I joined the Node and Development out of a postdoc in 2016 and now after five enjoyable years I’m moving on. I’ll write something a bit more reflective closer to my leaving date in June but here I thought I’d let you know what the job entails, since we’re searching for my replacement.
If you’re interested in science communication and helping the developmental biology community in various ways, this job might be ideal for you. And if you know anyone who is thinking of hanging up their pipettes but still wants to stay in touch with science and scientists, please send the job ad their way.
Here’s a collection of the kind of things you’d get up to:
Run the Node
Commission content – research stories, interviews, meeting reports etc.
Edit / give feedback on drafts for authors
Write your own content
Run competitions and series of posts
Maintain the site (including the now 900+ strong Node Network)
Develop the site’s future – we’re now 10 years old and well-established, but there are always opportunities for innovation
Social media
For the Node: Twitter (where all the fun stuff happens) and Facebook
For Development: Twitter, Facebook, more recently Instagram, and on our YouTube channel you’ll have opportunities for video editing
With these accounts you reach thousands of people, specialists and non-specialists, to spread the word about developmental biology
For Development
Write Research Highlights (usually one a week)
Conduct ‘The people behind the papers’ interview series (usually one per issue), and longer standalone interviews (could be a Nobel laureate or an up-and-coming star)
Write and manage press releases for topical papers
Development presents… – help out with our webinar series
Attend Editor meetings and strategy sessions – insight into the publishing world
Conferences
In a normal year, go to perhaps six conferences, some abroad, usually focusing on society events. Meet people, hear new science, promote our work, write meeting reports, interview prize winners
Help out at Development’s biennial human development meetings and Company of Biologists Workshops
Working for The Company of Biologists
Provide cover for and collaborate with the two other community sites, preLights and FocalPlane
Promote our work as a not-for-profit publisher
Work with 50 other great colleagues near Cambridge (/home office)
During their practical classes the students produced some beautiful images and so, as we did in 2018, we’re going to use them in a competition to find a Development cover. Participating is easy – just vote for your favourite image from the following selection (click to get full size images, voting below the pictures). The winner will then be immortalised in print and on screen in a future issue of the journal – testament to the bright future of developmental biology in Latin America.
2. Drosophila larval body wall. Third instar larva body wall muscle with nervous system innervation. Phalloidin (magenta), HRP (cyan), ppk > GPF (yellow). By Pablo Guzman Palma
3. Drosophila eye discs and brain lobes. In blue: nuclei (DAPI); in red: ganglion mother cells and neurons (PROSPERO); in magenta: F-actin (Phalloidin) and in green: all neurons (HRP)). By Tonatiuh Molina Villa.
4. Parhyale(amphipod crustacean). F-actin (green-Phalloidin), nuclei (blue, DAPI) and eye (red-Elav). By Diana Carolina Castañeda-Cortés, Nicolas Eduardo Cumplido Salas, Felipe Andres Gajardo Escobar
5. Sea urchin late blastula. Green: Pax3/7; red Hoecsht. By Shurti Purushothaman
6. Drosophila larval body wall. Phalloidin (red), HRP (green), ppk > GPF (blue). By Marycruz Flores Flores, Felipe Berti Valer, Emiliano Molina.
7. Parhyale embryo. Labelled with DAPI and a membrane marker. By Marycruz Flores Flores, Felipe Berti Valer, Emiliano Molina
One vote per person – voting closes Monday 29 March!
Last week, we held the sixth webinar in our series, which was chaired by Development editor Thomas Lecuit (IBDM).
Below you’ll find recordings of the talks and live Q&A sessions.
Hongzhe Peng (from Bo Dong’s lab at Ocean University of China) ‘Ciona embryonic tail bending is driven by asymmetrical notochord contractility and coordinated by epithelial proliferation
Camille Curantz (from Marie Manceau’s lab at Collège de France) ‘Cell shape anisotropy and motility constrain self-organised feather pattern fidelity in birds’
The annual Young Embryologist Network Conference is happening this year on May 4th! Put the date in your calendars now!
YEN is thrilled to announce that Nobel Laureate Christiane Nüsslein-Volhard from the Max Planck Institute of Developmental Biology in Tübingen, Germany will present this year’s Sammy Lee Memorial Lecture. We are also honoured to host two special speakers: Matthias Lutolf from EPFL in Lausanne, Switzerland and Alexander Aulehla from EMBL in Heidelberg, Germany. Finally, we are delighted that Marianne Bronner from Caltech, USA, Ana Pombo from MDC Berlin, Germany and Patrick P.L. Tam from CMRI, Australia will share invaluable insights from their life as a scientist in our “Scientific Perspectives” session.
