Say goodbye to the lab books. They may let you keep it. But usually, sadly, it must stay. Despite being illegible to anyone but you, and never mind the amusing cartoons. The best you can do is a photocopy. If like me you favour the ‘pop-up lab book’ approach to data recording, the job may look slightly daunting. Personally, my lab book is a three dimensional work of art. A photocopy is just not going to convey the essence of my meaning. Yet for many of us, the urge to copy large tracts of our lab books is irresistible.

Remove all those personal touches you took years to accumulate around you. You know the ones. We all have them. For example, I have in front of me right now:

A rainbow stress ball in the shape of a brain. Courtesy of some trade display, company long since forgotten
Ditto a rubber duck wearing a lab coat.
An amusing picture of a lemur that was sent to me during my Ph.D. and is now somewhat of a mascot
One of those fluffy microbes that got popular a while back that you could give to people and joke about gifting them with mono or Ebola. This one is a rather adorable fat cell.
Countless post-it notes with essential information nuggets such as passwords, chemical formulae, how to skip blank cells in Microsoft Excel and a choice selection of French vocabulary

Unbelievably, your successor is unlikely to treasure these as you have, so you may choose to bequeath them to the like-minded souls around you, or give them a one-way trip into the bin on top of the lab book copies.

Get rid of all your solutions. There is nothing more lonely than a collection of old buffers. Here’s a sad fact: no one really trusts your buffer. It’s a personal thing, this is my buffer, I made it, and in it I trust, even though I know you made your buffer exactly the same way and you look reasonably clean. But I’ve seen that amusing bit of fungal fluff you found in your media bottle that you’ve been nurturing on your shelf to see how big it gets and it’s nothing personal, but I’m going to make my own buffer. Incidentally, now is the time to also get rid of any of your own fungal media pets.

Vintage journal articles. Is it just me or does reading other people’s article copies feel weird? Pre-loved literature (scribbled notes are the worst), makes me terribly uncomfortable, to the extent that, shamefully, I will print another copy rather than read someone else’s vintage papers. At this point it may be kindest to consign the whole pile to the recycling bin and think seriously about planting some trees.

Wipe your hard drive. Copy your data, purge your personal stuff and make sure that novel you’ve been writing during ten minute incubations is safely out of the way. Because someone is going to inherit your computer and unless you want to give them a unprecedented window into your life via your old emails, it’s time to search and destroy.

Fridge stocks. Sadly, they will either go off or grow stuff. Possible exceptions are pricy or rare things like antibodies which you should put back where you found them immediately (see next point).

Freezer stocks. Are you the one who took the second last tube of that reagent from the communal box that time you were working really late at night and forgot to put it back? We’ve all been there. It’s time for us to do the walk of shame back to the freezer with all the expensive things we’ve been hoarding. Best done last thing with as few witnesses as possible.

Now walk over to the minus 80C freezer. That cold, frozen wasteland of very important and largely forgotten samples. Samples labelled 1-10, or something similarly inscrutable that doesn’t even make sense to you anymore since the day you tucked them down the side of a box rather than safely inside it because it was only going to be in there for a couple of days. It’s time to let go and move on to…

Liquid nitrogen stocks. The pinnacle of storage paranoia. Exercise some caution here (not just for the very real possibility of frostbite). Things in here are most likely expensive and temperamental and very, very useful. Often best to walk away quietly.

All the rest of your various samples that someone might use someday. If you don’t care for your name being taken in vain throughout the ages, it’s nice to treat your tubes to a label. With a date. And perhaps even a lab book reference. When it comes to your samples, is there any such thing as Too Much Information?

So you’ve cleaned out your desk, your fridge is empty, and apart from the frostbite, you’re in good shape. You may be slightly hung-over from the leaving party, and you’ve definitely got a giant novelty goodbye card. Congratulations, you’re the perfect leaver.

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We have an opening for a PhD student at the University of Amsterdam in the Netherlands.

This research project will investigate the behaviour and control of Wnt-responsive stem cells in the mammary gland. You will be part of a young research team that uses a combination of in vivo and in vitro approaches to understand normal stem cell behaviour, with the ultimate goal of translating principles of developmental and stem cell biology to cancer research and regenerative medicine. Our lab has strong ties to the Wnt-signaling community and to the field of mammary gland biology and we are looking for an ambitious PhD candidate to strengthen our team.

