Postdoc (f/m/d) – Comparative genomics in planarians –
(Code number 11-20)
Planarians are fascinating animals that can regenerate from tiny pieces, harbor adult pluripotent stem cells, scale their bodies over a wide size range and, as a taxonomic group, display a fascinating spectrum of regenerative abilities, body sizes, reproductive strategies or life expectancies from a few months to seeming immortality. In collaboration with Gene Myers, our group has pioneered planarian high-quality genome assemblies and we have established a large and phenotypically diverse species collection through world-wide field expeditions. Comparative genome mining now promises access to a wealth of intriguing research questions. Current project opportunities include probing of the genomic consequences of asexuality by means of comparisons between the sexually and asexually reproducing strains of S.mediterranea; body size evolution in the giant planarians of Lake Baikal or genomic adaptations to life in the lake’s abyssal zone (~ 1600 m depth); intra-organismal population genomics amongst the many independently replicating pluripotent stem cells or the dynamics and functional relevance of the new class of giant planarian retroelements that we discovered. We have a number of fully funded postdoc positions available for talented individuals to pursue these or other questions.
Your Profile
You have a PhD or equivalent degree in a relevant subject area, e.g., biology, computational biology or computer science and extensive hands-on experience with genomic data.
You have a proven track record in one or more of the following: genome assembly, multi-genome alignments; comparative genomics; structural genome variance; transposon mobility; cancer or evolutionary genomics; phylogenetics and or population genomics.
You are passionate about the scientific endeavor and you are not afraid of pursuing your questions beyond the current scientific frontier.
You are self-motivated and independent and enjoy being part of an international and interdisciplinary work environment.
About us
We are a brand-new department at the Max Planck Institute for Biophysical Chemistry in the historic science town of Goettingen. We represent the organismal end of biophysical chemistry at the institute and investigate the mechanistic and evolutionary underpinnings of planarian regeneration. The department hosts a large zoo of planarian species for comparative analyses and we just established a field station at Lake Baikal in Russia, the Galapagos of planarian biodiversity. We are a thoroughly international and interdisciplinary group of people and based at one of Germany’s premier research campuses. We enjoy generous funding by the Max Planck Society and the proximity to picturesque Goettingen with its bustling student bars.
The Position
The payment and benefits are based on the TVöD guidelines. The Postdoc position are limited to two years with a possibility of extension.
The Max Planck Society is committed to increasing the number of individuals with disabilities in its workforce and therefore encourages applications from such qualified individuals.
Interested? Submit your application including cover letter (explaining background and motivation), CV, transcripts, and publication record preferably via e-mail as one single PDF file to
TB: The joy of seeing an article finally published is always slightly tempered by the long-drawn out process of peer review, re-writing, re-submission, re-review, proof-reading, required to get to that point. But the publication of our article ‘Auxin export from proximal fruit drives arrest in temporally competent inflorescences’ represented the end of a much longer journey. And to be honest, even a third round of peer review didn’t diminish the joy in fulfilling a long held personal ambition. Here, we look back at some of the key moments in the making of this paper.
2003: Inspiration
TB: I don’t know when exactly I first read ‘The fate of inflorescence meristem is controlled by developing fruit in Arabidopsis‘ by Linda Hensel and the late Tony Bleecker. Even 2003 is something of a deduction. What I do remember is that it was one of a bundle of articles photocopied out of the physical journal (those were the days!), and given to me early in my PhD by Jon Booker, one of the post-docs in Ottoline Leyser’s lab. And I remember being immediately struck by the paper upon first reading it. For the uninitiated, Hensel et al (1994) is an absolute masterpiece of experimental plant science, a combination of meticulous observation, meticulous experimentation and nuanced interpretation. It is a bona fide ‘classic’.
Hensel et al focuses on an important but somewhat overlooked developmental phase, namely ‘end-of-flowering’. Flowering itself is the reproductive phase in the most abundant group of land plants, the angiosperms (or ‘flowering plants’). Flowering occurs by the production of specialised shoots (inflorescences), which generate flowers. Each flower typically has male and female organs (staemen and carpels) that produce gametes (pollen and ovules respectively). Pollination of ovules leads to the formation of seeds containing embryos, and conversion of the carpels into a fruit that holds the seeds. Given that the majority of the world’s food supply is derived from the seeds and fruits produced by flowering, it’s a pretty important process. For the plants themselves, it is critical that flowering begins at the right time of year, but also that it ends at the correct time. While we know a lot about the developmental mechanisms that control the start of flowering, we know much less about those that control end-of-flowering.
In looking at end-of-flowering, Hensel et al chose to work on what was rapidly becoming the dominant plant model species, the small, short-lived weed Arabidopsis thaliana (or just ‘Arabidopsis’). Arabidopsis reproduction occurs in a single coherent burst, elaborated through a branching inflorescence system. What Hensel et al found was that Arabidopsis flowering seemed to end by the simultaneous developmental arrest of all inflorescences on the plant, in a ‘global proliferative arrest’ (GPA) event (Figure 1). They then showed that this arrest required the presence of fertile fruit, and that removal of fruit could delay arrest, or even re-start flowering if arrest had already happened. Further, they demonstrated that it was very specifically the seed inside the fruit that really seems to drive arrest. Ultimately, they proposed a model in which the cumulative build-up of a fruit-derived signal triggers the simultaneous arrest. I thought this was a stunningly elegant mechanism for coordinating development across the whole plant body, and I knew there and then that I wanted to work on this problem, although not right there and then…this was something I was going to save for the future.
Figure 1: Global proliferative arrest. A wild-type Arabidopsis plant undergoing ‘global proliferative arrest’…except look more closely and it isn’t…
12th March 2016: Inception
TB: As it turned out, the future was a long time in coming. Originally, I’d thought about this as something to work on towards the end of my PhD, but other tasks took precedence. And then I moved away to post-doc on somewhat different areas of plant development; I never forgot about GPA, but for a long while it was mostly at the back of my mind. Luckily for me, everyone else seemed to forget about GPA for quite a while. There was no follow up from Hensel et al, and no one else picked up the baton in the meantime. Thus, when I finally picked the idea back up in earnest in late 2015, we knew little more about GPA than we had done back in 2003. At the time, I was in the process of applying for academic positions, and GPA was clearly something that I was going to work on when I started my own group. In February 2016, I accepted a position at the University of Leeds to start later that year, and shortly thereafter, I set up my first GPA experiment (the imaginatively titled ‘GPA1’). When I started, I never really doubted that the phenomenon was already defined, and what I was looking for was just the mechanism. But GPA1 didn’t quite go as expected; yes, the plants arrested as expected, but I kept watering the plants just to see what would happen. To my surprise, the plants initiated new inflorescences and started flowering again (Figure 2). Clearly, this wasn’t going to be quite so straightforward as I’d thought…
Figure 2: When is arrest not arrest? “Plant 1” completely misunderstands what it is supposed to do during GPA.