YEN 2021 will be held entirely online, which will allow for unprecedented international participation. Spread the word, and let us take the Young Embryologist Network worldwide!
Talks will be held throughout the day, beginning at 9.15am (BST). We will be using the online conference platform Remo, enabling us to recapitulate that in-person networking feeling of conferences that we are all missing. Interactive poster sessions will also be held via Remo, with further discussions taking place in dedicated Slack channels both during and after the event.
Register here to submit an abstract or to attend as a delegate (and hear what your fellow young embryologists are up to). Registration is free and the deadline for abstract submission is April 4th, so be sure to sign up as soon as possible!
In 2020 the Node turned 10 and, along with a virtual networking birthday party and a Development editorial, we ran a community survey for advice on what to improve and where to go next. We gathered some fantastic ideas for content that we’re going to develop soon but also heard many suggestions for things we’d done before. This made us think about how we could better promote historical Node content (going all the way back to 2010), pieces that are currently quite hard to find in the archive. We also felt that the homepage needed a refresh – it hadn’t been updated since 2015 – and identified a few more tweaks we’d like to implement, both from reader and author perspectives. These discussions happened to coincide with a necessary upgrade in our WordPress system to their Gutenberg editor, which gives a lot more freedom in terms of page design, and also changes the user experience for writing posts. And so, towards the end of 2020 we started working on giving the Node a new look: not a full on revolution, more an upgrade, which we’re happy to launch today. Here are the main features we’ve changed:
Homepage tweaks
One of our first decisions was to refresh our header images. This being the Node, we tapped our greatest resource: the developmental biology community. A competition in February led to over fifty entries which we winnowed down to the final five (you can skip through by refreshing your page). Congratulations to competition winners Markus Schliffka, Rory Cooper, Evan Bardot, Gonzalo Aparicio and Daniel Castranova – you can find out more about their images in our ‘About us’ page.
We’ve also removed the static ‘Featured posts’ bar and replaced it with a moving carousel above the blog posts – we hope this better showcases the diverse range of our recent content. The new, more flexible, homepage will also allow us to better highlight other content and information – you can expect to see the homepage evolving further over the coming months.
Something we discovered in the survey was that many of you still don’t know just how easy it is to contribute to the Node – all you need to do is register for an account, and you’re then free to post without the need for our ‘official’ approval (though we are of course always happy to provide feedback to people interested in writing for us). Hopefully the new ‘welcome’ message at the top of the page reemphasising the fact that the Node is your site will encourage even more community engagement.
Topic pages
To help readers navigate our extensive archive of content, we are now collating blog posts on particular themes into one place – its own topic page. Here are some examples:
A day in the life… Our series of posts detailing what it’s like to work with a particular model organism
Behind the paper stories. We regularly commission scientists to tell us the stories behind their new publications.
Forgotten classics. A series on unjustly neglected papers in the literature.
SciArt Profiles. Profiles of scientists who do art, or artists who dabble with science.
You’ll find links to the topics pages in the ‘Archive’ tab at the top of the page, and we’ll continue adding more pages as they become relevant – if you have an idea for a new collection, just get in touch.
Jobs page
The jobs page now only shows active job adverts – once a job advert expires, it goes into the archive (all job adverts posted before today can be found in the archive – if you want to see your own advert back on the jobs homepage, simply post it again). We’ll soon make job adverts filterable by categories like location and position – watch this space.
The author experience
If you’re a returning author, you’ll notice a few changes in how posts are created, as we’ve upgraded to a newer version of WordPress that uses their Gutenberg Editor. This uses a ‘block’ system – blocks can be headers, paragraphs, images, YouTube links, and more, and can be used in any order. We hope that creating a post will still be relatively self-explanatory, but we have a walk through video and a written ‘how to’ over on our FAQ page. If you have any issues, just email us.
Posting a job is now different to posting a blog post – for example, you need to include an expiry date. Just check out our FAQs for more information.
We hope you enjoy our new look and, as ever, would love to hear your ideas for where we can take your community site.
Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY, USA
The neural crest has long been referred to as “the fourth germ layer” for its remarkable ability to give rise to a number of cell types in the vertebrate embryo including neurons, glia, bone, and cartilage. Specified at the border of the neural plate, the neural crest is intimately linked to this adjacent cell population, which will give rise to the central nervous system. Directing the partitioning of the ectoderm into these two territories are inductive interactions driven by signaling systems including Wnt, BMP, and FGF. These signals form overlapping spatial gradients across different ectodermal territories, driving the regulatory programs required to induce the neural crest and the neural plate. Many developmental biologists have studied the timing and levels of signaling required for proper neural crest formation, but fundamental questions remain: How do distinct combinations of signaling molecules give rise to different cell types? Furthermore, how do fields of cells interpret and respond to these signals?
Fig. 1. Patterning of the ectoderm during early vertebrate development is guided by opposing concentration gradients of Wnt and FGF signaling.
A conceptual framework for understanding these questions was established by Lewis Wolpert in 1969 with his seminal paper “Positional Information and the Spatial Pattern of Cellular Differentiation”1. Wolpert’s “French Flag Model” proposed that spatial gradients of signaling molecules known as morphogens drive subdivision of cellular fields based on concentration. Although Wolpert’s model offered foundational insights, today we know these processes are much more complex. For example, there must exist mechanisms by which cells can produce binary responses to distinct ranges of signaling levels. One such mechanism relies on the transcriptional control of signaling system activity through activation of agonists/antagonists. However, transcription can be a leaky process, and may not confer the optimal levels of signaling activity needed for cell fate decisions. Therefore, other modes of regulation may offer robustness in these developmental programs.
When I began my first year of graduate school at Cornell University I had never even heard of Lewis Wolpert or the neural crest, for that matter. I was first made aware of this cell population after hearing a rotation talk from my now mentor Marcos Simoes-Costa. Although I had no background in development, I was amazed by the beautiful movies of migrating neural crest cells and the chick model system’s tractability for investigating gene regulatory programs. After Marcos’s talk, I was very excited to rotate in his lab and eager to discuss rotation projects. Prior to my rotation, Marcos had published his first article as a new PI, investigating the role of the Lin28/Let-7 axis in neural crest multipotency2. From this work he became interested to look further at the post-transcriptional regulation of this cell type. As an undergraduate, I studied genetic interactions associated with pre-mRNA splicing in Saccharomyces Cerevisiae. Through this work, I developed an immense interest in post-transcriptional gene regulation, which I consider the underdog of the central dogma of molecular biology. As luck would have it, our interests aligned, and we embarked on a new project which culminated in a recent publication in PNAS3.
It has been known for roughly a decade that Dicer, a key enzyme in the miRNA biogenesis pathway, is critical for neural crest development and differentiation. Conditional Dicer knockout mice exhibit severe craniofacial defects due to lack of neural crest-derived structures, highlighting the importance of Dicer, and therefore mature miRNA species, in the formation of this cell type4-6. However, few studies had investigated the mechanistic roles that miRNAs and their gene targets may play in this cell type. This led us to our major goal of identifying and characterizing miRNA function during early neural crest formation.
Fig. 3. Bilateral electroporation scheme utilized for Dicer knockdown in gastrulating chick embryos. Immunohistochemistry for specification marker TFAP2B revealed loss of neural crest cells upon Dicer knockdown
It would be quite difficult to assay the phenotypic outcome of inhibiting every individual miRNA expressed in the chicken genome. So, to get an idea of the role miRNAs might be playing during neural crest specification, we first turned to Dicer, examining its expression in relation to that of the neural crest specification marker TFAP2B. What came as quite a surprise was that Dicer, which is thought to be a ubiquitously expressed protein, was enriched in neural crest cells. Furthermore, through interrogating the Dicer locus, we uncovered a neural crest-specific enhancer driving Dicer upregulation in this cell population. This was an exciting finding, as it demonstrated that there may be increased processing and turnover of miRNAs within neural crest cells. This idea made a lot of sense to us, as neural crest cells undergo rapid genomic and morphological changes in their relatively short lifetime, which may be facilitated by different groups of miRNAs.
The chick embryo offers a beautiful system in which we can perform bilateral electroporations to observe control and knockdown phenotypes within the same organism. Using this method, we injected gastrulating chick embryos with a Dicer protein-inhibiting morpholino. Since the phenotypic effects of morpholino based knockdown can be quite broad, we performed a Nanostring analysis in order to more globally assess the effects of Dicer knockdown during neural crest specification. To our surprise, knockdown of Dicer not only resulted in a loss of neural crest markers but was also accompanied by increased expression of several neural plate-specific factors. Observing knockdown embryos, we indeed saw an expansion of the neural plate at the expense of neighboring neural crest cells.
