Posted by Journal of Cell Science, on 2 September 2015
This cartoon was first published in the Journal of Cell Science. Read other articles and cartoons of Mole & Friends here.
Part I- ‘The imposter’
Part II- ‘The teaching monster’
Part III- ‘The Pact’
Part IV- ‘The fit’
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Posted by Domingos Henrique, on 2 September 2015
Great success, at least 25 Masters and PhD students applied to these fellowships.
We want to encourage the participation at our meeting (www.spbd-meeting2015.com) of the future generation of developmental biologists, and found some extra funding that allows us to offer up to 10 fellowships to Masters students (with lab experience already) and 1st year PhD students. Normally, these students do no participate for lack of sponsorship, but with these fellowships they can now join us at Algarve for the best Dev Biol meeting of the year!!
Fellowship cover registration and all other expenses (except travelling!) and you can find more information at www.spbd-meeting2015.com
Encourage students in your lab to apply!
Do not lose this special opportunity and join us at Algarve!
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Posted by Xiaofei Sun, on 1 September 2015
The process of embryo implantation consists of multiple steps: blastocyst apposition, adhesion to uterine luminal epithelial (LE) cells, and removal of the epithelial cells encasing the blastocysts. How the blastocyst trophectoderm breaches the luminal epithelial barrier has been studied for decades, the mechanism of the abstraction of LE cells was not clearly understood. Since the discovery of cell apoptosis mechanism, a putative thought has been that LE cells around the implanting embryo undergo this programmed cell death once they are attached with the blastocyst (Joswig et al, 2003; Parr et al, 1987). This mechanism indicates that degeneration of LE cells is a maternal intrinsic response to implanting embryos (Finn & Hinchliffe, 1964; Krehbiel, 1937). Although others suggested that trophoblast cells have a role in triggering epithelial cell apoptosis (Joswig et al, 2003), it is believed that trophoblast cells need to wait passively for the autolysis of apoptotic epithelial cells in order to get in contact of stromal cells.
However, our study shows that embryos play an active role in removing LE cells (Li et al, 2015). We have shown that LE cells in direct contact with the blastocyst are endocytosed by trophoblast cells by adopting the nonapoptotic cell-eat-cell process (entosis) in the absence of Caspase3 activation. About half a century ago, Finn and McLaren observed that degenerated uterine epithelial cells are taken up by the trophoblast cells (Finn & McLaren, 1967). The endocytosed epithelial cells were named as “W-body”. However, these notions were primarily based on observations of cell integrity and structure, but it was not clear whether it is entosis or phagocytosis, since both of them involve engulfment of one cell by another cell. In phagocytosis, only dead or dying cells are engulfed, whereas live cells are internalized in entosis. Our results showed that trophoblast cells actively engulf proximate live epithelial cells. This observation challenges the dogma that uterine epithelial cells undergo apoptosis attributed by maternal responses with minimal role played by embryonic cells in eliminating the LE cells.
Although our results demonstrated that trophoblast cells are able to entosize epithelial cells both in vivo and in vitro, we cannot rule out the possibility that the involvement of other mechanisms to remove LE cells during implantation. In fact, we observed that in the absence of embryos, epithelial cells undergo apoptosis in a longer time span in pseudopregnant mice. It would be interesting to examine whether blockage of entosis or epithelial cell apoptosis could completely block implantation and cause pregnancy failure. It is possible that embryos will still be able to complete implantation without entosis, although the implantation process may be delayed. However, most defects during the early implantation events result in either pregnancy failure or late stage pregnancy defects (Cha et al, 2012; Wang & Dey, 2006).
Although trophoblast cells are known to be invasive, our report is the first one to show that they are able to endocytose live cells. Trophoblast cells also play a key role during placentation. It has been shown that maternal endothelial cells are substituted by trophoblast cells (Cross, 2005). The mechanism is still not clear. Is it possible that entosis also plays a role during placentation?
