Fully Funded PhD Places available in Developmental Biology and Neuroscience

Syracuse University, New York, USA.

Interneuron specification in the zebrafish spinal cord.

The Lewis Lab recently moved to Syracuse University from Cambridge University in the UK. We use Genetics, Cell Biology and Developmental Biology to investigate how the correct number and pattern of different neurons forms in the vertebrate spinal cord, and how these neurons acquire their specific characteristics and functions.

PhD Projects are available to investigate the roles of specific regulatory genes (Transcription Factors) in determining different neuronal characteristics (such as neurotransmitter phenotypes and axon morphology) in the zebrafish spinal cord.
We primarily use zebrafish embryos as a model system, as the embryos develop outside the mother and are transparent and their relatively simple nervous system facilitates studies of neural circuitry and function. We use GFP lines (see picture) to study neurons in live and fixed embryos. As most of the genes involved in spinal cord development are conserved between vertebrates, the insights that we gain should be widely applicable, including to humans.
See http://biology.syr.edu/faculty/lewis/lewis_research.htm for more details
Application Deadline:
Deadline for August 2012 admission is January 2012.
Applications will be considered in the order that they are received – so if you are interested please apply soon! We will start assessing applications in December 2011.
Notes on Funding and PhD Program
Funding will be a mixture of teaching and research assistantships and is guaranteed for 5 years.
Students usually rotate in 3 different labs and then choose a lab for the PhD.

Information on other labs in the department can be found here: http://biology.syr.edu/directories/fac_dir.htm
For more details on the graduate program see http://biology.syr.edu/grad/graduate.htm
Syracuse has its own airport (15 minute drive from downtown) and is close to Toronto, New York City, Philadelphia, Montreal as well as the natural beauty of Upstate New York (Niagara Falls, The Finger Lakes, Adirondack lakes and mountains).
Syracuse University shares a campus with SUNY Upstate Medical University that has active research programs which include Cell Biology, Developmental Biology and Neuroscience http://www.upstate.edu/research/research_dept.php and the Lewis Lab is also part of their graduate program in Neuroscience (for which there is a separate application).

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It’s the end of the month, which means it’s time to download next month’s desktop calendar. Put it on your own computer and/or on the computers in your lab. There, now you’re all ready for October!

Mouse embryo showing Wnt1/Cre-YFP transgene (yellow), 2H3 antibody (red), and DAPI (blue). This image, taken by Elsa Denker of the Sars International Centre for Marine Molecular Biology, was one of the candidates in the fourth Development cover image voting round of images taken at the 2010 Woods Hole Embryology course.

Visit the calendar page to select the resolution you need for your screen. The page will be updated at the end of each month with a new image, and all images are chosen from either the intersection image contest or from the images we’ve featured from the Woods Hole Embryology 2010 course.

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-By Nitin Sabherwal, Eugen Nacu, Heike Laman, Irene Gutierrez Vallejo and Anna Kicheva

The second day of the workshop has finished and it is the reporting time now.

We had a wonderful day with fantastic talks and a nice walk around the area. The weather had also been beautifully supportive for these kinds of excursions and this added to the joy of walking around such a splendid place.

The first session on the second day had talks with the general question and theme- is it possible to control the cell fate decisions, particularly in context of neural development, by manipulating/controlling the cell cycle?

The session started with a talk by Philipp Kaldis who investigated the brain of CDK2/CDK4 double knock out (DKO) mice embryos. He found that the brain of these mice showed similar gross structures as the normal brain from control mice, however, the cortical plate and the intermediate zone areas showed reduced thickness indicating reduced differentiation, while the subventricular zone and the ventricular zone containing progenitors were largely unaffected. His work conveyed 2 important points:

1)   in the absence of CDK2 and CDK4, cyclinD will pair up with CDK1 and CDK6 instead.

2)   CDK2 and CDK4 have an effect on differentiation of neural stem cells. The effect is mediated by a change in the length of cell cycle and potentially by a direct effect of CDK2 and CDK4 on differentiation.

In the second talk, Federico Calegari, followed up on the theme of “cell cycle length (particularly the length of the G1 phase) being a determinant of cell fate during division of neural stem cells in the developing mouse brain”.  He started by describing the process of neurogenesis in mice, which follows thepath: apical progenitor -> basal (intermediate) progenitor -> neuron. He followed with explanation of previous work that supported this idea; work which showed that:

1) the G1 length of neural progenitors increases during development

2) cortical areas with higher neurogenesis have a longer G1 than proliferating progenitors

3) an artificial lengthening of G1 induces premature differentiation.