These observations led us to hypothesize that miRNAs (synthesized via Dicer) may play an important role in the cell fate decision between the neural crest and neural plate. To test this hypothesis, we needed to isolate these cell populations in order to identify the abundant and unique miRNAs present in each. For this we turned to a commonly used system in our lab, in which we can inject chick embryos with cell type-specific enhancer reporters and then perform FACS to isolate pure populations of cells. Since we were interested in the neural plate and the neural crest, we isolated cells from each of these populations and performed small RNA-sequencing. Admittedly, getting small RNA-sequencing to work was a feat in itself. Most of my rotation and my first summer in lab were spent optimizing the protocol for small numbers of sorted chick neural crest cells. This involved dissecting hundreds of chick embryos but was accompanied by lots of time with Marcos at the electroporation station discussing what miRNAs could be doing in crest.
Fig. 4. DICER mediates the biogenesis of FGF-targeting miRNAs in neural crest cells, leading to posttranscriptional attenuation of FGF signaling for proper neural crest cell formation.
Once we finally optimized a protocol for small RNA-sequencing, we were off to the races, identifying miRNAs and determining their modes of action. Through several analyses including miRNA target prediction, we ultimately identified a group of neural crest miRNAs that target components of the FGF signaling pathway. This was an “aha!” moment for us as we knew levels of FGF must be quite precise for neural crest induction: too much and the cells are fated towards the neural plate, but not enough, and neural crest will not form at all. We hypothesized this group of miRNAs was required in crest to keep levels of FGF low, inhibiting a neural plate fate, and confirmed this through several functional approaches. One of my favorite experiments we performed, that truly wrapped up the paper, was the rescue of the Dicer knockdown phenotype by adding back our FGF-targeting neural crest miRNAs. Getting back to post-transcriptional regulation being the underdog of the central dogma, this was amazing to me. miRNAs typically have very modest repressive effects (less than 1.5 fold) on gene expression. Given this, I was not sure if by putting back our FGF-targeting miRNAs we would rescue the Dicer knockdown phenotype. But to my surprise, by working in a concerted fashion to target different FGF pathway components and attenuate levels of FGF, these three miRNAs were quite capable of rescuing the neuralization switch observed upon Dicer knockdown.
I am quite proud of this paper, not only because it is my first publication in graduate school, but because it tells a story of how small RNAs can work together to drastically influence the cell fate decisions of neighboring cell populations in the ectoderm. I also appreciate how it unifies two opposite ends of the of neural crest regulatory spectra: signaling system inputs that jumpstart the neural crest GRN and post-transcriptional regulation of these signaling systems to ensure the proper thresholds of activity are met. Moving forward, I would like to explore regulation of signaling systems via miRNAs at a broader level, considering their contribution to patterning events related to other tissue types, as well as the regulation of the miRNAs that reside in those tissues. I also hope that this work can inform upon other developmental scenarios where tuning of signaling systems via miRNAs is critical for cell fate commitment.
Two Postdoctoral Research Associate positions (PDRA) are available in the Spagnoli lab. in the Centre for Stem Cell & Regenerative Medicine at King’s College London. Our team uses interdisciplinary approaches to study pancreatic development and stem cells. The candidates will join a Wellcome Trust-funded research programme aiming at studying the pancreatic tissue microenvironment in all its complexity using cutting-edge models.
Single-cell sequencing has unveiled a high degree of cellular heterogeneity within the pancreatic microenvironment and has opened the way for a systematic study of intercellular interactions. We seek to spatially reconstruct the organisation of functional niches in the pancreas and study how they induce distinct pancreatic differentiation programmes using mouse models and human pluripotent stem cells. This will set the stage for manipulating combinatorial 3D organ niches towards engineering pancreatic cells for regenerative medicine.
The research programme will require expertise in transcriptomics, high-resolution imaging, stem cell culture, human tissue, mouse genetics, computational analytical methods. Applicants should have a recent Ph.D. degree or have submitted his/her Ph.D. thesis. We wish to appoint one PDRA with background in development and stem cell biology and one PDRA with computational background interested in single-cell omics, spatial transcriptomics and image analysis.
The Spagnoli lab. is a young dynamic team, member of the outstanding Centre for Stem Cell & Regenerative Medicine at King’s College London. This is a world-class research environment with all facilities essential for this ambitious research programme.