20th January 2017: Proclamation
TB: As the ’new boy’ at Leeds, I was asked to give the ‘keynote’ talk at our annual Centre for Plant Sciences symposium, shortly after I started there. I’d never talked about my plans to work on GPA before, but I decided that’s what I was going to talk about, I think mainly because I was excited by the prospect of getting ‘stuck in’ to the project. I had very little actual data to present, but I pitched the talk on the importance of the phenomenon, and talked mostly about the theoretical background. I wasn’t sure how well it would go down, but as it turned out, it was something of a masterstroke…
CW: I had no idea who Tom was at the start of the symposium (other than the tall man who I occasionally passed in the corridors at work), but by the end of his talk, I had basically decided that I also wanted to contribute to understanding GPA. Tom had outlined some of what he planned to do, but I was particularly interested in the fact that he pointed out it could be relevant in crop species such as oilseed rape – I had an agricultural background, and wanted to do more work with crops. At this stage I had no interest in working with Arabidopsis, and figured I could provide some crop knowledge and avoid Arabidopsis. I wasn’t working for Tom at the time, so I figured any research I did contribute, I would just do in oilseed. Funnily enough, that’s not how things ended up working out.
5th June 2017: Recruitment
CW: Not only did I end up working for Tom, I also ended up spending the majority of my time working on Arabidopsis. With hindsight, my naivety about Arabidopsis was key to me completely buying into the end of flowering being a fascinating process. Very early on, I was carrying out an experiment where I was going to treat plants at floral arrest. During a routine check of the plants, Tom asked why I hadn’t carried out the treatments yet. I was confused by this – clearly the plants hadn’t finished flowering. Tom indicated that the primary inflorescences had all arrested – I countered that many of the lower inflorescences were still vigorously flowering. At this stage, we began really questioning GPA as a concept. If floral arrest was synchronous, how could these plants have some inflorescences that had arrested, and others which were still flowering several days later? The next step was to closely examine the flowering lifetimes of every individual inflorescence of a set of plants, where we clearly showed that floral arrest isn’t synchronous, it follows a basipetal wave, with the upmost inflorescences on the plant arresting first, followed by each inflorescence below it in turn. Each inflorescence class (primary, secondary, tertiary etc) also displayed a characteristic lifetime, where the timing of arrest appeared to be controlled specifically by the time since that inflorescence had initiated. I was hooked on the project from this point on; I needed to know how this was controlled!
1st November 2017: Nottingham
TB: Back in May 2016, a paper on GPA had been published in Plant Physiology, suddenly breaking the radio silence on the subject after 22 years (and giving me that terrible sinking feeling, until I realised that their approach was very different to what I was planning). So I was very much aware that interest in the area was starting to emerge again, but I had very little idea who else might be working on GPA. As it would turn out, at least two other research groups had also recently developed interests in GPA – Cristina Ferrandiz’s group in Valencia, and Zoe Wilson’s group in Nottingham.
It was therefore very serendipitous that my first seminar as a group leader on the ‘academic circuit’ was in Nottingham. I think it came as a surprise to Al Ware (the PhD student working on the project) and Zoe that there was someone else working on GPA, just as it came as surprise to me that my audience was really interested in what I had to say on that subject! Happily, we sat down to talk some more GPA after my seminar, and it rapidly became clear that our data and approaches were completely complementary. We agreed to collaborate there and then, and over the next few months, began to sketch out a plan for a manuscript that combined our data. Collaborating with Al and Zoe has been thoroughly enjoyable, and of massive benefit to both groups, so it really was a genuine stroke of luck to meet them so early in the project!
June 2018: Broken
CW: This was an ‘interesting’ period in the development of the GPA research. In each experiment we set up, we were convinced that – this time – we knew what the outcome would be, but each time the results were completely different to what we had expected (Figure 3) and led to multiple new hypotheses and experiments.
Figure 3: Wrong, wrong again. Our hypothesis for GPA27 turns out to be exactly wrong…
Ultimately, this resulted in GPA 27 (we’d come a long way from GPA 3 when I started a year ago) – simultaneously one of my favourite and most-hated experiments to date. The plan was to remove all open flowers from plants daily; I think at this stage we were expecting the plants to arrest at a ‘normal’ time – we were wrong. Not only was floral arrest delayed, but with no fruit production, the plants kept producing more branches, meaning flower production was becoming exponential. What had started out as half an hour each morning removing flowers became the majority of every day pulling flowers off increasingly more gnarled, brittle Arabidopsis (Figure 4). It wasn’t quite as fun as it sounds. I was doggedly insistent that I was going to see this experiment to a close, but was away at a conference for three days, so asked Tom if he’d look after the plants while I was gone – it was only a few days, what could possibly go wrong?
Figure 4: We did this experiment so that you never have to. What happens when you pull every opened flower off an Arabidopsis plant for 5 weeks…
By the second day, Tom had emailed me to tell me that it was probably a good idea to halve the number of plants we were treating; we didn’t need as many as we had, and he’d leave the rest as a ‘recovery’ treatment (traitor). Funnily enough, my horror at this suggestion wasn’t enough to change Tom’s mind, and I returned to the lab to find that the ‘recovery’ plants had produced fruit and…arrested. The treated plants were still flowering on, but the recovery plants had happily arrested and stopped flowering, despite only producing a few fruits per inflorescence. I began to forgive Tom for the ‘recovery’ treatment, and we started questioning how many fruit were actually needed for arrest. Hensel et al. had suggested around 40% seed set was required for arrest, but hadn’t specified whether this was per fruit, per inflorescence… We’d removed hundreds of flowers from these plants, so clearly they hadn’t produced that much seed in the few days of the recovery treatment. We began to question whether it was the position of the fruit, rather than the number, that was crucial to arrest.
After GPA 27 finally finished, I ‘decided’ to take a few weeks of holiday to recover, and swore never to repeat another flower removal experiment. Obviously, when I came back, I’d forgotten the trauma of GPA 27, and carried out another flower removal experiment, only this time we focussed on individual inflorescences. Only a few inflorescences per plant had flowers removed, while the rest of the plant remained untreated. Pleasingly, I found that only the treated inflorescences had a delayed arrest – the rest of the plant arrested when we would expect. Not only had we shown that floral arrest wasn’t synchronous, now we’d also shown that it wasn’t global – it was local, and it was dependent on a small number of fruit.