4) shortening of G1 by CDK4 and cyclinD1 inhibits neurogenesis and promotes the expansion of basal progenitors during embryonic development

And finally he showed the amazing results that it is possible to conditionally control the expansion of NSC in the adult mouse brain by temporarily overexpressing CDK4 and cyclinD1 (called 4D), which would initially expand the progenitor pool and then, after stopping the 4D overexpression by genetic manipulation, the expanded pool would eventually differentiate into the neurons. In essence, this new system allows the increase of neuron number in the adult hippocampus, which may have important implications for understanding the role of adult neurogenesis in cognitive function and controlling this process for therapy of neurodegenerative diseases

So we found out that controlling cell cycle length by CDKs and cyclins influences fate decisions in neural progenitors. But the next bigger question becomes- what is downstream of these Cyclin/Cdk molecules responsible for the fate change? And here came Anna Philpott’s insightful talk to our rescue.She looked at the posttranslational modifications of Neurogenin2 which drives neurogenesis. Neurogenin2 has multiple sites for phosphorylation and these different sites show different sensitivity to Cyc/CDK levels, with more sites being phosphorylated at a higher level of CDK. These phosphorylations were shown to negatively affect the stability of Neurogenin promoter binding in a cumulative fashion. Anna nicely showed that the efficiency of Neurogenin2 induction of neuronal markers is inversely proportional to the number of phosphorylated residues.

Linking the data together from Federico’s and Anna’s work, it is tempting to speculate that CDK4 and cyclinD1 induce proliferation of basal progenitors by decreasing the activity of Neurogenin2 and similar differentiation factors.

The last talk of the session was from Kristen Kroll who talked about the role of Geminin in setting up the epigenetic landscape for neural fate acquisition. Kris has long standing interests in how neural fate acquisitionis regulated by Geminin, which she cloned long time back in Mark Kirschner’s lab, as a regulator of both neurogenesis and cell cycle.  Kris nicely showed that knockdown of Geminin, a nuclear protein had no effect on the ability of ES cells to maintain or exit pluripotency, but when she overexpressed Geminin, it promoted neural fate acquisition, even in the presence of growth factors that normally antagonize neural induction. She followed this observation and showed that the mechanism behind Geminin’s ability for neural induction was due to its ability to maintain a hyperacetylated and open chromatin conformation at neural genes. She nicely showed that in ES cells, Geminin had the ability to enhance the histone acetylation on neural promoters and also it binds to the acetylated neural promoters and activate the expression of neural genes, leading to the neural fate acquisition caused by the Geminin overexpression. Thus Kris showed that Geminin functions as an intrinsic factor regulating the neural fate acquisition, by establishing an appropriate epigenetic signature on neural promoters.

During the Monday afternoon session we continued with two talks that link polarity and cell proliferation.  Dr. Helena Richardson presented her work in Drosophila eye imaginal discs about the role of lgl in proliferation.  lgl is a polarity protein that has been implicated in human cancers. Helena found that lgl mutant cells show an increase in proliferation without apparent defects in apical basal polarity. This proliferation mis-regulation is due to a perturbation of the Salvador/Warts/Hippo pathway, and she also presented her preliminary data on novel mechanisms that couple the polarity to the Hippo pathway.

Dr. Nancy Papalopulu spoke on her work on the early neural plate progenitor cells from Xenopus, In this system, cells with different apical-basal polarity properties showed different potentials for proliferation and differentiation. Her work shows that a membrane-bound, active form of aPKC, an apical polarity protein, is able to directly phosphorylate some components of the cell cycle regulatory machinery.  This caused protein destabilization with consequent effects on shortening the length of G1 phase, and promoting proliferation. She proposed that cell polarization is one mechanism that controls the length of the cell cycle, with consequent effects on the differentiation potential of the cells.

The fun (for scientists) continued in the evening with a mini grant writing session where five teams of randomly-paired discussants were asked to come up with a fundable proposal, that incorporated both team members expertise, in 15 minutes!! Proposals included microRNA regulation of oscillatory networks, proteomic screens on limb regeneration, uncovering links between patterning and proliferation, molecular requirements for NSC differentiation, and the importance of G2 phase.  Reflecting the current economic climate, none of the proposals was funded

(2 votes)

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Whether you’re familiar with the web comic or not, most of you will probably recognize your own current or past career as a graduate student in the new PHD Comics movie.

PHD Movie Trailer from PHD Comics on Vimeo.

It’s playing at university campuses across the world. If your city is not on the list, don’t fret: the website contains information on how to organise a screening at your own institute. Now if someone in Cambridge would like to host a screening, I’ll be there!

(See last year’s interview with Jorge Cham on the Node.)