To apply, please visit the vacancy website. If you have any further questions, please contact dr. Renée van Amerongen

Applications will be accepted until 10 December 2013.

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Professor Daniel St Johnston is a prominent developmental biologist and the current director of the Gurdon Institute in Cambridge (UK). The St Johnston lab recently retracted two papers, in what Retraction Watch lauded as a poster case of ‘doing the right thing’. The Node interviewed Daniel and discussed the case, and how his experience highlighted the shortcomings of the current system of ‘setting the record straight’.

Tell us a little bit about the background of this case

We had published two papers, one in The Journal of Cell Biology and another in Developmental Cell, on a low energy polarity pathway. In each case the basic observation was that mutant follicle cells, marked by the loss of GFP, showed a loss of polarity under starvation conditions. Specifically they lost apical aPKC and lateral Discs large. When we tried to follow up this research we could see the phenotype, but it was frustrating because sometimes it was there and sometimes it wasn’t. We initially assumed that we weren’t starving our flies properly. We tried all sorts of drugs that mimic starvation but were not able to change the frequency at which we could see the phenotype. Two members of my lab, Dan and Timm, started to suspect that there was something wrong technically, and came up with this idea that the GFP negative cells weren’t actually real clones but damaged cells. Between our two papers coming out and realizing what was going on, Lynn Cooley’s lab showed that follicle cells remain attached to their sisters after mitosis, generating clones of cells that are connected by small cytoplasmic bridges. This meant that if you just nicked one cell, GFP – and polarity markers – could leak out from a whole cluster of cells, looking exactly like a mitotic clone. The killer experiment was marking the clones in a different way: if you positively mark them with GFP and repeat the experiment, you can observe some GFP-marked clones where you never see the polarity phenotype, and GFP-negative clones where you do. The final bit of the explanation was to clarify why the phenotype seemed to be starvation-dependent. If you starve flies, their ovaries are much smaller, it’s harder to dissect them apart and so you cause damage more frequently. Once we discovered this artefact it basically invalidated the main conclusion of both papers. We felt obliged to set the record straight.

Why did you think that a retraction was necessary? Was there an alternative way to correct the papers?

We wrote a paper (now out in Biology Open) explaining this artefact, which I forwarded to the editors of both JCB and Developmental Cell. I told them that it was important that this work was linked to the original papers, because it showed that many of the results are due to an artefact. They both came back with the same message – that this looked like a case for a retraction.

We had collaborated in both papers with labs that provided the key mutants. In the JCB paper, Jay Brenman had done a very large screen that isolated the first AMPK mutants in Drosophila on the basis of a neural phenotype. That data was in the original paper and is all still true. Actually that paper was probably more highly cited for the identification of those alleles than for the spurious low energy polarity pathway! Jay wasn’t very happy to have to retract what was a major piece of work from his lab that was still true and still being cited.

Was there a way to republish this data?

We asked JCB whether we could retract only part of the paper, but we were told that this was not possible- a retraction is a retraction. Furthermore once a paper is retracted no one can cite it because it ceases to exist after a while. That held things up for quite a long time because we were stuck at an impasse. At this point I called up Jordan [Raff, Editor-in-chief of Biology Open] and asked him whether he thought Biology Open would be prepared to republish this part of the work, as it is important data and will be cited in the future. Jordan immediately said yes.

The next step was to make sure that everything happened simultaneously, because otherwise this data would be published twice, which would also have been a major offence. The three journals, Developmental Cell, JCB and Biology Open, agreed on a date to publish our paper explaining the artefact, Jay’s paper republishing his original mutants, and the two retraction notices.

You mention your concerns regarding your collaborator. Were you worried about the impact in your lab members and your own career?

I am worried about the career of the first author, who was a member of my lab. But what can you do? –  the data aren’t true! As for the impact in my career, time will tell. In an ideal world it will be fine, as long as people look carefully enough to realise that we willingly retracted the papers. The alternative strategy would have been to just publish a paper saying that those results were wrong and hope that people would make the link. No one would have noticed, and it would have probably been better for the careers of everyone involved. But it would have meant that people, especially those in more distant research fields, might carry on citing these papers that aren’t correct.