7th February 2019: Submission
TB: By the end of 2018, we’d managed to collect all the data we needed for the planned manuscript, and we spent the first month of 2019 putting the manuscript together. We’d always planned to submit to Nature Plants; I’d been given some encouragement by one of the editors (Guillaume Tena) at a conference the previous summer, and I felt like our story was of sufficient general interest. Nevertheless, it’s always a tense wait to hear if the journal is going to send the manuscript for review. And often you don’t actually here anything from the journal at all until the reviews land in your inbox. Fortunately, Guillaume let me know fairly quickly that the manuscript was going out for review, making the whole process that bit less stressful!
Summer 2019: Redux
TB: The reviews — all four of them — came back at the start of April. Two of them were very positive, while the other two were positive, but had some serious reservations, particularly with respect to our divergences from the GPA model. But I have to say that, the comments were all very fair, and ultimately very helpful. Overall, this was by far the best experience I’ve had of peer review; I really feel like the reviewers helped us make a better and more coherent paper. We got straight to work on trying to provide new data to address the comments.
CW: Following the reviewers’ comments, we set up several key experiments to really focus in on the numeric and positional fruit requirement for arrest. My primary focus for the paper at this stage involved removing fruits at different timings prior to arrest, and allowing recovery periods to see under what conditions arrest occurred. Through this, we showed that only a small number of fruit are required to bring about arrest – and that the closer they are to the meristem, the faster the arrest; whereas a large number of fruit far from the meristem will not bring about arrest at all.
Interestingly, I accidentally further refined the number of fruit required for arrest while working on a totally different area of my PhD. I was looking at whether removing increasing numbers of flowers along an inflorescence (every other flower, 2 out of every 3, etc.), increased the final size of fruits. It didn’t. But nor did it really affect arrest either. If I removed 4 in every 5 flowers, the inflorescences arrested only a couple of days later than untreated inflorescences, despite only having 20% of the fruit. I particularly love that this experiment, which had a completely different purpose, ended up helping us to answer a different question we were working on. It’s so satisfying to see different areas and ideas link up in unexpected ways, but I hadn’t really experienced that in my own research before this time.
4th April 2020: Acceptance
TB: We finished re-writing the paper just in time for Christmas, and re-submitted on 17th December. I was pretty confident we’d addressed the reviewers comments, but after a second round of peer review (17th February), there were one or two new issues to address, though it was pretty clear publication was going to happen, as long as we addressed those issues. Fortunately, we already had the data, so we resubmitted within a week, and went back out for a final round of review. Then, finally, on 4th April, we received the good news…
CW: Looking back over the lifetime of this project, it’s incredibly satisfying to see how things have progressed so much – not just the research, which I’ve loved, but also generally how our approach and understanding developed as a whole. The first summer I was in the lab was very much a case of trying to get to grips with a new concept and species. The second summer was incredibly productive, but also very draining, both physically and mentally. We got great data out of that time, but it did come at a cost (although I did learn that 30+ consecutive days in the lab really is my limit). By the summer of 2019, we really knew what we were doing. Granted, we still found answers in accidental ways, but our whole approach was much smoother and more refined. Having the manuscript accepted really provides a satisfying point of perspective over how things have developed in the last few years. Now we’re on to the next exciting thing, and I can’t wait to find the answer. It won’t even involve any flower removal. Probably.
Of the many virtual seminar series that have sprung up in response to the COVID-19 pandemic, one in particular caught our eye – the New PIs in Cell and Developmental Biology Forum (you can follow updates and find information by following #NewPICellDev on Twitter). To find out more about the series we met Salah Elias, new PI at the University of Southampton and organiser of the forum (you can read Salah’s bio at the end of the interview).
How did you come to run your own lab and what are your main research questions?
My move to the University of Southampton in 2017 and appointment to a lectureship enabled me to start my own independent laboratory building on my postdoctoral research. This has involved bringing together expertise from cell biology, physics and mathematics to investigate new microtubule- and actin-mediated mechanisms of oriented cell divisions (OCDs) in the normal mammary epithelium, and determine how this influences stem cell fate and dynamics during development and homeostasis. OCDs represent an essential mechanism during development that ensure proper epithelial integrity and differentiation in several epithelial systems. Yet their functional requirement for mammary epithelial biology remains subject to deliberation. This is a fundamental and important question for my lab, particularly in the mammary gland where tissue turnover is very high. Moreover, given increasing evidence linking dysregulation is OCDs to breast cancer, my lab aims to understand how imbalance in OCDs can lead to the abnormal cell fate and behaviour that contributes to the initiating events of malignant transformation. Our multidisciplinary approach has allowed us to develop a set of cutting-edge tools and novel ideas that open up new research directions and help us establish our own niche.
How has your research been affected by the lock down?
The COVID-19 pandemic has caused unprecedented disruptions within the entire research community. It has also exacerbated existing inequalities, with new PIs representing one of the most affected groups. As a new PI, closing my lab, which I have managed to get up and running after a challenging and time-consuming process, was heart-breaking. After I joined the University of Southampton, I have been able to secure major grants, hire talented PhD students and postdocs and develop excellent collaborations. We have started to work on our ideas and get exciting findings, which we were looking forward to sharing this year at conferences. The pandemic reminded me how vulnerable and precarious my position as a new PI was. In few days we have had to cull several experimental mouse cohorts which we have been preparing several months in advance and thrown away many long-term in vivo imaging experiments which have taken months to prepare. We stopped all our research within a week. Suddenly, I also found myself with childcare responsibilities, which I couldn’t share with my wife who is a key NHS worker. This has considerablydisrupted my productivity and challenged my ability to run my lab. All this would delay time to publish my lab first independent publications, putting at risk the competitiveness and sustainability of my research program.
How did the idea for a young PI forum in cell and developmental biology come up?
One of the immediate consequences of the lockdown was the cancellation of conferences. For my lab, this has taken away many opportunities to showcase and discuss our research. We know how conferences are important particularly for new PIs, by offering excellent networking and career development opportunities. They are also the place where we can make the scientific community aware of our accomplishments and thereby build a reputation that is important for our careers. For me, working from home has also been very isolating and challenging mentally. Many peers around the world have shared their frustrations and struggles through social-media platforms such as Twitter. It was great to see many established PIs relaying actively those concerns and urging the scientific community to protect new PIs during and after the pandemic. However, I thought that new PIs, as a community, could be proactive and help each other. This is how the idea for the New PIs in Cell-Dev-Biol Forum emerged. The forum would include e-seminars, but I also wanted it a platform that maintains connections and fosters peer support. I discussed the idea with Dr. Bethan LIoyd-Lewis, new PI at the University of Bristol, which she endorsed immediately. Then, everything went fast, the first colleagues we have contacted responded positively, and within a week we had our e-seminars with a fantastic fist line-up of speakers. We advertised on Twitter, it was really heartening to see how positively the scientific community has responded and helped us promote the forum. The e-seminars have started already with success.