We have shown previously that LE cells begin to lose their apicobasal polarity pending blastocyst implantation (Cha et al, 2014; Daikoku et al, 2011). The transition of LE cells from a high to a low polar state is critical to implantation, since the LE retains high polarity in mice with uterine inactivation of Msx, Klf5 or overexpression of Wnt5a, and blastocysts remain encased within the intact epithelium past day 6 of pregnancy which results in implantation failure (Cha et al, 2014; Daikoku et al, 2011; Sun et al, 2012). Therefore the initial phase of the implantation process requires a transition from high to lower polar state in the epithelium. In addition, usually epithelial cells in vivo are anchored onto the basement membrane, adhered to neighboring epithelial cells by junctional proteins, and aligned as a single layer. The cell-in-cell structure of entosis suggests that the engulfed cell loses connections to its neighboring LE cells and basal lamina, causing epithelial cells to be more flexible and thus easier to be engulfed. Therefore, it would be interesting to examine whether entosis requires decreases in epithelial polarity.
Our results showed that some trophoblast cells on the surface of the blastocyst became enlarged and formed dome-shaped bulges during entosis. The mechanism of reorganization of trophoblast cytoskeleton is not clear. Our study also showed that entosis is only observed in mural trophectoderm, which differentiates into trophoblast giant cells. The giant cell layer is the border between fetal and maternal tissues, and functions as a protective shell for fetal growth. We speculate that the early entosis of maternal cells by the cells in mural trophectoderm makes the future giants cells chimera of maternal and fetal origin, and thus facilitating the protective role of trophoblast giant cells.
References:
Cha J, Bartos A, Park C, Sun X, Li Y, Cha SW, Ajima R, Ho HY, Yamaguchi TP, & Dey SK (2014). Appropriate crypt formation in the uterus for embryo homing and implantation requires Wnt5a-ROR signaling. Cell reports, 8 (2), 382-92 PMID: 25043182
Cha J, Sun X, & Dey SK (2012). Mechanisms of implantation: strategies for successful pregnancy. Nature medicine, 18 (12), 1754-1767 PMID: 23223073
Cross JC (2005). How to make a placenta: mechanisms of trophoblast cell differentiation in mice–a review. Placenta, 26 Suppl A PMID: 15837063
Daikoku T, Cha J, Sun X, Tranguch S, Xie H, Fujita T, Hirota Y, Lydon J, DeMayo F, Maxson R, & Dey SK (2011). Conditional deletion of Msx homeobox genes in the uterus inhibits blastocyst implantation by altering uterine receptivity. Developmental cell, 21 (6), 1014-25 PMID: 22100262
Finn CA, & Hinchliffe JR (1964). Reaction of the Mouse Uterus during Implantation and Deciduoma Formation as Demonstrated by Changes in the Distribution of Alkaline Phosphatase Journal of reproduction and fertility, 8, 331-338 PMID: 14248593
Finn CA, & McLaren A (1967). A study of the early stages of implantation in mice Journal of Reproduction and Fertility, 13, 259-267 : 10.1530/jrf.0.0130259
Joswig A, Gabriel HD, Kibschull M, & Winterhager E (2003). Apoptosis in uterine epithelium and decidua in response to implantation: evidence for two different pathways. Reproductive biology and endocrinology, 1 PMID: 12801416
Krehbiel RH (1937). Cytological Studies of the Decidual Reaction in the Rat during Early Pregnancy and in the Production of Deciduomata Physiological Zoology, 10, 212-234
Li Y, Sun X, & Dey SK (2015). Entosis allows timely elimination of the luminal epithelial barrier for embryo implantation. Cell reports, 11 (3), 358-365 PMID: 25865893
Parr EL, Tung HN, & Parr MB (1987). Apoptosis as the mode of uterine epithelial cell death during embryo implantation in mice and rats. Biology of reproduction, 36 (1), 211-225 PMID: 3567276
Sun X, Zhang L, Xie H, Wan H, Magella B, Whitsett JA, & Dey SK (2012). Kruppel-like factor 5 (KLF5) is critical for conferring uterine receptivity to implantation. Proceedings of the National Academy of Sciences of the United States of America, 109 (4), 1145-1150 PMID: 22233806
Wang H, & Dey SK (2006). Roadmap to embryo implantation: clues from mouse models. Nature reviews. Genetics, 7 (3), 185-199 PMID: 16485018
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Posted by alexandraspencer, on 1 September 2015
Biology Week showcases the important and amazing world of the biosciences, getting everyone from children to professional biologists involved in fun and interesting life science activities.