(1 votes)

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Eric Wieschaus is a Professor at Princeton University, USA. He was awarded the Nobel Prize in Physiology or Medicine in 1995, together with Christiane Nüsslein-Volhard and the late Edward B. Lewis, for their work “uncovering the genetic control of embryonic development”. Throughout his career, he has been interested in the mechanisms underlying patterning and morphogenesis in the early Drosophila embryo. You can find a short film featuring Eric, made at The EMBO Meeting here.

 Marcos González-Gaitán‘s main interest lies in fly development as well. He started his lab at the MPI-CBG in Dresden, Germany, and in 2006, his group moved to the University of Geneva, Switzerland. Marcos has made major contributions to our understanding of how morphogen gradients are formed and regulate tissue growth. In his work, he combines cell biology and biophysics to address developmental problems in a quantitative manner.

I spoke to Eric and Marcos at The EMBO Meeting in Vienna last week. We talked about model systems, tackling details versus fundamentals, the future of developmental biology, and how to successfully collaborate with non-biologists. I hope you’ll enjoy reading about their experiences and thoughts!

What are currently the big scientific goals in your labs?

EW  I think I’ve always been interested in things that I can see. For me the focus is on morphological change – how cells change shape, how they move. I’m trying to do something slightly more biophysical, partially because I have this prejudice that physicists never have to remember much detail and you can get to an understanding without knowing all the details.

MG  What we are increasingly caring about is how tissues proliferate and grow, also taking a biophysical and cell biological approach. Of course I care about the details, but I try to see what can be fundamental beyond the details. I don’t know if it’s possible, because the details are contaminating the fundamentals to a large extent.

EW  Yes, and we’ve almost never done well when we don’t look at details.

MG  Exactly.

EW  I think this is actually a little frustrating about the time we’re living in, because overall in the field, we have this desire to go to a systems level, and yet at least for me how to do science is really grounded heavily in particulars. Describing something in a general, global way isn’t as helpful for me….

MG  I have very strong opinions about this, where I might be completely wrong in fact, but that’s how I think these days about this problem. We all speak about model systems, like Drosophila and I also work in fish, and with these you want to do something that can be general to other animals.

So, you start off thinking that the general description is at the level of genes. I don’t know what’s Eric’s opinion is on this, but over my career, I realised that that’s not really true – beyond saying that this gene is doing signalling, and this other one is a transcription factor. Beyond that it’s difficult to say that what Ubx does in Drosophila is the same as the homologous gene in another animal.

Then I became a cell biologist, because I thought these details might be general. I studied endosomes and endocytosis thinking that I’m going to find the principles of how endocytosis interfaces with signalling, and that’s going to be general. But, you also find out that that’s not the case, at least that’s my perception. The same endosome in the next system has totally different properties. It’s not general.

So then I moved into some biophysics and physics, thinking the universality is going to be in these physical properties, whatever they are – tension, mechanics or scaling of gradients. And now I’m getting to the point where this is probably also not true! Why is this? – I think its probably evolution; in every single system evolution has tinkered around with properties. So then where is our value?

My thinking today is that the real value is the approach. You ask questions to have solutions to these questions, and you develop tricks, assays – intelligent and elegant ways of thinking about the problem differently. In your little system, where the details are very important, you come up with a solution. I don’t think this solution is going to be universal. But the value, in my opinion, is that someone working in a different system can look at my study in flies or in fish and say, this is an interesting way of looking at the problem. You can measure degradation rates by doing FRAP, and then they can use these tricks or this way of thinking to apply to their system – the solution is probably going to be totally different.

EW  One thing that struck me was, you said that model systems are model systems because we think of them as leading to generalities. That is actually what the word means. The reality is that model systems, at least in the fields we work in, exist not because it has anything to do with generality, but because experiments were easy to do in them. We stupidly call them model systems, but we really work in them because I can go into the lab and have a chance of setting up an experiment in a way that leads to a conclusion that’s admittedly very specific. However, you’re not going to be able to do those experiments in anything other than the five or ten model organisms. So the real generality maybe is close to what you are saying, that the generality is that model systems allow the approach, allow us to pursue a scientific approach.

The curious thing, as biologists, we worry a little about generality, but one of the accusations the physicists make about biologists is that we don’t see the forest for the trees. We see trees all the time, it’s all we see, we see little specific trees. And my physicist friends worry a lot about whether what we’re doing is important, or generalisable? They always ask that question, and my reaction with time has become: Oh yes, it’s going to be generalisable, and somebody really smart some time down the road is going to see all of this, it’s all going to fit together in some picture – maybe! But right now I’m happy with trees, I’m happy that I can go into the lab and get something that is admittedly specific about flies, but at least is probably true, and measurable.