How does the forum work?
The primary goal of the forum is to be a platform for peer support and collaboration, supported by an e-seminar series where talks are organized every two weeks. Our top priority, particularly during the lockdown, is to offer opportunities for new PIs to give and host talks. Speakers will be encouraged to present unpublished results to promote discussions and collaborations. We advertise through Twitter, where we post a link for each talk. We have also created a Slack (@NewPI_CellDev), which allows us to maintain connections, support each other and exchange ideas about the future of the forum. I am pleased to see how everyone is taking ownership of the forum, which I believe is the best way to maximize contributions and achieve our goals together.
If people are interested in giving a talk, what do they have to do?
Three weeks after its creation, 30 new PIs from 20 UK and European research institutions have joined the forum already. We have a full program of talks until May 2021. Everyone who joins the forum is invited to give and host a talk. As I mentioned above, priority will be given to preliminary results, so colleagues who have just opened their labs are also welcome to share their research, particularly if they are seeking help for their grant applications. Advertising the forum and talks on Twitter allows us to reach the wider scientific community. Generally, when we receive expression of interests from colleagues, we ask them to send us their contact details through direct messaging or e-mail, so we can add them to our mailing list and send them an official invite. Our members are doing a fantastic job in promoting the forum within their own networks and institutions. However, we are also aware that not all our colleagues have a Twitter account. We hope that societies such as the Company of Biologists will help us to be more visible to increase our membership.
Do you expect to keep the forum going when the lockdown ends, whenever that may be?
Our first successes reinforce our ambition to create an international forum for new cell and developmental biologists, which lasts beyond the lockdown. We are aware that the consequences of the COVID-19 pandemic will affect our research and careers for the next few years at least. The forum will offer opportunities for peer support, networking and collaboration, andl represent a powerful mechanism fostering long-term equal partnership with mutual benefits. The forum will also be rewarding on a personal level, and I am looking forward for some really great friendships.
Do you think COVID-19 will change the way scientists share their work with each other?
Unquestionably, the COVID-19 pandemic has brought new opportunities for science communication. It is amazing to witness how proactive and altruist the scientific community is, by turning big conferences virtual, and creating a variety of webinars and e-tutorials and open resources, in such a very short time. We have learned effective ways to make conferences more accessible and more ecologically friendly, while minimizing the costs. I am proud that our forum is taking part of this revolution in science communication. As a community, we need to continue in this vein to bring open science a step closer to reality.
Biography
Salah Elias studied cell biology and Physiology at Rouen University, France. He then did a PhD in neuroscience at INSERM U982, France, where he investigated the mechanisms of secretory vesicles biogenesis and trafficking in neuroendocrine cells, under the co-supervision of Prof Maite Montero-Hadjadje and Prof Youssef Anouar. During his first postdoctoral work in the lab of Dr. Sandrine Humbert at the Curie Institute, France, he showed that huntingtin and kinesin-1 regulate spindle orientation and apical polarity in mammary epithelial cells during development and homeostasis. He then moved to Prof Elizabeth Robertson lab at the Sir William Dunn School of Pathology, University of Oxford, where he identified a new subset of mammary stem cells, expressing Blimp1, that drive gland morphogenesis and homeostasis. In 2017, Salah was appointed Lecturer at the University of Southampton. His lab aims to understand the mechanisms of oriented cell division (OCD) in the normal mammary epithelium to discover cell division defects that are unique to breast cancer cells. Salah is the recipient of an MRC New Investigator Research Grant and Wellcome Trust Seed Award in Science.
Contact details:
School of Biological Sciences, University of Southampton, Highfield Campus, Southampton SO17 1BJ, United Kingdom
Highly motivated postdoctoral candidates are invited to lead several new projects to address fundamental questions on RNA homeostasis (Zhang et al. Molecular Cell 2018; Haeusler et al. Nature 2014) and protein homeostasis (Lu et al. Nature Neuroscience 2019; Liu et al. Genes & Development 2018; Periz et al. PLoS Biology 2015) related to neurodegenerative diseases in the laboratory of Jiou Wang. The position is open to candidates with a wide range of backgrounds including biochemistry, molecular biology, cell biology, and structural biology on all topics of biology. Those with experience in RNA biology, protein biochemistry, and bioinformatics are particularly encouraged to apply.
The Johns Hopkins Medical Institutions provide a stimulating and collaborative environment for biomedical research. Our lab is affiliated with the Department of Biochemistry and Molecular Biology at the Bloomberg School of Public Health and the Department of Neuroscience at the School of Medicine. The Baltimore/Washington D.C. area also offers rich professional and living opportunities.
Candidates should have a doctoral degree and strong research background. Please send a statement of research experience and career goals, a copy of Curriculum Vitae, and contact information of at least one reference to Dr. Jiou Wang at jiouw@jhmi.edu.
A complete listing of PubMed-accessible publications can be accessed at the following URL: http://www.ncbi.nlm.nih.gov/pubmed/?term=Jiou+Wang.
More information available at: http://www.jhu-bmb-phd.org/faculty/jiou-wang. The Johns Hopkins University is an Equal Opportunity Employer.
The ongoing pandemic has resulted in many scientific conferences moving to an online format, and researchers who can no longer attend seminars at their institutes have been organising and attending various virtual seminar series (here on The Node there are currently over 40 online events listed in developmental biology and beyond). Several considerations about virtual events have been brought up (see for example here and here), but a better understanding of participant experience is crucial to inform conference organisers on specific areas that could be improved in future virtual events.
A group of early-career researchers who contribute to preLights have designed a survey and are seeking responses from students, researchers, journal editors, or anyone who has attended a virtual scientific event.
Please take our anonymous survey and feel free to share it with your colleagues.
The survey will be open until 31 July 2020. The results of the survey will be shared on the preLights website.
Study of the molecular mechanism of Endothelial to Mesenchymal Transition during muscle regeneration and crosstalk with the immune system in vivo and in vitro.
A 3 year PhD studentship is available within the Heva Research Group, School of Medicine and Surgery, University of Milano Bicocca, Milan, Italy (https://hevaresearch.unimib.it/), under the supervision of Prof. Silvia Brunelli.
The position is the framework of the H2020 Marie Skłodowska-Curie ITN funded project RENOIR (REcreating the ideal Niche: environmental control Of cell Identity in Regenerating and diseased muscles, https://renoir-itn.eu/).