Biology Week 2015 will run from Saturday 10th – Sunday 18th October. Get involved with the biggest week in the biology calendar by organising your own event, finding out what’s happening in your local area, or sharing and following #BiologyWeek.
Biology Week 2014 was a huge success with over 100 events taking place nationwide from 11th – 18th October. Take a look at Biology Week 2014 highlights on Facebook, Storify, or by reading our blog.
It was great week of biological activities with our own annual awards ceremony, malaria eradication debate and the launch of the Starling Murmuration Survey. We also produced resources for schools which teachers can use all year round.
Other events included bug hunts, competitions, dinosaur digs, online experiments, and lectures, organised by our members, member organisations, schools, and individuals – anyone can get involved!
We hope that you will run your own event for Biology Week 2015. This could be anything from a Big Biology Day science festival to a Biology Week quiz with some friends. Please contact us if you would like to discuss any Biology Week ideas.
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Posted by Seema Grewal, on 1 September 2015
Here are the highlights from the current issue of Development:
Formation of the blood vessels involves complex endothelial morphogenesis, including directional cell migration and lumen formation. Understanding the cell biological processes underlying vessel formation in vivo requires the ability to analyse the behaviour of single cells at high spatiotemporal resolution within developing tissues, which has been challenging. Taking advantage of the genetic tools and optical clarity of zebrafish embryos, Brant Weinstein and colleagues (p.2951) develop a robust method to label both the nuclei and membranes of individual endothelial cells (ECs) and monitor their behaviour using two-photon imaging. Using these tools, they first investigate the cellular basis of the plexin D1knockdown phenotype. Their data suggest that the defective migration of ECs in plexin D1morphants can be attributed to differences in the protrusive activity of wild-type versus morphant ECs. In a second set of experiments, the authors show that lumens form both within and between ECs, suggesting that multiple mechanisms contribute to tubulogenesis in this system. In addition to providing insights into the cellular basis of vessel formation, this work presents a set of tools that should be valuable to the community for future analyses.
It is known that adult neural stem cells are found in a hypoxic environment and are sensitive to oxygen tension. However, whether oxygen tension also regulates neural progenitor behaviour during development has been unclear. Now (p. 2904), Alexander Storch and co-workers investigate the effects of maternal hypoxia or hyperoxia on cortical development in mice. They find that exposure of pregnant mothers to different atmospheric oxygen tensions causes changes in foetal brain oxygenation, and that this has consequences on overall brain volume: hypoxic embryos have smaller brains, whereas hyperoxia causes increased brain size. At the cellular level, the hypoxic foetal cortex shows reduced proliferation of progenitors and increased apoptosis. By contrast, hyperoxia induces the accumulation of a population of proliferative progenitor cells in regions of the cortex more basal to the main zones of proliferation. These cells, similar to the outer subventricular zone progenitors that are normally rare in rodents but more common in primates, apparently contribute to increased corticogenesis. Although the mechanisms by which oxygen signalling regulates cortical development remain unknown, these intriguing results point to an important role for oxygen tension during foetal neurogenesis.
The zebrafish caudal fin is a powerful model for understanding the cellular and molecular processes underlying regeneration. Following amputation, a proliferative blastema forms, from which all the tissues of the fin regrow. Many aspects of this regenerative process are still poorly understood. For example, what is the source of the various lineages, how do these diverse cell types differentiate in appropriate proportions, and how is their spatial patterning controlled? In two related papers, Nicola Blum and Gerrit Begemann investigate the regeneration of the fin rays, uncovering crucial roles for retinoic acid (RA) signalling – which is known to be important for bone formation during development – at multiple steps of the process.
On p. 2894), the authors uncover a complex series of requirements for active or suppressed RA pathway activity in the bone lineage. RA is known to be synthesized in the blastema immediately following amputation, but the authors find that this inhibits dedifferentiation of osteoblasts to a proliferative preosteoblast state. Subsequently, RA signalling promotes proliferation of the preosteoblasts, then inhibits their differentiation, and is finally required for new bone matrix production. Given these apparently opposing roles for RA at different stages of ray regeneration, levels of the RA-synthesizing enzyme Aldh1a2 and the RA-degrading enzyme Cyp26b1 appear to be tightly regulated in the blastema, in both a spatial and temporal manner.