MG  The question is whether the problems we are addressing now, are comparable to trying to understand the double helix etc. We have the tendency to believe that it’s not, because we’re so much into our thing. But then, very often when people look back, they say, “These guys were doing absolutely fundamental research!”, but at the time they were just looking into this very particular thing. I ask this question all the time, are we looking at something fundamental or just the details. Because when I started to do developmental biology, I thought all my colleagues who did botany were completely boring, because they were just describing petals and sepals, while I was doing something fundamental. But with age, I’m not sure that I’m not just looking at petals and sepals, I’m not sure…

EW  Well you know, some day, somebody will know, but we will fortunately not be around!

In your view, what will be the future of developmental biology?

MG  I organise retreats in my lab, which often have this question – What is going to be the future in 5, 10 years. And it’s funny, my students and postdocs in the lab would say that the future is physics and to measure things. I think that’s not the future, that’s now! I have the feeling that we are neglecting some other things that might be the future, and that is chemistry. We think of proteins and genes, but there are all also lipids and sugars, and we are ignoring them completely! Maybe the future could be to measure them, find out where they are and how they influence things. Chemistry could be the future.

EW  Maybe the future is ignorance! Meaning where the future is, is where we’re ignorant today. So, in a way, asking where the future is, is to ask what are the things that we don’t know. That’s the question I never ask because if I would make a list of all the things I don’t know, I’d just spend all my time making that list. Beyond the idea that it’s just in the things we don’t know today, your job as a scientist is to find something you don’t know and figure it out.

MG  I think the future is determined by new ways of looking at things and then you can just ask different questions. For example, when I started my PhD with Garcia-Bellído, I was looking at work that he was proposing, and that Eric was proposing, which back then, meant to look at cells. At that time, developmental biology was not looking at cells at all – I’m talking 1985. So I thought the future is in cells, single cells, and it became the future in the 90s and 2000s. The same now with physics, people started to do this, so that can change the way we look at things and we will find things that we don’t know now. In this sense the new way of looking at it is maybe chemistry, but perhaps other things that my students may see one day, but not me.

EW  I suppose if you were an administrator at a university deciding where you’re going to throw money, clearly one of the places that you could decide to throw money is in re-vamping chemistry departments, which many places now do. And that might be another test of where the future is – it’s where the people who have money are throwing it!

So they might set the future by throwing money there, because money usually makes things possible?

EW  Yes, and when things become possible, unless people are cruelly incompetent, something good comes out of… going to the moon.

How did you start your collaborations with physicists, and do you have advice for others who are trying to do this?

EW  I’m totally dependent on proximity. I don’t like talking on the phone, I type badly, I don’t write – I have to have people who are next to me, and I have to get along personally with them. What helps me a lot is that I’m at a university that has a very strong commitment to undergraduate teaching. It’s a great university with a lot of very smart people, but we all teach undergraduates, and we all often teach together. And so a lot of my contacts with physicists or with computer scientists are through my teaching. It’s odd, because you think, “God if I didn’t have to do so much teaching I could be really, really good and accomplish all kinds of stuff!”, but for me, teaching has been a very important part of my scientific development over the past 30 years. It’s brought me into contact with colleagues and people that I wouldn’t necessarily have found common ground with.

MG  First, I think that very often biologists, when they go into these quantitative things have an agenda. They want to be proved right, and then they use these guys to prove them right. That is a short-term agenda. I think doesn’t work. In my case, I probably started in this way, but my main collaborator, Frank Jülicher, he’s a very deep person, and we have had to take our time to understand each other. Fortunately, we never had time pressure – we saw a problem and stepped back to the fundamentals. And we went slowly. It takes time; to me not rushing is something important. Second, I’m discovering that there is a component of personal chemistry and respect that is very important. The physicist needs to respect, appreciate and value, and want to understand the experiment and the details of it. And you need to do the same with their science; you need to understand how they solve the differential equations at some point because there is value in that.

What career advice do you give to your students and postdocs?

EW  Work hard! Really, work hard, and be successful. Meaning that make choices always based on “Is this going to be successful?”, and be able to make that judgement. Be able to change, be flexible. You have to work really hard; you have to work on the weekends and all these things. But it’s not an excuse after a year or two to say, “Well, I worked really hard, somebody should hire me.” They’re not going to hire you because you work really hard; they’re going to hire you because you’ve actually accomplished something. And it’s impossible to accomplish something unless you work hard, and you have to finish stuff. You have to bring things to conclusions.