It is actually worse to discover your own mistakes than other people’s. As scientists, we publish plenty of papers contradicting the results of previous papers from a different lab. That is how science works and it’s normal. But if you do it to yourself then you are in much worse state, career-wise.

Did you get positive feedback from the community?

I gather that it was discussed on Twitter with generally positive responses. I did talk to the author of one of the papers that erroneously attributed a polarity phenotype to a mutant because of this artefact. I asked him if he minded that we included in our Biology Open paper a repeat of his experiment, showing that you didn’t get that phenotype when you made sure that the artefact wasn’t occurring. He was great about it- he agreed that it needed to be corrected and was happy that I mentioned that his result is wrong. I think we have done the best we possibly could in terms of correcting the scientific record.

Do you think this experience highlighted problems with the current process of getting the record straight?

The main concern is that the majority of retractions take place because someone has done something deliberately wrong: manipulating figures or something worse. Those retractions are the ones that attract all the attention and people’s careers deservedly suffer as a result. Once you realise someone is faking their data, you cannot really trust anything else that they do. I view being a lab head almost as being a trademark- you have to protect the integrity of what you produce. Our case is almost the opposite of a retraction due to data manipulation. We withdrew the paper because we made an honest mistake and we wanted to clear up the record – so people know that when we make a mistake we admit it and we sort it out. The fact that these two different kinds of retractions are indistinguishable when you look at the citation does make things more complicated. Without reading the retraction notices in detail, or going to Retraction Watch, you just think: ‘oh, so and so has retracted two papers, they must be dodgy in some way’. It would be useful to have some way to distinguish between these two types of retraction.

My feeling is that the current set-up discourages people from acknowledging their mistakes. The incentives are not right for trying to get the most accurate description of what is known and what is known to be wrong in the public domain. And what we are talking about here is just the tip of the iceberg. There is much more stuff in the literature that is wrong and never gets corrected. If everyone was honest about it, and retracted papers that they found to be seriously wrong, there would be many more retractions and much less stigma.

The other problem is that, as far as I can understand, you can correct things if you get them slightly wrong but if you get things majorly wrong then you have to retract the whole paper, even if some of the data are perfectly sound. It seems wrong that reagents that are extremely useful can disappear from the literature at a blink of an eye.

– Retraction notice: LKB1 and AMPK maintain epithelial cell polarity under energetic stress, Journal of Cell Biology, vol 177 nr 3, 2007

– Retraction notice: Dystroglycan and Perlecan provide a basal cue required for epithelial polarity during energetic stress, Developmental Cell, vol 16, 2009

– St Johnston lab Biology Open paper describing the artefact: Damage to the Drosophila follicle cell epithelium produces “false clones” with apparent polarity phenotypes, Biology Open, ePress

– Brenman lab Biology Open paper republishing mutant screen: Isolation of AMP-activated protein kinase (AMPK) alleles required for neuronal maintenance in Drosophila melanogaster, Biology Open, ePress

– Retraction Watch article on this case: Data artifact claims two fruit fly papers from leading UK group- who offer model response

Image from the St Johnston lab’s Biology Open paper showing damage-induced false clones

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Here are the highlights from the current issue of Development:

One-step transdifferentiation

Terminally differentiated cells are generally considered to be in a developmentally locked state in vivo; they are incapable of being directly reprogrammed into an entirely different state. Now, on p. 4844, Joel Rothman and co-workers show that the expression of a single transcription factor can trigger the transdifferentiation of fully differentiated, highly specialised cells in C. elegans larvae and adults. They show that brief ectopic expression of ELT-7, a GATA transcription factor that regulates intestinal differentiation, can specifically convert non-endodermal cells of the pharynx into fully differentiated intestinal cells. This conversion is accompanied by an increase in the expression of intestine-specific genes and a concomitant decrease in the expression of pharynx-specific markers and structural proteins. The reprogrammed cells also exhibit morphological characteristics of intestinal cells. These, together with other findings in the study, demonstrate that terminally differentiated cells can be reprogrammed to an alternative fate without the need for cell division, without the requirement for a dedifferentiated intermediate state and without prior removal of an inhibitory factor.