Interested candidates should get in touch with Francesca Spagnoli (francesca.spagnoli@kcl.ac.uk) for further information. Please send your CV, research interests, and names and contact information of three references.
Positions will be available starting in October 2021.
More information on the group, publications and research topics in the group can be found in the laboratory website: https://www.spagnolilab.org/
In the latest episode of Genetics Unzipped we’re delving into the science behind so-called ‘genetic superheroes’, and explaining why you might have hidden powers within your genes. Despite the name, these superheroes don’t have the ability to shoot webs from their fingers or save the universe, but something with a lot more real world relevance to human health.
Instead, these people have a much more down to earth ability: carrying genetic alterations that should make them seriously ill, yet they are apparently healthy.
We take a closer look at the search for genetic superheroes, the science behind their secret powers, and what their existence means for our understanding of genetics.
If you enjoy the show, please do rate and review on Apple podcasts and help to spread the word on social media. And you can always send feedback and suggestions for future episodes and guests to podcast@geneticsunzipped.com Follow us on Twitter – @geneticsunzip
The HOUART lab is seeking to appoint three postdoctoral research associates to join a 5-year Wellcome Trust-funded research programme in developmental neurobiology. The programme aims to understand the role of axonal splicing factors and intron retaining transcripts in neuronal maturation and degeneration. Our nervous system crucially relies on local fast decisions taken long distance from the neuronal cell body. The mechanisms by which these decisions are spatio-temporally controlled remain obscure. We found that axonal splicing factors and intron-retaining mRNAs are key players in the process. We seek to understand the fundamental molecular and cellular roles they play locally in the dynamic control of neuronal connectivity, using animal models (zebrafish) and cell culture approaches.
The research programme will require expertise in zebrafishgenetics, transcriptomics, proteomics, high-resolution (live and fixed) molecular imaging, and sophisticated computational analytical methods. We wish to appoint one scientist with expertise in cutting-edge high-resolution/molecular imaging technologies; one with strong zebrafish neurobiology background and one with very strong protein/RNA biology experience.
Prof. Corinne Houart is a member and Deputy Head of the outstanding Centre for Developmental Neurobiology and MRC Centre for NeuroDevelopmental Disorders at King’s College London. Her lab is affiliated member of the Francis Crick Institute. This rich research environment provides world-class research facilities to the post holders.
Deadline for application 31st March 2021. For further information, please contact Prof. Corinne Houart, corinne.houart@kcl.ac.uk
The Ward Lab (https://www.ward-lab.org/) at the University of Texas Medical Branch is seeking a Postdoctoral Fellow to lead core projects focused on cardiovascular functional genomics.
The goal of the Ward Lab is to dissect the global role of regulatory elements in directing gene expression in healthy, stressed and disease states in cardiovascular disease-relevant cell types. We use a variety of population and evolutionary genomics approaches and induced pluripotent stem cell-based tools to tackle this problem.
Projects are available in several areas including:
-gene regulatory dynamics during differentiation to cardiovascular cell types
-gene regulatory processes in response to disease-relevant perturbations
-inter-individual variation in response to disease-relevant perturbations
We are looking for a highly motivated, enthusiastic individual to join our growing team. Candidates should have received their Ph.D. within the last year in Molecular Biology, Cell Biology, Evolutionary Biology, Cancer Biology, Genetics, Systems Biology, Computational Biology, or a related field. They should have excellent communication skills and a good track record of productivity, including a first-author paper.
The University of Texas Medical Branch, located on the island of Galveston, is a member of the University of Texas System, the Texas Medical Center (the largest medical center in the world based in Houston -approximately 50 miles away), and the Gulf Coast Consortia in Quantitative Biomedical Sciences. This environment provides a vibrant research community. There are excellent Core facilities on campus including Next Generation Sequencing, Flow cytometry and Proteomics.
Please apply by sending a cover letter, C.V., and contact information for three references via email to Dr. Michelle Ward (miward {@} utmb {.} edu). Review of applications will begin immediately and continue until the position is filled. Informal enquiries are welcome.
UTMB Health strives to provide equal opportunity employment without regard to race, color, national origin, sex, age, religion, disability, sexual orientation, gender identity or expression, genetic information or veteran status. As a VEVRAA Federal Contractor, UTMB Health takes affirmative action to hire and advance women, minorities, protected veterans and individuals with disabilities.
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