MG  I’m more of a dreamer, I’m not so pragmatic. What I tell them is, value your career of course, but be beyond that, you want to understand something, and that is the uncompromisable thing. Do what is important to you, do work hard indeed, but go for a problem, understand something. I think that is the fuel to work hard and to improve your career. It allows you to relax a little bit about this pressure that everybody is feeling now, about crises, problems; you just focus on your problem. If you cannot do this, it does not work.

EW  Yes, it’s really hard to work hard if you’re not passionate. It is the passion I guess that allows you to believe that if you work hard, you’ll accomplish something.

(12 votes)

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Here are the highlights from the current issue of Development:

ApoE: a role in neurogenesis

Hippocampal neurodegeneration occurs in most forms of dementia, including Alzheimer’s disease. There is, therefore, intense interest in unravelling the mechanisms that underlie adult neurogenesis in this region of the brain. Now, on p. 4351, Steven Kernie and colleagues report that the cholesterol carrier apolipoprotein E (ApoE) is required for the maintenance of the neural stem/progenitor cell pool in the adult dentate gyrus region of the mouse hippocampus. The researchers show that ApoE is minimally expressed within the neural progenitor pool during early dentate gyrus development, when neural stem/progenitor cells are rapidly proliferating and differentiating into neurons. However, ApoE expression is markedly upregulated in adult dentate gyrus stem/progenitor cells, which proliferate more slowly. Notably, in ApoE-deficient mice, dentate gyrus neural stem/progenitor cells continue to proliferate rapidly, which ultimately depletes the neural stem cell pool. These and other data suggest that ApoE helps to regulate hippocampal progenitor cell fate and provide a mechanism by which human APOE polymorphisms might contribute to late-onset hippocampal neurodegenerative diseases.

A gutsy new model for intestinal development

The mechanisms that drive early intestinal development are poorly understood, but it is widely believed that the foetal intestinal epithelium is multilayered (stratified). Here (see p. 4423), Deborah Gumucio and co-workers overturn this dogma. By analysing cell polarity, cell shape and cell dynamics in the foetal mouse intestine, they show that the early intestinal epithelium is single-layered (pseudostratified) and undergoes interkinetic nuclear migration (a process seen in other pseudostratified epithelia, in which nuclei move from the basal to the apical surface of the epithelium during the cell cycle). They report that microtubule- and actinomyosin-dependent apicobasal elongation drives the growth of intestinal epithelium girth that occurs at mid-gestation and that villus formation occurs by expansion of the apical surface. Finally, they show that, as in the pseudostratified neural tube, the actin-binding protein Shroom3 is crucial for the maintenance of the foetal intestinal epithelium. These results suggest a new model for intestinal morphogenesis in which the epithelium remains single-layered and apicobasally polarised throughout early intestinal development.

Excretory systems: regeneration and evolution

Because planarians can regenerate a complete body from a tissue fragment they present a powerful system in which to study cell, tissue and organ regeneration, and to look for conserved developmental mechanisms. Peter Reddien and colleagues now describe a regulatory programme for the regeneration of the planarian Schmidtea mediterranea excretory system, the protonephridia (see p. 4387). The S. mediterranea protonephridia consists of tubules, which are dispersed throughout the animal’s body, two types of tubule-associated cells, and ciliated terminal cells, which drive filtration from the extracellular space into the tubule lumen. The researchers use RNAi screening assays and microarray analyses to show that Six1/2-2, POU2/3, hunchback, Eya, Sal1 and Osr, which encode transcriptional regulators, are involved in protonephridia regeneration. Notably, apart from hunchback, all these genes are also required for vertebrate kidney development. Moreover, the researchers show that planarian and vertebrate excretory cells express several homologous proteins involved in reabsorption and waste modification. Together, these findings suggest that metazoan excretory systems share a common evolutionary origin.

TPR-GoLoco moves to orientate division

Cell divisions must be correctly oriented, usually through mitotic spindle orientation, to ensure normal development. Extrinsic signals sometimes control division orientation, but how? To address this question, Adam Werts and co-workers have been investigating the localisation of the TPR-GoLoco protein pair GPR-1/2 in C. elegans embryos (see p. 4411). In four-cell stage embryos, GPR-1/2 is enriched at the junction between two cells – the endomesodermal precursor EMS and the germline precursor P₂ – and both cells align their division towards this cell-cell contact. The researchers report that, unexpectedly, GPR-1/2 distribution is asymmetric in P₂ but not in EMS. Instructive intercellular signalling through MES-1/SRC-1 determines the asymmetric localisation of GPR-1/2 in P₂, they report, and this distribution (which is established through GPR-1/2 destabilisation at one cell contact, and its diffusion and stabilisation at another cell contact) is important for normal development. Overall, these results identify the dynamic localisation of GPR-1/2 as a key mediator of cell division orientation in response to external signalling.