Stem cells and regeneration in a new light

Zebrafish have a remarkable capacity to regenerate and, as such, are being used increasingly to study stem cells and organ regeneration. Here, Chen-Hui Chen, Kenneth Poss and colleagues establish a luciferase-based approach for visualising stem cells and regeneration in adult zebrafish (p. 4988). The researchers generate several transgenic lines that enable ubiquitous or tissue-specific expression of both firefly luciferase and mCherry. They show that, unlike the fluorescence signal, bioluminescence in these lines, which they term zebraflash, readily penetrates through adult tissues and can easily be detected. Using the cardiac zebraflash line, they demonstrate that this approach can be used to monitor the extent of heart injury and subsequent regeneration in animals in a non-invasive and high-throughput manner. Furthermore, they report, this approach can be used to detect quantitatively the progeny of engrafted stem cells in recipient animals at high spatial resolution. This methodology, along with the transgenic lines presented here, offer a valuable resource for the study of stem cells and regeneration.

Rocking the Wnt pathway

Wnt signalling plays important roles during embryonic patterning and in tissue homeostasis, and mutations that affect the Wnt pathway are associated with cancer. Despite this, the exact way in which the Wnt pathway is regulated is still not fully understood. Now, Amy Bejsovec and colleagues uncover a novel regulator of Wnt signalling (p. 4937). Previous studies have shown that the Drosophila RhoGEF Pebble (Pbl) might influence patterning mediated by Wingless (Wg), the primary fly Wnt. Following this, the authors show that both loss- and gain-of-function Drosophila pbl mutants exhibit defects that are consistent with a role for Pbl in negatively regulating the Wg pathway. Furthermore, both Pbl and ECT2, the human homologue of Pbl, downregulate Wnt reporter activity in cultured Drosophila and human cells, highlighting a role for ECT2 as a potential proto-oncogene. Finally, the researchers show that, unlike most negative regulators of the Wnt pathway, Pbl acts downstream of Armadillo/β-catenin and may act through Rho1 to negatively regulate Wnt/Wg signalling.

Opening a passage for hair growth

The hair follicle epithelium forms a tube-like structure that is continuous with the epidermis, but how the lumen of this structure is created during morphogenesis and regeneration remains unclear. Now, Sunny Wong and colleagues identify a novel population of cells that initiates hair follicle lumen formation in mice (p. 4870). The researchers first provide a detailed characterisation of the infundibulum, the region encompassing the hair follicle mouth, and identify a population of keratin 79 (K79)-positive epithelial cells within this region. Using lineage tracing, they show that these cells are specified early during hair follicle development and migrate outwards from the hair germ into the epidermis prior to lumen formation. This migratory event is also observed during regeneration of the hair follicle; K79-positive cells are specified in the secondary hair germ and migrate out, eventually forming a continuous layer with pre-existing K79-positive cells. These findings identify both a novel mode of epithelial tube morphogenesis and a unique population of cells that migrate throughout the life cycle of the hair follicle.

Insm1 controls pituitary endocrine cell development

The pituitary gland is an endocrine organ that plays a role in various physiological processes, including growth, metabolism and reproduction. The development of various pituitary endocrine cells is influenced by a number of transcription factors and signals. In this issue (p. 4947), Carmen Birchmeier and colleagues report that the transcription factor Insm1 controls the differentiation of all endocrine cells in the mouse pituitary. The researchers show that Insm1 is expressed in pituitary progenitors and continues to be expressed in differentiated endocrine cells. Using Insm1 knockout mice, they demonstrate that Insm1 controls a pan-endocrine differentiation programme; genes encoding pituitary hormones or proteins involved in hormone production and secretion are downregulated in Insm1 mutant pituitary glands. By contrast, Notch signalling components and skeletal muscle-specific genes are upregulated, suggesting that Insm1 also represses inappropriate gene expression programmes in the pituitary. Finally, the researchers show that the SNAG domain of Insm1 is required for its function, acting to recruit histone-modifying proteins and transcriptional regulators.