On p. 2888), Blum and Begemann analyse the role of RA signalling in the spatial control of ray regeneration, such that each ray is separated by an interray region. They find that Cyp26a1 (a paralogue of the blastema-expressed Cyp26b1 discussed above) is expressed in the basal epidermal layer overlying the osteoblasts but absent from the cells overlying the interray tissue. Thus, a low-RA environment exists in the epidermis around the regenerating ray. This permits expression of Sonic hedgehog (Shh), again specifically in the epidermis around the ray, which in turn promotes proliferation of osteoblasts. When this spatial restriction of RA is abolished – using Cyp26a1 inhibitors – osteoblasts spread into the interray regions and the patterning of the regenerating fin is disrupted. Together, these two studies reveal multiple roles for RA in ray regeneration, and highlight the complex signalling dynamics required to achieve efficient and precise regeneration.
Vascular smooth muscle is derived, in part, from the neural crest in a differentiation programme regulated by the Jagged1-Notch signalling pathway. However, there is also evidence that Hippo signalling regulates vascular smooth muscle development. Several studies have detailed mechanisms by which the Hippo and Notch pathways interact and, on p. 2962, Jonathan Epstein and colleagues identify a new level of cross-talk between these two pathways – via direct interaction between Yap (a Hippo pathway-regulated transcription factor) and the Notch intracellular domain (NICD). They first show in mice that deletion of Yap and the functionally related protein Taz in the neural crest leads to loss of crest-derived vascular smooth muscle; this phenotype is reminiscent of that caused by deletion of Rbp-J – the transcription factor downstream of Notch. They then provide evidence in cell culture models that Yap and NICD physically interact and co-occupy the enhancers of a subset of known Notch target genes, and that the Yap/NICD/Rbp-J complex is important for induction of vascular smooth muscle differentiation. Thus, as well as shedding light on how the vascular smooth muscle forms, this work provides insights into the mechanisms of signalling pathway cross-talk and its importance during development.
PLUS:
Didier Stainier is a Principal Investigator at the Max Planck Institute for Heart and Lung Research in Bad Nauheim, Germany. Having spent most of his career in the USA using zebrafish to study organ development, Didier recently moved back to Europe and is now branching out to study organ development in mice. At a recent conference, we caught up with Didier and asked him about his career, his thoughts on funding, view on morpholinos and his advice for young researchers. See the Spotlight on p. 2861
Neuromesodermal progenitors (NMps) contribute to both the elongating spinal cord and the adjacent paraxial mesoderm. It has been assumed that these cells arise as a result of anterior neural plate patterning. However, as the molecular mechanisms that specify NMps in vivo are uncovered, and as protocols for generating these bipotent cells from mouse and human pluripotent stem cells in vitro are established, the emerging data suggest that this view needs to be revised. See the Hypothesis by Storey et al on p. 2864
Polycomb and Trithorax group chromatin proteins play important roles promoting the stable and heritable repression and activation of gene expression, respectively. Here, Geisler and Paro review recent advances that have shed light on the mechanisms by which these two classes of proteins maintain epigenetic memory and allow dynamic switches in gene expression during development. See the Review on p. 2876
Our latest featured movie shows ocular morphogenesis in a zebrafish embryo. It is from a recent paper where Link and colleagues show that the transcriptional regulators Yap/Taz and Tead are necessary and sufficient for optic vesicle progenitors to adopt retinal pigmented epithelium identity. Read the paper here: http://bit.ly/1KJIPqP [OPEN ACCESS]
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Posted by the Node, on 1 September 2015
This interview first featured in Development.
Didier Stainier is a Principal Investigator at the Max Planck Institute for Heart and Lung Research in Bad Nauheim, Germany. Having spent most of his career in the USA using zebrafish to study organ development, Didier recently moved back to Europe and is now branching out to study organ development in mice. At a recent conference, we caught up with Didier and asked him about his career, his thoughts on funding, view on morpholinos and his advice for young researchers.
What first got you interested in developmental biology and was there anyone in particular who inspired you?