Mediator complex sizes up plant development

Final organ size is regulated by coordinated cell proliferation and cell expansion, which control cell number and cell size, respectively. Little is known about how organ size is determined in plants, but now, on p. 4545, Ran Xu and Yunhai Li report that MEDIATOR COMPLEX SUBUNIT 25 (MED25) regulates organ size in Arabidopsis thaliana. The researchers discover this new role for MED25 – a gene that controls shade avoidance and stress responses in Arabidopsis and is involved in transcriptional regulation – through a genetic screen for mutations that enhance the floral size of the da1-1 mutant; DA1 is a negative regulator of seed and organ size that restricts cell proliferation. Loss-of-function mutants in MED25 form large organs, they report, whereas plants overexpressing MED25 have small organs. These alterations in organ size are caused by changes in both cell number and cell size. Thus, the researchers suggest, MED25 acts within the transcriptional machinery to regulate plant organ size by restricting both cell proliferation and cell expansion.

Axons set oligodendrocyte myelinating potential

Myelination facilitates the transmission of electrical signals along axons and ensures their long-term viability, and most axons in the central nervous system are eventually myelinated by oligodendrocytes. But are the timing and extent of myelination regulated by the intrinsic properties of oligodendrocytes or by axons? To address this question, David Lyons and colleagues examine myelination by single oligodendrocytes in vivo in zebrafish (see p. 4443). As in mammals, zebrafish oligodendrocytes myelinate either a few large caliber axons or numerous smaller axons, they report. They further show that the large caliber Mauthner axon is the first axon to be myelinated. Then, using two independent genetic manipulations, the researchers generate zebrafish that have additional Mauthner axons. In these fish, oligodendrocytes that typically myelinate one Mauthner axon in wild-type fish myelinate multiple Mauthner axons, and oligodendrocytes that exclusively myelinate smaller caliber axons in wild-type fish also myelinate the supernumerary Mauthner axons. Thus, the researchers conclude, individual axons regulate the myelinating potential of single oligodendrocytes.

Plus…

The Wnt signaling pathway controls lineage specification and axial patterning in vertebrate embryos and, as reviewed here by Sergei Sokol, recent studies have uncovered a new mode of Wnt signaling that acts to maintain pluripotency in embryonic stem cells.
See the Review article on p. 4341

The International Workshop on Molecular Mechanisms Controlling Flower Development took place in Italy in June 2011. As reviewed by Francois Parcy and Jan Lohmann, the results presented at this workshop underlined how mechanistic studies of both model and diverse species are deepening our understanding of the cellular processes involved in flowering.
See the Meeting Review on p. 4335

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We are looking for a highly motivated PhD student to study development and regeneration of the thalamus in zebrafish.

Stroke is a prevalent and devastating disorder, and no treatment is currently available to restore lost neuronal function after stroke. In 10% of all stroke patients, a remote damage of the thalamus has been documented.

We utilize the genetic model organism zebrafish to explore innovative strategies for the improvement of regeneration by means of tissue engineering. The main focus is on the analysis of the development of the zebrafish thalamus and on the design, and testing of an 3D-cell culture system for reconstructing this complex brain part in-vitro. In order to optimize the strategy for tissue engineering, the project is aimed at reaching a new level of innovation which brings together (in a transdisciplinary approach) the main pillars of tissue engineering, namely 1) Developmental biology, 2) Microsurgery and Transplantation of tissues and cells, and 3) Material science. The project is set in a collaboration Dr Stefan Giselbrecht (IBG1, KIT; http://www.ibg.kit.edu/ibg1/57.php ).

The ability to quickly integrate into a team and to work within an academic research environment is essential. You must show initiative, should be well organized and must pay attention to detail. General laboratory management skills are required. You should have a very good degree in a subject related to molecular biology or cell culture. Previous experience with zebrafish would be an advantage.

The position is implemented in the Graduate School of the Biointerfaces Program of the KIT   ( www.bif-igs.kit.edu ) and is available for 3 years. The project could start any time.