Split thoughts on the neural crest

The neural crest (NC) is a transient structure that gives rise to multiple lineages. Despite intense studies, it is still unclear whether the NC represents a homogeneous population of cells. Here, Jean Paul Thiery and colleagues examine this issue (p. 4890). The authors first characterise the cranial neural fold in chick and mouse embryos and show that, prior to delamination, it contains two phenotypically distinct domains: neural ectoderm and non-neural ectoderm. The researchers then show that the two domains display temporally distinct delamination patterns. Cells specifically within the non-neural ectoderm are the first to delaminate, whereas a second population of delaminating cells then originates from the neural ectoderm in both chick and mouse embryos. Importantly, they report, cells within the two domains have distinct fates: those from the non-neural ectoderm give rise to ectomesenchymal derivatives, whereas those within the neural ectoderm give rise to neuronal derivatives. These, together with other findings, prompt the authors to revisit current definitions of the NC and the origin of ectomesenchyme.

PLUS…

Mechanisms of scaling in pattern formation

Many organisms and their constituent tissues and organs vary substantially in size but differ little in morphology; they appear to be scaled versions of a common template or pattern. Here, David Umulis and Hans Othmer investigate the underlying principles needed for understanding the mechanisms that can produce scale invariance in spatial pattern formation and discuss examples of systems that scale during development. See the Review article on p. 4830

Conveying principles of embryonic development by metaphors from daily life

How can the revolution in our understanding of embryonic development and stem cells be conveyed to the general public? Here, Ben-Zion Shilo presents a photographic approach to highlight scientific concepts of pattern formation using metaphors from daily life, displaying pairs of images of embryonic development and the corresponding human analogy. See the Spotlight article on p. 4827

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Meeting report for Genetics Otago symposium 28-29^th November 2013.

The annual Genetics Otago symposium was held in the newly refurbished HD Skinner Annex of the Otago Museum in sunny (yes, really!) Dunedin, New Zealand at the end of November.   This two-day symposium is run annually by Genetics Otago, a Research Centre of the University of Otago, which has over 240 members based at Otago and right across New Zealand. This year the meeting brought together plenary, guest and postgraduate speakers from Otago and across NZ, in addition to invited speakers from overseas (Australia, Czech Republic). Highlighting the diversity of genetics research, presentation topics ranged from the genomics of NZ stick insects, liver disease, gout, brain development, chordate evolution through to cancer genetics.  Below are a few highlights; for more details check out the Storify of the live tweeting from the symposium: http://storify.com/ANZSCDB/geneticsotago-symposium-2013.

Professor Vicky Cameron’s (Christchurch Heart Institute) group has been studying the genetics of susceptibility to Takotsubo cardiomyopathy or broken heart syndrome, cases of which increased following the two Christchurch earthquakes, especially in post-menopausal women. She and Professor Martin Kennedy, also of University of Otago Christchurch, are championing differing hypothesis for the genetic origin of this condition – a single, rare causative gene mutation versus a ‘perfect storm’ of contributing SNPs.

Dr Amy Osborne (Laboratory for Evolution and Development) spoke about her work identifying the mechanisms behind transgenerational inheritance and the predictive-adaptive response (“Are you what your great grandmother ate?”) where various behaviours or health conditions can be inherited without DNA sequence changes.  In work leading on from the PhD of Sarah Morgan, Dr Osborne has been making use of Drosophila to investigate nutritionally derived transgenerational inheritance in the F3 population following feeding of the F0 generation on a restricted diet.

Sophia Cameron-Christie, a PhD student with Professor Stephen Robertson, presented on the genetics of biliary atresia, a developmental disorder of the bile duct, which is usually only treatable by liver transplants in children affected by this condition.  Sophia is using exome sequencing and linkage analysis on samples from a NZ family to identify susceptibility loci.  Two other PhD students from Professor Robertson’s group also presented their PhD work, Adam O’Neil on periventricular heterotopia and neuronal migration, and Emma Wade on mechanosensing and bone density.

Professor Neil Gemmell (Department of Anatomy) spoke on his work on the increasing evidence that the mitochondrial genome has an important impact on sperm fertility and function, through a phenomenon termed ‘Mother’s Curse’ – whereby incremental mutations can accrue of no selective disadvantage to the mother, but are detrimental to sperm performance, sperm having far fewer mitochondria and more intense energy requirements than oocytes.