When I was young, my mother worked in the Zoology Department at the University of Liège, Belgium, and when she was busy at work we would often go to the department museum. So I spent a lot of time there. At that time, my dad was also working in a lab – he trained in the Pharmacy Department where his father was a professor. Most of my extended family was actually in the medical field, practicing as doctors or pharmacists, so science was a major part of my environment growing up. Then, when I was 15, I moved to the UK, actually to Wales. I studied at the United World College of the Atlantic, and there I had a very inspiring biology professor called Alan Hall. He was a somewhat quirky, Cambridge-educated fellow who was a most enthusiastic and committed teacher. I then went back to Liège for university, but essentially this was not very satisfying as the biology textbooks we were using there were older than those I had used in high school in Wales. I also wanted to start doing research during my undergraduate studies and in Belgium, at the time, this wasn’t possible until the masters level. So, I transferred to the USA. There I worked in an immunology lab at Brandeis University and took a developmental neurobiology course with Eve Marder, who was my academic advisor. From there, I moved to Harvard for my graduate studies, where Doug Melton had recently arrived. I did several lab rotations – my first was actually with Doug – and eventually joined Wally Gilbert’s lab to work in developmental neurobiology.
How, why and when did you start working with zebrafish?
When I joined his lab, Wally had just come back to Harvard from Biogen and was starting some new projects. His lab was very eclectic: there was the sequencing technology subgroup, the origin of introns subgroup and the immunology subgroup. As you might imagine, Wally was a very inspiring person – he’s probably the person who shaped me the most scientifically. One of the projects that he wanted to start was to look for cell surface molecules involved in axon guidance and target recognition in the developing mouse brain, and I thought that this would be a very interesting project to take on. A couple of years later, a psychiatry fellow came to the lab and set up the zebrafish model with the goal of developing insertional mutagenesis techniques. Although I did not work with fish in Wally’s lab, I was of course exposed to them and so they were very much on my mind when I was looking for a post-doc position in 1989. One of the people I applied to work with was Mark Fishman, who’d just received a large chunk of money to set up a cardiovascular research centre at Massachusetts General Hospital, Boston. We discussed the possibility of doing some zebrafish work and, shortly thereafter, he asked me to get a zebrafish heart project off the ground and then put some major resources into it. He also recruited Wolfgang Driever as a junior faculty member to the centre; Wolfgang had recently finished his PhD with Jani (Christiane) Nüsslein-Volhard, in Tübingen, Germany, and so had also been exposed to zebrafish. Wolfgang first went to Eugene, Oregon, for several months to train with Monte Westerfield, Chuck Kimmel and Judith Eisen, and during that time Mike Pack and I got started with a few tanks on a bench. Wolfgang then came back from Eugene to start his own lab, we moved to a new building and set up the first fish room, and things really took off from there.
How did the big zebrafish screen, which was published as a Special Issue of Development in 1996, come about?
Well, many of us wanted to do genetic screens; one of the reasons Mark and I wanted to work with zebrafish was to be able to carry out a screen for heart mutants, and Wolfgang, of course, also wanted to do screens. Thus, there was some prior arrangement to decide who would ultimately focus on specific developmental processes and follow up on the mutants relevant to these processes, but it really was a team effort. There were many interesting characters in the team, several of whom have become very prominent in the field. We certainly learnt a lot from each other and it was a very productive period. The large screen taking place in parallel in Jani’s lab at the time also added to the excitement, and it was Jani who suggested and coordinated the Development Zebrafish Special Issue. The Special Issue was a great opportunity to present our work, although much of the writing was done without me – at that time, communication was not as easy as it is now – as I had left to set up my own lab at UCSF in 1995. One also has to remember all the pioneering work done in Eugene, as it played a major role in attracting people into the zebrafish field. In addition, many people, including myself, spent time in Eugene learning how to work with zebrafish.
Recent advances in genome engineering have raised lots of debate about the use of morpholinos – in both zebrafish and other model organisms – with regards to how and when they should be used and whether they’re actually reliable. I know you have commented on this in a few recent publications (Schulte-Merker and Stainier, 2014; Stainier et al., 2015; Rossi et al., 2015), but what are your thoughts on this now?