For further information and/or application with CV and a short statement of your current research please contact:

Dr. Steffen Scholpp

Karlsruhe Institut of Technology (KIT); Institute of Toxicology and Genetics (ITG); Email: steffen.scholpp[at]kit.edu; WWW: http://www.itg.kit.edu/scholpp.php

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Okinawa institute of Science and technology (OIST), situated on Okinawa Island is an ideal and inspiring place to discuss and learn science. The student participants and mentors of the developmental neurobiology course (July 17- 31, 2011) were from every corner of the globe. The course began with a wonderful talk about history of developmental neuroscience by David Van Vactor. M.A Price spoke about the signaling mechanisms during early development of Drosophila embryo.  James Briscoe from MRC London discussed about brain and neural tube development in vertebrates. Explained, “How does neurogenesis begin and how do neural stem cells maintain their fate”.  Chris Q. Doe from Oregon USA very elegantly described the mechanisms involved. Prof. Ischiro Masai from OIST Japan explained factors involved in spatial and temporal pattern of neurogenesis in Zebra fish retina. Kozo Kaibuchi from Nagoya University, Japan presented how internal and external signals regulate neuronal polarity. How do axon find their right partners and make neural connections, were the major focus of Elke Stien, Hitashi Sakano and J Huang. Students very enthusiastically and actively discussed their work too during the poster sessions in between.  After two days of intense lab work at the main campus, participants could also visit the labs of various groups. Personally talk to researchers and use the lab facilities for experimental work. Drosophila and Zebra fish were mainly used during the practical sessions in the course.  Students learned dye injection into embryonic Zebra fish eye to visualize the connections in wild type animals and then compare with the mutant animals. They got opportunity to do live imaging using Zebra fish and Drosophila embryos. Dissection of embryonic and larval Drosophila nervous system was also performed during the session. Participants could visualize and experience good microscopy by trying out their samples on microscopes from the Institute imaging facility. We also utilized and tried out different kinds of microscopes, which were provided by various companies in the workshop. Image analysis soft wares were also used for data analysis.

Second week of the course started with session on axon targeting and synapse specificity. Akiko Nose from Tokyo University taught how the connections are made and then refined to form a proper functional synapse. He showed some nice movies using optogenetics as a tool. The molecular mechanisms for dendritic self-avoidance and tiling, how is dendritic field size regulated and how are these maintained over time were the major themes of the Prof. Yuh Nung Jan’s talk. He also explained how fruit fly maggots avoid sunlight and described in detail how class IV dendritic arborisation neurons with elaborate dendrites tiling the entire body wall, act as light-sensing antennae. Van Vactor from Harvard school of Medicine shed light on the posttranscriptional machinery of growth cone involved in regulation of synapse assembly. He also discussed his recent findings from the lab about modelling spinal muscular atrophy, a severe neurogenic disease in Drosophila. Vijay from NCBS India explained, how the behaviour output is generated, once the neural circuits are established. He illustrated various assays to quantify behaviour deficits in mutant animals. At the end of the session Hitoshi Okamoto from RIKEN brain Institute described how Zebra fish could be used as a model to study vertebrate behaviour. He explained various behaviour assays to study learning and memory in Zebra fish. We relaxed and also got chance to show our non-scientific talents in the party and dinner at faculty house located nearby the seaside house. We also visited Castle and Aquarium during the course. After fun and enjoyment we attend talk by David Feldhiem, who described how graded expression of Ephrins is involved in generation of topography in vertebrate visual system. Bernando sabatini discussed about various high resolution imaging techniques utilised to study active synaptic connections. In the last of course Takeharu Nagai described broad range of fluorescent probes to image the synaptic structures and how to choose a good fluorescent probe for your experiments. Prof Hideyuki Okano discussed about iPSCs and their use in treating various neurological disorders and injury. Prof. Lee Rubin at the end of the course demonstrated how we could do large-scale drug screening in the lab in collaboration with pharmaceutical companies to treat challenging nervous system disorders. Last but not least, at the end of the last supper, we enjoyed the traditional Japanese dance and Judo Karate. In short this course was full of fun and learning.

You can read more about OIST and Course here

http://www.oist.jp/en/press-room/news-articles/151/1062-dnc2011.html

and watch this video also.

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In the series of The Company of Biologists Workshops a select group of roughly 30 scientists have gathered at Wiston House, West Sussex, UK, from September 18 to 21, 2011, to discuss the topic of “Growth, division and differentiation: Understanding Developmental Control”. This workshop series aims at fostering collaboration and conceptual advancement by bringing together researchers from various backgrounds and by facilitating close scientific exchange and cross-pollination to tackle challenges in current biological research.

We are a group of workshop participants – PhD students, postdocs and lab heads – who will be updating the Node with collectively written posts from the meeting. All speakers have approved the text before it was posted.

The scientific program of the opening afternoon session on Sept. 18 included a series of four excellent plenary talks followed by an evening poster session.