Tess Sanders (a PhD student from Dr Christine Jasoni’s group) spoke on how the maternal environment affects foetal brain development. It is well established in humans and other mammals that if the mother is obese, there is a much higher risk of the child being obese.  Tessa is studying gene expression changes and axon guidance in the arcuate nucleus, the part of the brain that receives signals whether to eat or not to eat, and has found molecular evidence that gene expression in this part of the developing brain of the embryo alters depending upon the diet of the mother.

Dr Nic Waddell  (Centre for Medical Genomics, University of Queensland) gave a excellent talk updating us on the ICGC (International Cancer Genome Sequencing) initiative, in particular where they are at with the Australian focus of the project, whole genome sequence analysis of pancreatic cancer, which has a very high mortality rate in those afflicted.

Associate Professor Andrew Shelling from the University of Auckland spoke on the role of Foxl2, a transcription factor they identified as playing a role in premature ovarian failure in NZ families. In initially unrelated work, his group also found point mutations in FoxL2 in many granulosa cell tumors and are now carrying out knockdown and overexpression studies in cell lines to determine how Foxl2 acts to cause ovarian cancer, and comparing this to its misfunction in premature ovarian failure

We were very pleased to have the ANZSCDB support a postgraduate speaker prize and with 12 high quality student speakers it was a hard decision for the judges. In the end, the award was presented to Megan Leask, currently writing up her PhD with Associate Professor Peter Dearden, who investigated the molecular mechanisms behind phenotypic plasticity using the honeybee as a model – whereby dietary differences (i.e. the feeding or otherwise of royal jelly to larvae) drive the development of very different adult organisms (queens vs workers).  In the hive, worker bee ovaries are repressed due to the presence of a queen in the hive; in the absence of the queen, the worker ovaries become activated and they start to lay eggs.  Megan used microarray and RNA-seq, chromatin-immunopreciptation (for epigenetic marks) and drug inhibitor functional studies to understand the molecular changes that occur, both gene expression and chromatin organization, for ovary reactivation, and hence may give us a better idea of how this phenotypic plasticity works at the molecular level.    Sophia Cameron-Christie and Tess Sanders won the GeneticsOtago Speaker award.

This was the 5^th year for the Genetics Otago Annual Research Symposium, and it was again a big success.  It is becoming so popular that registrant numbers had to be capped this year, but given the strong interest from outside Otago, next year’s meeting will be extended, with more researchers from the North Island encouraged to attend.  Looking forward to it already!

—– Dr Megan Wilson, ANZSCDB New Zealand representative and Genetics Otago member; Developmental Biology Laboratory, Department of Anatomy, University of Otago.

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This month saw many interesting posts on the Node, in addition to several job and PhD studentship adverts in our jobs page. Here are some of the highlights!

Node series

Our two series continued at full steam this month:

– In our outreach series, the Cosy Science team presented their ongoing project of bringing science to the relaxed environment of the pub, while Worm Watch Lab is a citizen science project in which the public helps scientists study egg laying in C.elegans. The Biology Builders participated in our series by sharing their experience of organising a stand in a science festival, as well as suggesting an easy outreach activity involving ping-pong balls!

– In our ‘A day in the life’ series Stephen Freeman described a day in the life of a chick lab, while James Lloyd wrote about the mysteries of working with moss.

Research

– Atsushi Miyawaki and colleagues wrote about their recent paper in Development using Fucci technology to comparatively characterise endoreduplication and endomitosis.

– The Chicago Journal club is back  and their first post of this academic year was a Cell Stem Cell paper on the importance of cell sorting in spatial patterning.

– and Christele considered a recent paper assessing the role of dickkopf-1 (dkk1) in neural progenitors.

Meeting reports

– Megan attended ComBio, the largest annual life sciences conference in Australasia, and wrote about her highlights.

– Lauren and Ioanna reported from the UPMC/Curie Developmental Biology course 2013.

– the Node attended the first joint meeting of the French Society for Developmental Biology and for Genetics.

Also on the Node

– We interviewed cardiovascular developmental biologist and Development editor Benoit Bruneau.

– Olivier introduced Manteia, a database that allows the comparison of embryological, expression, molecular and etiological data from human, mouse, chicken and zebrafish simultaneously

– and the deadline for the next round of Company of Biologists Travelling Fellowships, to help cover the costs of visiting another lab, is fast approaching

 
Happy Reading!