My thoughts, which I believe are shared by many others in the field, are that we need to keep an open mind as key data keep being generated. Taking extreme views one way or another is not good for the field. There are of course many potential reasons why antisense technology can lead to artefacts, and people need to be careful and aware of the various caveats of the tools they’re using. I try to see opportunities when others may see downsides and, if some of the observations that we have made recently turn out to be widely applicable, they should open the door to some very compelling biology. There might indeed be some interesting and intriguing reasons for the discrepancies between mutant and morphant phenotypes as we have seen evidence of genetic compensation in mutants but not in morphants. Getting to the root of these discrepancies and understanding the mechanisms underlying compensation will not be easy, but it will certainly be a worthwhile endeavour. We will try to pursue these issues but, regardless, I think that morpholinos, much like siRNAs and other antisense tools, are reagents that can give you valuable information if used with appropriate care and scepticism. Understanding all the effects morpholinos are causing inside a cell is also an important goal that will provide further clarity on what is clearly a complex situation.
I gather that you’re now starting some mouse-based studies, again carrying out forward genetic screens to identify new players in developmental process. What was the motivation behind this?
When I was thinking about moving the lab from UCSF to Germany, we held a lab retreat and I asked the students and postdocs what projects or kind of work they would like to tackle, setting financial limitations aside. About half the scientists mentioned that they would like to do some mouse work. At the time we were mostly working on zebrafish; we had some collaborations with mouse people but we weren’t doing any mouse work ourselves. However, several scientists, some of whom had come from mouse labs, thought that they would like to complement their zebrafish studies with mouse studies, and there were others who were getting reviews of their papers with requests for mouse data. Mouse work was also something that I wanted to get back to, having been an extensive part of my PhD, and I wanted to get a deeper understanding of the work that was going on in other vertebrate development labs. There were many reasons to move from the USA to Germany, but when you move to an institution like the Max Planck, it gives you the opportunity to think about projects that you would not otherwise be able to do.
And so we thought about the various types of screens that we wanted to carry out and the phenotypes we should be looking for and, given that zebrafish don’t have lungs and that the Max Planck Institute we were moving to is a heart and lung institute, we decided to focus on the respiratory system. The goal of our screen is to look for cell differentiation phenotypes in the lung and trachea, and we are starting to see some very interesting phenotypes, including some that should represent informative disease models. Importantly, now that the activation energy to work on mouse has been lowered substantially, several people in the lab are pursuing their own projects using both fish and mice.
During that big move from the USA to Germany, did you notice any obvious differences in lab culture or in the funding situation between the two countries?
There are various ways of funding scientific research around the world. At one end of the spectrum, one goes to a university or research institute, they give you a little start-up money and then expect you to come up with grant money to fund everything else. At the other end of the spectrum would be a Max Planck Institute, where the Max Planck Society provides substantial core funding. It’s a real privilege to be working in a Max Planck Institute. I appreciate that there are advantages to writing research proposals and grants, because it forces one to think carefully through every step of the project, but after a while this mode of thinking becomes automatic before starting up any new project. In terms of lab culture, I think that we’ve been able to maintain the same kind of culture and set-up that we had in the USA: a physically wide-open lab to stimulate communication with a mostly flat hierarchy.
What is your advice to young researchers today?
I would like to tell young researchers to follow their dreams of course, but I also want to stress that they need to reach out to society and inform them about the value of basic science as well as the value of working with model systems, even very basic model systems. In the USA, and in other countries, the emphasis – and hence the funding – is increasingly being placed on translational research. This switch in focus is one of the reasons I moved from the USA to Germany: I felt that, in order to keep running a lab in the USA investigating several different topics, I would have had to move to more translational work. I had a hard time imagining myself not being able to pursue the kind of basic research required for innovative translational work. I’d like to think that the tide will turn and that there will be renewed appreciation of seeking knowledge for the sake of knowledge itself, for one never really knows when a basic science finding will transform translational research – the CRISPR/Cas9 technology is just one recent example of such a transformative finding arising from basic science. In this context, I really appreciate the value that the Max Planck Society places on basic science.
What would people be surprised to find out about you?
Well, I played quite a bit of rugby when I was young, first in Belgium, then of course in Wales, and then when I went back to Belgium. Actually, just before I moved to the USA, I played very briefly on the Belgian national junior team. I also played with the Harvard Business School team when I was a graduate student at Harvard. Moving to San Francisco to set up my lab, and starting a family at the same time, brought an end to this hobby.