Ludger Hengst from Innsbruck Medical University (Austria) opened up with a talk elucidating the role of the CDK inhibitor p27, specifically its regulation by growth factor-related signaling molecules such as JAK2, exemplifying how tyrosine kinase signals can directly modulate cell cycle regulators and underlining the immediate clinical relevance, for example, in the context of JAK2 mutations in proliferative diseases such as polycythemia vera.

Jackie Lees from MIT presented work on the role of the Rb tumor suppressor in fate commitment and cancer. To elucidate tissue tropism and heterogeneity of Rb-associated tumors (here: osteosarcoma) this work exploited Rb-/-, p53-/- as well as Rb/p53 double mutants in Osterix-positive bone precursor cells [see Calo et al., 2010]. In an E2F-independent mechanism, Rb appears to potentiate Runx2 serving as an activator in osteogenesis. While Rb mutants did show surprisingly little effect, the combined Rb/p53 deletions not only lead to blockage of differentiation at the pre-osteoblast stage, but to a reversion toward even earlier stages, enabling this earlier stage mesenchymal precursor to give rise to an extended spectrum of derivatives including brown fat tissue tumors (hibernoma). Re-introduction of Rb reinstated terminal bone differentiation. This work also illustrated how the heterogeneity of tumors could arise from the dedifferentiation of more mature stages, so that tumors may contain cells with stem cell character without necessarily having arisen from a “cancer stem cell”.

While Ludger Hengst’s earlier presentation had primarily drawn attention to N-terminal interaction partners of p27 during late G1, the next talk by P. Renee Yew from the University of Texas focused on its C-terminal regulatory interaction. To this end, the work presented here introduced the Xenopus inhibitor of CDKs Xic1 (exhibiting both p21 and p27 features) and showed novel regulatory interactions with PCNA during S-phase of the cell cycle.

Peter Sicinski, Harvard Medical School, presented data on a cell cycle regulation-independent role of Cyclin-E on CDK5 in the generation and functionality of neuronal synapses and demonstrated its relevance for cognitive behavior in mouse models. In this context, CDK5 appears to partner with p35 and p39 to execute its essential function in neuronal differentiation and synaptogenesis. On the other hand, formation of a cytosolic complex with Cyclin-E and p27 appears to render it inactive and profoundly interferes with synapse formation and learning.

This concluded the first day’s session of oral presentations. A common thread were the identification of novel linkages between classic cell cycle machinery and a range of signaling pathways involved in the control of differentiation. So inspired, ample discussion continued throughout the evening poster session and beyond.

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Scheduled Node Maintenance:

This weekend (September 16-18) we’re upgrading the system that the Node runs on (WordPress), so you may not be able to access the site at times. Everything should be working again on Monday, but as always, if you spot anything unusual, let us know.

Update 18/9: the site upgrade is now complete, and everything works – as far as we can tell (again, do let us know if something seems weird.)

Dates for your calendar
In the recent survey about the Node, a few people asked to be kept up to date of various scholarships and registration deadlines. Here is a selection of upcoming dates of interest, but this is by no means an exhaustive list. We’ll try to do these once in a while, but don’t hesitate to write your own posts to let people know about similar deadlines, or leave a comment below. Also make sure to check the eligibility of all scholarships and grants before applying.

Conference registration deadlines.
Keystone announced a few upcoming deadlines for conference abstract submissions, including dates for the following meetings:
September 19 – abstract & scholarship deadline for “Angiogenesis: Advances in Basic Science and Therapeutic Applications” (January 16-21, 2012)
September 20 – abstract & scholarship deadline for “Epigenomics” joint with “Chromatin Dynamics” (January 17-22, 2012)
September 21 – abstract & scholarship deadline for “Cardiovascular Development and Regeneration” (January 22-27, 2012)
October 6 – abstract & scholarship deadline for “Gene silencing by small RNAs” (February 7-12, 2012)

Grants and fellowships:
October 11 – The NSF announced an application deadline of October 11 for Postdoctoral Research Fellowships in Biology (PRFB). For 2012 this fellowship is limited to certain areas: (1) Broadening Participation in Biology; (2) Intersections of Biology and Mathematical and Physical Sciences; and (3) National Plant Genome Initiative Postdoctoral Research Fellowships.
November 1 – Sir Henry Wellcome PostDoctoral Fellowships. See their website for other grant deadlines.
November 18 – NSF Graduate Research Fellowship Program (GRFP)

Travel funding:
September 30 – Deadline for The Company of Biologists Direct Travel grants, which fund travel for conference attendance.
October 31 – EDEN has research exchange funds available for US-based eco-evo-devo researchers (graduate students, postdocs, faculty).

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