, muscles genetically depleted of satellite cells show the same increase in muscle mass and similar hypertrophic fibre cross-sectional areas as non-depleted muscles but reduced new fibre formation and fibre regeneration. Thus, muscle fibres can mount a robust hypertrophic response to mechanical overload that is not dependent on satellite cells.

Together, these studies suggest that satellite cells could be a source of stem cells for the treatment of muscular dystrophies but also highlight the potential importance of fibroblasts in such therapies. Importantly, the finding that muscle regeneration and hypertrophy are distinct processes suggests that muscle growth-promoting exercise regimens should aim to minimise muscle damage and maximise intracellular anabolic processes, particularly in populations such as the elderly where satellite activity is compromised.

Plus…

Notch signaling: simplicity in design, versatility in function.

The evolutionarily conserved Notch signalling pathway operates in numerous cell types and at various developmental stages. Here, Andersson, Sandberg and Lendhal review recent insights into how versatility in Notch signalling output is generated and modulated.

See the Review article on p.3593

Evolution of nervous system patterning: insights from sea urchin development

Recent studies have elucidated the mechanisms that pattern the nervous system of sea urchin embryos. Angerer and colleagues review these conserved nervous system patterning signals and consider how the relationships between them might have changed during evolution.

See the Review article on p. 3613

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For the past 24 years, the Mouse Molecular Genetics meeting has been a leading forum for researchers who apply the methods of genetics and genomics to fundamental problems in mammalian biology, including stem cell biology, early development, and models of human disease. In particular, the meeting showcases the latest technical developments in genetics and engineering of the mouse genome, and this year will feature a session devoted to imaging. The Mouse Molecular Genetics meeting assembles leaders in the field to present unpublished research findings, encourages junior investigators to participate in oral and poster presentations, and provides a stimulating environment for the exchange of ideas and information.

Sessions:
Epigenetics
Genetics and Genomics
Imaging
Models of Human Disease
Organogenesis
Patterning
Stem Cells and Germ Cells
Technology

Scientific Programme Committee:
Allan Bradley, Wellcome Trust Sanger Institute, UK
Kat Hadjantonakis, Sloan-Kettering Institute, USA
Haruhiko Koseki, RIKEN Research Center for Allergy and Immunology, Japan
Michael Shen, Columbia University Medical Center, USA

Keynote speakers:
Kathryn Anderson, Sloan Kettering Institute, USA
William Skarnes, Wellcome Trust Sanger Institute, UK

Speakers include:
David Adams, Wellcome Trust Sanger Institute, UK
Shinichi Aizawa, RIKEN CDB, Japan
Phil Avner, Institut Pasteur, France
Yann Barrandon, EPFL, Switzerland
David Beier, Harvard Medical School, USA
Richard Behringer, MD Anderson Cancer Center, USA
Shuomo Bhattacharya, University of Oxford, UK
Neal Copeland, Institute of Molecular and Cell Biology, Singapore
Xiaoxia Cui, Sigma-Aldrich Corp, USA
Elizabeth Fisher, UCL , UK
Scott Fraser, Beckman Institute, USA
Matthias Merkenschlager, MRC Clinical Sciences Centre, UK
Olivier Pourquie, Institute of Genetics and Molecular and Cellular Biology, France
James Sharpe, Centre for Genomic Regulation, Spain
Ludovic Vallier, Cambridge University, UK
Magda Zernicka-Goetz, The Gurdon Institute, UK

Conference Programme Information:
The conference will start on Tuesday, 20 September with registration at 14.00.
The conference will finish after lunch on Friday, 23 September 2011 at approximately 13.30.

https://registration.hinxton.wellcome.ac.uk/display_info.asp?id=258

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I’ve just added some 2012 conferences to the events calendar, and thought I’d give a quick reminder on how to add events here. If you have an account on the Node, you will have received these instructions when your account was approved. (And if you don’t have a Node account, you can get one here.)

When logged in, click “add/edit events” in the sidebar of the Node admin panel.

You’ll now get to the page where you can add an event. In the following picture, the numbers correspond to the list below:

1. Add name of event
2. Select both boxes (skip the first if there is no website)
3. Add start and end date of event
4. Add location
5. This is set to “conference” by default, but can be changed to “workshop” or “course”
6. Add website address

Don’t forget to save. Your event now appears on the events calendar!

If you want to share more detailed information about conferences (eg. if you’re organising one) you can write a post about it, but don’t forget to also add it to the calendar!

(Get these instructions as a pdf)

(NB – events that are not relevant to the developmental biology community, or commercial/sales events (such as product demos) will be removed from the calendar. If you’re not sure whether an event is suitable, you can contact us or leave a comment below.)

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