References:
Rossi, A., Kontarakis, Z., Gerri, C., Nolte, H., Hölper, S., Krüger, M. and Stainier, D. Y. (2015). Genetic compensation induced by deleterious mutations but not gene knockdowns. Nature 524, 230–233.doi:10.1038/nature14580
Schulte-Merker, S. and Stainier, D. Y. R. (2014). Out with the old, in with the new: reassessing morpholino knockdowns in light of genome editing technology. Development141, 3103–3104.doi:10.1242/dev.112003
Stainier, D. Y. R., Kontarakis, Z. and Rossi, A. (2015). Making sense of anti-sense data.Dev. Cell 12, 7–8.doi:10.1016/j.devcel.2014.12.012
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Posted by Katherine Brown, on 1 September 2015
At Development, we’re always thinking about how we can best serve our community, and striving to ensure that the journal is publishing the most important and relevant research for its readership. To help us going forwards, we’re now asking for your feedback with a community survey designed to gauge how well Development represents and serves the modern developmental biology community. Do our papers reflect the cutting edge of the field? What do you think about the recent expansion of our stem cell content? This is your chance to tell us what you think about the journal, and to help us shape the future of Development.
Please take the time to complete this survey – it shouldn’t take more than a few minutes to fill in, and your feedback is invaluable to us. Thanks for your help!
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Posted by the Node, on 1 September 2015
Our jobs page was very busy this month, with 15 new positions advertised! Here are some of the other highlights:
Discussion:
– What is the best way to encourage peer reviewing? Share your thoughts in the latest Question of the Month!
– In a piece originally published in the Journal of Cell Science, Martin Schwartz argued that learning how to separate self interest from the scientific process should be an important part of scientific training.
Resources:
– Do you want to teach school students about stem cells? João collaborated with an artist to create a comic book called ‘A stem cell adventure‘, that you can download for free. He wrote about the project for our outreach series.
– We collated a new list of societies, databases and other useful resources. Help us make this a comprehensive list!
– And here is some of the career and outreach advice shared at the recent SDB meeting.
Interviews:
– We reposted two interviews originally published in Development: An interview with Lewis Wolpert, winner of this year’s BSDB Waddington Medal, and an interview with plant developmental biologist Caroline Dean.
– And the interview chain continues, with an interview with SDB poster prize winner Valeria Yartseva.
Also on the Node:
– Mike Levin wrote about recent papers in his lab on long-range signaling via gap junctions.
– Allison and Tamara reported from the first meeting of the Pan American Evo Devo Society.
– and Héctor shared his experience visiting the Rivolta lab at the University of Sheffield, sponsored by a Development travelling fellowship.
Happy reading!
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Posted by Hector Galvez, on 31 August 2015
Thanks to the travelling fellowship, awarded by the Company of Biologists, I was fortunate enough to undertake a period of research in the laboratory of Prof. Marcelo N. Rivolta at The University of Sheffield, England.
I am a 3rd year PhD student in the Laboratory of Developmental Biology at the Universitat Pompeu Fabra in Barcelona. The laboratory researches into the development of the inner ear. The ear is the sensory organ responsible for hearing and balance, and consists of two main cell types which form the sensory epithelia of the inner ear: neurons and hair cells. Our laboratory is particularly interested in the molecular generation of inner ear hair cells, which are responsible for transducing sound waves into neural activity.
Hearing is important for daily interaction with others and the surrounding environment. Loss of hearing can have large social and emotional implications on health and well-being. According to the World Health Organisation (WHO) 360 million people worldwide have hearing loss, which is commonly the result of damage to the inner ear hair cells (HCs). Mammals have lost the potential to regenerate hair cells and neurons and therefore cannot repair damage in the inner ear. Therefore our research is of particular importance, in order to develop techniques which will allow for inner ear hair cell replacement. In recent years, stem cells have appeared as a potential therapeutic solution, at least in the case of neurons. The laboratory of Prof. Marcelo N. Rivolta at The University of Sheffield is a centre of excellence in stem cell research. The group are specialists in the isolation of otic like progenitor cells form human embryonic stem cells. Their main goal is to develop stem cell therapies that can be used to cure deafness. Therefore it was in the best interest of both laboratories to establish a collaborative project in order to learn from each other’s expertise.