The PhD project (https://renoir-itn.eu/esr1/) focusses on how the inflammatory and vascular components integrate to coordinate muscle regeneration and how the process of Endothelial to Mesenchymal Transition (EndoMT) contributes to fibrosis in pathological conditions, using in vitro and in vivo models.
The student will be enrolled in the Ph.D. Programme in Translational and Molecular Medicine (DIMET), University of Milano Bicocca (www.dimet.org).
The animation is a result of collaborative work of scientists from the Novo Nordisk Foundation Center for Stem Cell Biology (DanStem) and visual storytellers from the Animation Workshop (VIA), telling the story of a scientific attempt to learn what happen to the liver when damaged and how this knowledge could be translated in the future and help healing liver diseases and improve patients quality of life.
One night, during the summer of 2012, I found myself sitting in a cottage in Woods Hole, trying to explain to my parents why I’d spent much of my professional life studying the little skate (Figure 1). I was a postdoctoral fellow at Dalhousie University at the time, and working almost exclusively with skate as a model system was hard: I could only access animals while visiting the Marine Biological Laboratory (Figure 2), and while I was fortunate enough to spend my summers in Woods Hole (thanks largely to generous support from the MBL Whitman Center Fellowships programme and the MBL Embryology Course), there were relatively few tools and resources available for the skate at that time, and limited access to animals meant that I was under a great deal of pressure to design, optimise and complete experiments during a relatively short time window each year. Why would anyone do this to themselves?!
Figure 1: A hatchling of the little skate (Leucoraja erinacea)
Up until that point, I’d worked exclusively on skate embryonic development. I explained to my parents that skates occupied a very important position in vertebrate evolutionary history, and that by studying skate embryos, and comparing our findings with what we know from work in mouse, chick, frog and zebrafish, we are able to make inferences about anatomical features (and developmental mechanisms) that were present in the last common ancestor of jawed vertebrates. That’s a perfectly good and valid reason for studying skate embryos, isn’t it? So why was I getting the “blank look” that many of us scientists know and dread? Could it be that aspiring to infer ancestral developmental mechanisms, while a perfectly good and reasonable academic endeavour, is not necessarily the most compelling reason for studying an obscure marine organism, in the eyes of a non-scientist? Like a stand-up comic squaring off against a heckler, I felt the need to come up with something else – and fast.
Figure 2: The Marine Biological Laboratory in Woods Hole, U.S.A.
Sometimes, such moments of forced introspection push us to recognise things that we’ve long known, but rarely acknowledge. I started to think about how, for as long as I could remember, I’d been drawn to the sea, and fascinated by the amazing diversity of form that exists within it. Many marine organisms, with their remarkable (and, sometimes, downright bizarre) adaptations, have arrived at solutions to seemingly intractable biological problems – and if I was being honest, I was just as interested in understanding the skate’s oddities as I was in resolving deeply conserved features that were present at the origin of jawed vertebrates.
So, what’s weird and wonderful about the skate? Hmmmm, flat as a pancake? Electroreceptive? Toothy denticles on the skin? Oviparous mode of reproduction? I’ve always worked on skeletal development, and both my parents suffer from arthritis, and so, in that moment, I pivoted to my go-to organ system – the skeleton – and grasped at three relatively simple observations. The first observation was that cartilaginous fishes (the group of animals that includes sharks, skates and stingrays) do not form bone, but rather (as their name suggests), possess a skeleton that is composed almost entirely of cartilage. This stands in stark contrast to what is seen in mammals: in mammals, cartilage is predominantly an embryonic tissue, and the vast majority of cartilage is replaced by bone, through a process known as endochondral ossification. In adult mammals, cartilage persists in very few places within the skeleton – among them, as the thin pads of articular cartilage that are found within joints. The second observation was that, although cartilage is a rather homogeneous and simple-looking tissue (it only has a single cell type – the chondrocyte – Figure 3), it has very little capacity for spontaneous repair (for example, following articular cartilage damage), and it is surprisingly difficult to engineer in vitro. While much progress has been made in developing cell-based therapies for cartilage repair, many of these approaches are still hindered by the frustrating tendency of in vitro cartilage to differentiate toward a bony fate. The third observation related to the old adage that your pet goldfish will grow to the size of its tank. Of course, this is a gross oversimplification, but it is generally true that, unlike mammals (whose growth curves plateau), many fishes do, indeed, continue to grow (albeit very slowly) in a largely indeterminate manner.
Figure 3: Histological section of skate cartilage, showing chondrocytes recessed within typical lacunae. The proteoglycan-rich cartilage extracellular matrix has been stained with Safranin O.
And so, I pondered out loud, if the skate skeleton is composed entirely of cartilage, and if that skeleton exhibits some sort of indeterminate growth, could it be that skates hold, within their skeleton, a mechanism to generate new cartilage in adulthood? And could this mechanism not only allow them to generate new cartilage during normal growth, but perhaps also to repair injured cartilage? There is mounting evidence that the cartilaginous skeleton of sharks and skates is a derived condition – in other words, cartilaginous fishes didn’t primitively lack bone, but rather lost it (for the latest on this topic, see this exciting pre-print by Martin Brazeau, Sam Giles and colleagues). If, through evolution, cartilaginous fishes have come up with a way to make cartilage as a permanent, growing tissue (rather than as an embryonic stepping stone toward bone) – and if they did so from an ancestral bony condition – could studies of cartilage development, growth and repair in skate inform new approaches to cartilage repair in mammals? Needless to say, at this point, my parents were rapt, sold, and ready to get in on the ground level…
While it is absolutely true that my lab’s work on cartilage growth and repair was born from a conversation with my parents, it is an exaggeration to say that this project crystallised and rolled out as smoothly as I set out above… In reality, after that fateful conversation, this project came together very episodically, over nearly 8 years (and mainly as a side project). Below, I’ll briefly run you through some of the major findings of our recent paper on adult chondrogenesis and cartilage repair in the skate (in the order in which they occurred – which, probably unsurprisingly, is not the order in which they appear in the paper…). In many cases, the figures that I’ve included here show more detail than I can succinctly address in the text – so for further information, please do take a look at our paper.