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A four-year PhD position is available to combine computer modelling with experimental work investigating stem cell specification, activity, and cell migration in the development and maintenance of the vertebrate cornea.

Further details are available here:

http://tinyurl.com/pmxm2cy

The deadline for applications is 16th December.  Please feel free to contact Prof Martin Collinson (m.collinson@abdn.ac.uk) or Dr Silke Henkes (silkehenkes@gmail.com) to discuss the project further.

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What is the earliest Phylum of metazoans to possess what we would recognize as a nervous system?

Did earlier organisms have all the components of a nervous system in the absence of what we would recognize as neurons?

What is a neuron?

Did nervous systems evolve independently more than once?

Where were all the molecular tool boxes that define a nervous system harnessed from?

These and related questions will be discussed in a three-day international meeting to be held in Florida, May 13-15, 2014.

Participants include recognized experts in the phylogeny of lower metazoans, comparative biologists interested in the cell and neurobiology of the same groups, and molecular biologists interested in the evolution of processes and molecules that underlie nerve function.

Contributed papers are invited for both oral and poster sessions.

Travel awards are available for students.

For full details see our website at: http://efns2.whitney.ufl.edu/

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The 4th Annual UPMC / Curie International Course on Developmental Biology titled “From Stem Cells to Morphogenesis” took place in Paris during a 5-week period in September-October 2013. Participants included both Masters and PhD students coming from all over the world. Students from Brazil, Canada, Greece, Portugal, France, Germany, Spain, England, India, Russia and Italy gathered together to take part in this special course.

The course was comprised of two complementary components. The first part included the practical workshops on the development of different animal models including Drosophila, Mouse oocytes and embryos, Zebrafish, Xenopus, Chick and Nematode. The workshop took place at Université Pierre and Marie Curie (UPMC) every day (except Sunday) for three weeks. Professors and Assistant Professors from all over Paris directed us during a series of experiments aimed at exploring the different advantages of the model systems. We also had the opportunity to work together with prominent guest researchers from the Stowers Institute in Kansas and University College London (UCL). Throughout the workshop students were encouraged to ask questions and to discuss with the professors about the different techniques that can be used to study each model system. The high quality of our instructors combined with the availability of modern equipment at each bench and within the university provided appropriate conditions for us to acquire a thorough understanding of every model presented.

The practical workshop was followed by two weeks of scientific talks given by French and International speakers, and there was an option to only participate in this portion of the course. The conference took place at the Institut Curie, which is located in the historic and beautiful Latin Quarter of Paris. Professors and renowned researchers from institutions such as Harvard, Cambridge, the Stowers Institute, UCL, UPMC, Institute Pasteur and Institut Curie presented recent and often unpublished data spanning a variety of interesting topics in developmental biology in different model systems. Subjects ranged from planarian regeneration to Drosophila morphogenesis, and from regulation of cell cycle to embryonic stem cell biology. Each lecture was followed by an active panel discussion. We had the opportunity to ask the speakers, who are experts in their respective fields, questions about their subject and research. In addition, following the talks we had the chance to discuss with the speakers in a more informal way over coffee and biscuits about things like our own research and future careers. All of us would agree that this was a unique and beneficial opportunity.

Furthermore, students had the opportunity to present an article during the course chosen by the guest speaker and then to propose an experimental design for future research. The advantages of this exercise were bidirectional; we were able to present in front of the author of the article which gave us the opportunity to acquire constructive feedback and advance our scientific way of thinking. Likewise, the researchers benefited from the chance to listen to some new ideas and research proposals on their own work from a different perspective.

Overall, this course provided us with an excellent opportunity to broaden our knowledge and understanding of developmental biology in an ideal environment that promoted discussion, critical thinking and learning. We acquired many new theoretical as well as practical skills that will help develop our scientific careers. However the experience was not only academic. On a more personal level, we were exposured to not only to a different educational system, but also to new cultures. Lasting friendships were made between people all over the world. We were able to bond over our shared interests in developmental biology and in this way help to build a future network of young scientists. All in all this was an extremely rewarding experience.

Ioanna & Lauren

(2 votes)

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