My experience in the lab was ineffable; working with the otic progenitors was not easy during the early stages of my project, but with the help and support of the group it became significantly easier overtime. Protocols for otic cells isolation are very stringent and require a high level of dexterity, precision and patience.
People in the lab were very kind and the working environment was warm and welcoming. I had the fortune of accompanying the laboratory on a team day to Warwick Castle. As well as getting to know the people in the lab, I also had the opportunity of exploring South Yorkshire. I visited the Peak District, the first national park in Great Britain. It is one of the most beautiful landscapes I have laid eyes upon, blanketed in luscious greenery and framed (on a good day) by clear blue skies. There you can find marvellous scenery and nature, a perfect place for a runner like myself. The thick Yorkshire accent, continuous rain, and cold weather made my native Barcelona seem a world away. I did, however, succumb to the charm of the North in the end!
In summary, my fellowship has given to me the opportunity to experience research and life overseas. I have learned a lot about stem cells, which I know will help me in my career as a scientist. I would like to encourage other young scientists to take the opportunity to travel if they are fortunate enough to be given such an opportunity, since intercultural understanding is as important as scientific understanding when working in collaboration with overseas scientists.
In conclusion, I would like to give thanks to The University of Sheffield for facilitating my research, to Professor Fernando Giraldez for his continuous support and supervision and to Prof. Marcelo Rivolta, for his continuous supervision, guidance and patience. Finally, I would like to thank the Company of Biologists for granting me the fellowship.
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Posted by Peng Huang, on 29 August 2015
Closing Date: 15 March 2021
The Department of Biochemistry and Molecular Biology at the University of Calgary, Canada is accepting applications for an Eyes High Post-doctoral Scholar position in the laboratory of Dr. Peng Huang. The position is funded by the University’s Eyes High rising stars strategy, which targets candidates of the highest caliber with track record that would be competitive for national or international fellowships. This 2 year postdoc fellowship commences in late 2015/early 2016 and includes a stipend of $50,000/year, plus health benefits.
We use zebrafish as a genetic model to understand human muscle diseases such as muscular dystrophy. Using a combination of reverse genetic tools, transgenesis, in vivo imaging, and small molecule screens, we study how muscle integrity is maintained. In particular, we investigate how cell signaling pathways and cell-cell interactions regulate muscle maintenance. The goal is to identify new cells and novel molecules modulating muscular dystrophy. For more information about the lab, please visit: http://people.ucalgary.ca/~huangp/index.html
We are looking for a highly motivated individual who shares our passion for science and would like to work in a friendly and collaborative environment. The candidate should have a PhD in Developmental Genetics or a related discipline, excellent molecular biology skills, and a strong interest in developmental biology. Previous experience with the zebrafish and imaging techniques is preferred but not required. Excellent written and verbal communication skills are critical. The candidate must have a track record of academic success as evidenced by peer-reviewed publications, awards and scholarships.
The call for applicants will be open until November 30, 2015. To apply, please send a cover letter with statement of research experience and interests, and CV with names of three references to Peng Huang, peng.huang@gmail.com, with the subject line “Eyes High Postdoctoral Scholar Position”.
About the University of Calgary
The University of Calgary is a leading Canadian university located in the nation’s most enterprising city. The university has a clear strategic direction to become one of Canada’s top five research universities by 2016, where innovative teaching and groundbreaking research go hand in hand, and where we fully engage the communities we both serve and lead. The strategy is called Eyes High, inspired by our Gaelic motto, which translates to ‘I will lift up my eyes.’ To succeed as one of Canada’s top universities, where new ideas are created, tested and applied through first-class teaching and research, the University of Calgary needs more of the best minds in our classrooms and labs. We’re increasing our scholarly capacity by investing in people who want to change the world, bringing the best and brightest to Calgary to form a global intellectual hub and achieve advances that matter to everyone.
About Calgary
Named a cultural capital of Canada and one of the best places to live in the world, Calgary is a city of leaders – in business, community, philanthropy and volunteerism. Calgarians benefit from the strongest economy in the nation and enjoy more days of sunshine per year than any other major Canadian city. Calgary is less than an hour’s drive from the majestic Rocky Mountains and boasts the most extensive urban pathway and bikeway network in North America.
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