The fin cartilages of adult skates are permeated by canals, containing blood vessels and other cell types
In the 1980’s, it was reported that the vertebral cartilages of some large sharks were permeated by a series of canals (Hoenig and Walsh, 1982, Can. J. Zool.60: 483-485). This isn’t something that is seen in the embryonic cartilages of other vertebrates (except for the transient invasion of cartilage by canals during endochondral ossification), and so it was speculated that these canals could function in the nourishment, maintenance and growth of cartilage in these sharks during adulthood. We decided to focus our study on the metapterygium (one of the basal fin cartilages) of the skate, as this element is easily recognisable at all life stages, and its location makes it easily accessible for surgical manipulation (Figure 4). We cut sections through the metapterygium of adult skates, and saw that this element is also permeated by cartilage canals. These canals originate in the perichondrium (the fibrous tissue that wraps around the outside of cartilaginous elements), and extend into the core of the metapterygium. In agreement with earlier reports, we found that these canals contained blood vessels as well as a number of other connective tissue-like cell types, and we found that the blind ends of these canals were sites of active deposition of type II collagen (the predominant collagen of cartilage extracellular matrix) (Figure 5). Could the perichondrium be a source of cartilage progenitor cells in adult skates? And could these canals serve as a means of delivering cells and generating new extracellular matrix deep within the cartilage of the metapterygium? Testing for label retaining cells within the adult skate skeleton, and attempting to trace their progeny, would have been a logical next step – and we would eventually get to that – but not before first asking…
Figure 4: The metapterygium of the little skate, Leucoraja erinacea. A radiograph reveals the skeletal anatomy of an adult skate. The metapterygium (false colored red in i) is the caudalmost basal fin cartilage. The plane of section through the metapterygium used for subsequent figures is indicated with a dashed line and x. Scale bar = 5 cm.
Figure 5: Histological features of the metapterygium in the adult skate.(a) Transverse vibratome and (b) histological sections through the adult skate metapterygium reveal cartilage canals (asterisks) originating in the perichondrium and extending into the cartilaginous core of the element. The surface of the metapterygium is covered by calcified tesserae (dashed outlines). (c) Cells within the hyaline cartilage core of the metapterygium exhibit typical chondrocyte morphology, and (d) are surrounded by abundant pericellular type II collagen. (e) Mineralized tesserae sit between the hyaline cartilage core and an overlying fibrous perichondrium. (f) Examination of the unmineralized hyaline cartilage of the intertesseral joint region reveals a population of flattened, spindle-shaped cells (black arrowheads in fi) sitting at the boundary between the cartilage and the perichondrium. (g) Cartilage canals (asterisk) can be seen entering the hyaline cartilage of the metapterygium through the intertesseral joint region. These canals originate in the perichondrium, and extend into the core cartilage of the metapterygium. (h) Cartilage canals are not lined by an epithelium, and contain some red blood cells (black arrows), but predominantly (i) connective tissue-like cells – many of which appear to be invading adjacent cartilage ECM (black arrows). (j) Cartilage canals are sites of active type collagen secretion, as indicated by positive immunostaining for Col2a1. (b-c) and (e-i) stained with modified Masson’s trichrome. hc, hyaline cartilage; itj, intertesseral joint region; pc, perichondrium; ts, tesserae. Scale bars: (a-b) 2 mm, (c-d) 30 μm, (e-f) 50 μm, (fi) 30 μm, (g) 50 μm, (h-j) 30 μm.
Can skates can spontaneously repair injured cartilage?
Why not shoot straight for the moon, right? I was interested in testing whether adult skates could spontaneously repair a cartilage injury that was comparable in scale to a very severe mammalian osteoarthritic lesion. The problem was, I had no money to carry out these experiments (adult skates require a large amount of tank space and care), and no experience working with adult skates. So I decided to apply for a Research Grant from the Fisheries Society of the British Isles (which would just cover the costs of animal care), and after a few failed attempts, I was eventually successful. I also joined forces with then MBL veterinarian, Dr. Amy Hancock-Ronemus, who had a lot of experience with the maintenance and care of adult skates, and who was keen to collaborate on this work. Amy and I developed a biopsy protocol to remove a ~3-4mm wedge of cartilage from the metapterygium of adult skates, and we performed this procedure on twenty-six animals, collecting two animals shortly after the procedure, and then two animals per month for the following year, to assess repair.
Mammalian articular cartilage injuries cannot spontaneously repair – rather, injury sites become filled with scar tissue, or with fibrocartilage, which is mechanically inferior to the hyaline cartilage that typically resides in joints. In skate, we noticed that at 2 months post-operation, the cartilage injury sites that we induced in the metapterygium were completely filled with an undifferentiated connective tissue, and that by 3 months, this tissue began to differentiate into hyaline cartilage. Histologically, this repair cartilage resembled adjacent uninjured cartilage – it contained chondrocytes, and an extracellular matrix composed of type II collagen that was continuous with the matrix of adjacent non-injured cartilage. This repair tissue progressively differentiated from the bottom of the injury site to the top, and by 11-12 months post-operation, the injury sites were completely filled with new cartilage (Figure 6). These observations suggested to us that skates do have the capacity to spontaneously repair injured cartilage, though they didn’t tell us where the repair tissue comes from. However, by chance, a small number of our cartilage biopsies were not completely successful, resulting only in damage to the perichondrium, without removal of a wedge from the underlying cartilage. In these cases, we observed the formation of a large mass of new cartilage between the native cartilage and the perichondrium. This led us to hypothesise that the perichondrium was the source of new cartilage during the skate’s injury repair response, and that mechanical disturbance of the perichondrium, even without the removal of underlying cartilage, was sufficient to trigger the onset of chondrogenesis.
Figure 6: Spontaneous repair of hyaline cartilage in the skate.(a) 3D reconstruction of a dissected metapterygium 2 weeks following experimental cartilage injury. Note the biopsy (red asterisk) has left a void of ~1/3 the diameter of the metapterygium. (b, bi) By 2 months post-operation (p.o.), the injury site has been filled with a fibrous connective tissue, and (c, ci) by 3 months p.o., this connective tissue begins to differentiate into cartilage. Note that the cells of the repair tissue adopt chondrocyte morphology, and the ECM of the repair tissue is integrated with adjacent cartilage. (d) By 12 months p.o., the injury site has been completely filled with repair cartilage. (di) Red staining of ECM at the surface of the repair tissue (*) could indicate the re-appearance of tissue with a perichondral-like nature, or the re-establishment of tesserae at the injured surface of the metapterygium. However, (dii) the vast majority of repair tissue is composed of typical hyaline cartilage. (e) Immunofluorescence reveals abundant type II collagen (Col2a1) in the ECM of repair cartilage. In (b-d), the red dashed line indicates the boundary of the biopsy, and the black dashed line indicates the extent of repair cartilage. In (e) the red dashed line indicates the boundary of the biopsy, and the white dashed line indicates the extent of repair cartilage. hc, hyaline cartilage; pc, perichondrium; ts, tesserae. Scale bars: (a) 1 cm, (b) 100 μm, (bi) 30 μm, (c) 100 μm, (ci) 30 μm, (d) 100 μm, (di) 50 μm, (dii) 50 μm, (e) 50 μm.
Skates possess label-retaining progenitor cells in their perichondrium, and these cells give rise to new chondrocytes in adults
Label retention experiments have long been used in the fields of cell/developmental biology and regeneration, as a means of testing for the presence of dividing cells (for example, putative progenitor cells) in vivo. Briefly, a label that will become incorporated into newly synthesised DNA is introduced into a system, and this label is then detected and visualised, with retention used as a proxy for cell division. Historically, tritiated thymidine or bromodeoxyuridine (BrdU) has been used for such experiments, though 5-ethynyl-2-deoxyuridine (EdU) has emerged as an increasingly popular alternative because of the relative ease, speed and simplicity of its detection. We conducted an EdU retention experiment in adult skates, with the aim of resolving whether/where cycling cells (i.e. putative progenitor cells) were located within the adult skeleton. We gave adult skates 3 intraperitoneal injections of EdU (with each injection spaced two days apart), and then we tested for the presence of EdU-retaining cells in the metapterygium. We noted that EdU-labeled cells were recovered exclusively within the perichondrium, with no label-retaining cells in the cartilage itself. We also noticed two morphologically distinct populations of EdU-positive cells within the perichondrium – the “outer” perichondral cells, with round nuclei, and the “inner” perichondral cells, which have flattened nuclei, and which sit at the boundary between the perichondrium and the underlying cartilage. These observations suggested to us that cartilage growth in adult skates likely involved a population of progenitor cells within the perichondrium, and wasn’t occurring through continuous proliferation of differentiated chondrocytes.
We reasoned that 1) as cell division was likely quite slow in the skate, 2) as EdU remains detectable in the progeny of labelled cells for several rounds of division, and 3) as label-retaining cells were located only within the perichondrium at the time of injection, we might be able to use this labelling approach to lineage trace these putative perichondral progenitor cells. So we conducted a set of EdU pulse-chase experiments, this time collecting animals at 1, 2, and 5.5 months post-injection – and this is where Aleksandra Marconi joined the project. By this time, I’d left Dalhousie University and started my own group in the Department of Zoology at the University of Cambridge. Aleks is a PhD student on our Wellcome-funded developmental biology PhD programme, and was interested in the problem of post embryonic cartilage growth in the skate. Aleks decided to do a rotation in my lab, and was keen to analyse the adult skate label retention experiments that had been sitting on my shelf for a couple of years. After confirming the presence of EdU-positive cells within the perichondrium of the metapterygium at the time of EdU injection, Aleks found that by 2 months post-injection, she began to see an increase in the number of EdU-positive cells within the perichondrium, and the appearance of EdU-positive cells within the cartilage canals. And by 5.5 months post-injections, she recovered EdU-positive cells within the perichondrium and cartilage canals, as well as EdU-positive chondrocytes at two places within the cartilage of the metapterygium: superficially, beneath the perichondrium, and deeper within the cartilage, adjacent to the blind-end of cartilage canals (Figure 7). These observations led us to propose that the perichondrium of the adult skate metapterygium houses a population of (likely self-renewing) label-retaining progenitor cells, and that these progenitors give rise to new cartilage throughout adulthood via two routes: superficially, by apposition from the perichondrium, and interstitially, via transport of progenitor progeny within cartilage canals.
Figure 7: Label-retaining perichondral cells are cartilage progenitors in the adult metapterygium. (a) After a 5.5 month chase, EdU-retaining cells are detected in abundance in the inner perichondrium, and also in peripheral chondrocytes, including (b) in the hyaline cartilage of the intertesseral joint region and (c) in hyaline cartilage beneath tesserae. (d) EdU-retaining cells are detected in greater abundance inside cartilage canals, and (e) can also be seen migrating from inside cartilage canals into adjacent ECM. (f) EdU-retaining chondrocytes are also detected in the core of the metapterygium, adjacent to the blind end of cartilage canals. For each panel, the same section was imaged for EdU detection (counterstained with DAPI), and subsequently stained with modified Masson’s trichrome. In histochemical images, EdU+ nuclei in the perichondrium or in cartilage canals are indicated with arrowheads, while EdU+ chondrocytes are indicated with an asterisk. can, canal; pc, perichondrium; ts, tesserae. Scale bars: (a-c) 50 μm, (d-f) 30 μm.
Skate inner perichondral cells express markers of embryonic chondrogenesis
In parallel with the above experiments, we were also looking at gene expression within the embryonic, juvenile and adult skate skeleton. Around that time, we began studying gene expression by hybridisation chain reaction (HCR) – a simple and sensitive method for multiplexed fluorescent mRNA in situ hybridisation, in any taxon, and with any tissue prep (Choi et al., 2018, Development, 145: dev165753). In mammals, differentiation of mesenchymal cells into chondrocytes is marked by the expression of Col2a1 (the gene encoding type II collagen), and Col2a1 is directly transcriptionally regulated by the SoxE and SoxD-class transcription factors Sox9 and Sox5/6. We found that, as in mammals, embryonic chondrocytes in the skate co-expressed Col2a1, Sox9, Sox5 and Sox6, pointing to the likely conservation of this cartilage gene regulatory mechanism across jawed vertebrates (Figure 8). Additionally, within the juvenile and adult skeletons, we found that Col2a1, Sox9, Sox5 and Sox6 were predominantly expressed in the periphery of the cartilage (consistent with our model of appositional growth, and the birth of new chondrocytes around the periphery of the metapterygium), and we noticed that the morphologically distinct “inner perichondral cells” (i.e. the flattened cells that sit at the boundary between the perichondrium and underlying cartilage, and that were identified as putative progenitor cells in our label retention experiments) express Sox9, Sox5 and Sox6, but not Col2a1 (Figure 9). This is consistent with the hypothesis that these cells have chondrogenic potential, but have not yet differentiated into chondrocytes.
Figure 8: Conserved co-expression of genes encoding ECM components and upstream transcription factors in skate cartilage. (a) At S32, chromogenic mRNA in situ hybridization reveals that chondrocytes within the developing metapterygium express Col2a1 and (b)Agc1. Multiplexed fluorescent mRNA in situ hybridization by chain reaction (HCR) reveals that skate chondrocytes co-expression (c-d)Col2a1 and Sox9, and (e-f)Col2a1, Sox5 and Sox6, pointing to conservation of transcriptional regulation of Col2a1 by SoxD- and E-class transcription factors in jawed vertebrates. Scale bars: (a-d) 50 μm, (di) 30 μm, (e-f) 50 μm, (fi) 30 μm.
Figure 9: Skate chondroprogenitor cells co-express Sox9, Sox5 and Sox6. In hatchling and adult skates, mRNA in situ hybridisation by HCR reveals co-expression of (a)Sox9 and Col2a1, and (b), Sox5, Sox6 and Col2a1 in peripheral chondrocytes. This experiment also reveals a population of perichondral cells that sit at the cartilage-perichondral boundary, and that co-express Sox9, Sox5 and Sox6 but not Col2a1. These cells (white dashed outline in a’ and b’) are morphologically similar to the label-retaining “inner perichondral cells” identified in our label retention experiments. Scale bars: (a-b) 25 μm.
We therefore propose that post-embryonic growth of cartilage in the skate occurs by the slow-but-steady development of new chondrocytes from a population of perichondral progenitor cells, and that these progenitor cells are recognisable, transcriptionally, by their expression of the pro-chondrogenic transcription factors Sox9, Sox5 and Sox6. We also show that the persistent presence of perichondral progenitor cells in adult skates correlates with an ability to spontaneously repair injured cartilage. We think that these are really exciting findings, though, of course, there are still a number of outstanding questions: Is the perichondrium homogeneous in its chondrogenic potential? Or, is there a specialised subpopulation of perichondral chondroprogenitor cells? To what extent is the endochondral ossification transcriptional programme conserved in cartilaginous fishes? And where does this programme arrest to permit the persistence of cartilage as a permanent skeletal tissue? Our work toward answering these questions is ongoing, and we look forward to sharing more of our progress with the developmental biology and regeneration community shortly.
So, what started off as a side project, inspired by a conversation with my parents and supported initially by a small society grant, has now become a major new line of research in my lab, and has renewed my curiosity in (and enthusiasm for) the bizarre little skate that I started working on as a graduate student fifteen years ago. Moreover, I think that this project illustrates a point that is made most eloquently by a quote attributed to the former MBL scientist, Nobel laureate Albert Szent-Gyorgi (and that is emblazoned on the wall leading into the tank room at the MBL Marine Resources Centre): “Research is to see what everybody else has seen and think what nobody has thought”. This research project stemmed from three observations – none of which were particularly novel or profound (or even our own to begin with!). But by digging a little deeper and conducting a few simple experiments, we were nevertheless able to learn something new and exciting about the unique skeletal biology of cartilaginous fishes.
As a side note: in 2021, my lab will be relocating to the Marine Biological Laboratory in Woods Hole, where I will be taking up a resident scientist position. I am very excited about this move, not least because it will allow us to develop the skate even further as a model system for developmental biology and regeneration. And I recently learned from my friend, colleague and fellow Woods Hole enthusiast, historian of science Shane Jinson, that the lab space we are moving into in the Lillie Building once belonged to, of all people, Albert Szent-Gyorgi (Figure 10)!
Figure 10: Third floor of the Lillie Building (circa 1926-1941), Marine Biological Laboratory, Woods Hole. Image credit: Shane Jinson.
I started off as quite little—just one cell, in fact. No heart, no brain, no blood flowed in me and yet, somehow I found the motivation in me to divide. One me made two and two mes made four, till many tiny mes made me a full-fledged embryo with a heart full of hope. As I grew older, my heart grew with me. My body and heart needed to synchronize their growths, you see, because if my heart grew slower, then it would pump less blood into my system, and my other organs that needed blood to grow would not be able to do so properly. This posed a challenge for me– how do I make sure that my body knows my vessels are growing, and my vessels know my heart is growing? Please don’t tell me that’s yet another thing my brain has to manage. Wait, do I even have a brain yet!?
Anyway, perhaps it’s easiest if I use some intrinsic property of my blood, the fluid that connects my body and vessels and heart, to transport this important message. This way, as my heart beats faster and more blood flows through my system, my vessels will take the hint and grow accordingly. Going back to connections, let me first focus on my outflow tract, which connects my heart to my aortic vasculature. Perhaps if I tell my outflow tract to widen as blood flow and contractility increase, it will maintain my blood pressure while also allowing information in blood to pass through to my other systems. Ugh, so how I do that?
Hmm. What if the cells in the inner endothelial lining of my outflow tract respond to blood flow and contractility by dividing? What if they accumulate cells from the neighboring vessels, in conjunction with neighboring vessels accumulating them from more distal vessels? Maybe I’ll do both—yes, that sounds like a good strategy. But how do I regulate this growth? Maybe I should have many opposing signals, reacting to multiple inputs, towards the unified goal of getting the outflow tract to a particular lumen size at a particular developmental stage. I’m feeling lazy, I’ll just repurpose my good ol’ TGFb pathway to do this—put some receptors in my endothelial cells and have my blood carry physical and molecular cues to activate them.
Great, I think I have a functioning cardiovascular system! And it’s caught in this self-regulating loop where function informs form, which feeds back to function. I feel so smart! Kudos to me figuring this out over evolution. Well, I guess I’ll give an additional kudos to this grad student who figured it out in 5 years.
We are looking forward to an exciting UK SouthWest Zebrafish Meeting at the 11 Sep 2020!
If you have not already, register and also submit your abstracts for either talks or posters. Talks and posters will be given to students, early career researchers and technicians. Our deadline for abstract submission is Friday 24th July, so submit your abstracts on our website: https://swzm2020.wixsite.com/swzm2020/registration. On the website you will find the online registration form, as well as the abstract form to fill out and upload.
Virtual Meeting:
We have been working behind the scenes to build our virtual meeting! We are planning to hold the meeting via a central hub on Padlet.com. This means we can host an online poster exhibition, secure to all delegates, where you will be able to browse and read posters, leave comments and interact with presenters and crucially vote for ‘best poster’! Prizes will be awarded for best talks and posters! We will also use Zoom to host our series of talks, break-out sessions, talks from sponsors, as well as an online ‘Zebrafish Zoom Café’ for breaks and general discussion. More details to come!
New Sponsors:
Good news! We can now confirm our meeting will be free from any registration fees for delegates. We can now confirm we have been kindly sponsored by The Company of Biologists, through a Scientific Meeting Grant, so we can waive registration fees. We can also announce we are kindly sponsored by Tecniplast and DanioLabs.
Special Issue:
We would like to announce that a Special Issue of ‘Histochemistry and Cell Biology’ focussing on ‘In vivo cell biology in zebrafish’ will accompany the meeting. Please email us for further details. We are looking forward to hearing from you with research!
Please pass this information on to anyone you think may be interested and feel free to tweet about the event using #SWZM20 and follow us on Twitter @Swzm20!
Looking forward to hearing from you all,
Steffen, Lucy, Holly, Michael, Josh, Chengting & Yosuke
(South West Zebrafish Organising Committee)
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