The ISSCR Annual Meeting, taking place in San Francisco, USA on 15-18 June, is a gathering of the brightest minds in stem cell research and regenerative medicine across geographies and disciplines. Nearly 3,500 scientists from around the globe will convene at ISSCR 2027 to take part in a 4-day program comprising the year’s most significant new advances in the fields of stem cell research and regenerative medicine.
Visit https://www.isscr2027.org/ to learn more about registration, abstract submission, and to view the full scientific program. Do not miss the opportunity to present your work at ISSCR 2027 – abstracts are due 27 January 2027.
As artificial intelligence, computational biology, and increasingly sophisticated stem cell-based models reshape the research landscape, ISSCR 2027 will showcase advances spanning fundamental discoveries in human development and disease, engineering biology, and emerging cell and gene therapies. ISSCR President Lorenz Studer, M.D., founding director of the Center for Stem Cell Biology at Memorial Sloan Kettering Cancer Center, USA, will president over the ISSCR Annual Meeting. The scientific program, led by Program Committee Co-Chairs Viviane Tabar, M.D., Memorial Sloan Kettering Cancer Center, USA, and Matthias P. Lutolf, Ph.D., École Polytechnique Fédérale de Lausanne (EPFL), Switzerland, will feature pioneering research, emerging discoveries selected from submitted abstracts, interactive poster sessions, and opportunities for collaboration across academia, industry, and clinical research.
Complementing the scientific program, the Exhibit and Poster Hall will highlight innovations in laboratory automation, advanced imaging, computational technologies, and cell manufacturing, connecting researchers with the tools, expertise, and partnerships driving the next generation of scientific discovery and clinical advances.
Abstract Submissions and Opportunities to Participate The ISSCR invites researchers at all career stages to contribute their latest discoveries and participate in global scientific exchange. Opportunities include:
Submit an Abstract: Deadline 27 January 2027. Share new research through oral or poster presentations at the world’s leading stem cell research meeting. Travel awards are available to ISSCR student and postdoctoral members who submit abstracts.
Submit a Science Spotlight Proposal: Deadline 27 January 2027. Student and postdoctoral members can help shape the scientific conversation by proposing sessions highlighting emerging research areas, innovative approaches, and new developments not already featured in the program.
Apply for a Child and Dependent Care Grant: Deadline 10 March 2027. Eligible ISSCR members can apply for grants to help offset care costs associated with attending the meeting in person. Awards are available on a first-come, first-served basis.
Organize a Meet-Up Hub: Deadline 19 April 2027. Connect researchers with shared scientific interests through informal gatherings in the Exhibit and Poster Hall.
Participate in One-on-One Partnering: Schedule face-to-face meetings with researchers, industry representatives, and potential collaborators to explore scientific partnerships, investments, licensing opportunities, and new ventures.
Research fellow in Cell and Developmental Biology, University College London
TLDR: Approach science with the mindset of a waterbender, be like the flow of a river, flexible, malleable, adapting, and most importantly, enjoy the ride and stay curious!
The philosophy of waterbending
Ok, I know you probably think I’m a bit wacky with that opening heading, but bear with me! There is this great cartoon series by Nickelodeon from the early 2000s that I grew up watching (and rewatching still) called Avatar: The Last Airbender. The show brings you into a world of four nations, where people from each nation can manipulate one of the four elements: water, earth, fire, and air through a type of martial art called bending. The show’s premise isn’t important for this piece, but one of the greatest things about it is the philosophy behind each bending form, and for me, the best has always been waterbending. “Water is the element of change.” Waterbenders “let their defence become their offense, turning their opponents’ own forces against them. The people of the Water Tribes are capable of adapting to many things.” As much as one might think this is just a kid show, this philosophy has stuck with me and underlies much of how I approach science.
This is the best cartoon show, both for the story and the philosophy, hands down!
After finishing my PhD in cancer migration and metastasis in 2020 at the Cancer Research UK Scotland Institute, I wanted change. I wanted to explore more complex systems than cell culture. I became interested in how cells respond to mechanical forces, particularly how immune cells integrate these signals to regulate a process called macropinocytosis, also known as cell drinking. I’m not sure where this fascination with immune cells came from, because before this, I had never worked with them. But the idea of a migratory cell type capable of morphing, branching, and constantly gulping up stuff piqued my interest and, honestly, sounded like a fascinating system to explore. I’d known of Roberto’s work for a while and knew his expertise in in vivo mechanobiology, so I approached him and proposed a project to look at the mechanobiology of early macrophages (also known as embryonic myeloid (EM) cells) in vivo and determine how substrate stiffness regulates macropinocytosis using Xenopus embryos. I applied for the Sir Henry Wellcome fellowship and was lucky enough to get funded. This marked my biggest career transition, moving from relatively neat, clean cultured cell lines to frog embryos. It was also daunting because, unlike transparent zebrafish, frog embryos remain a rather unusual model for immunobiology, and this project was about to be led by someone who had no prior experience working with live embryos. But just like the philosophy of waterbending, one can either look at changes as something to fear, or they can look at them as new opportunities for growth and adaptation, turning fear into excitement and curiosity.
The first goal
The first major goal of this project was to establish an ex vivo explant system of myeloid cells. If imaging through a Xenopus embryo is difficult because of yolk platelets present in every cell, then these same yolk platelets also allow Xenopus tissue to be isolated and cultured independently for an extended period. An ex vivo explant would allow us to perform high-resolution imaging and cellular perturbations. I remember those first few months of constant trials and errors vividly. We had three main concerns at the time. First, isolated primary blood cells are cumbersome to culture in humans and mice, so we had no idea whether the same problem would apply to Xenopus myeloid cells. The second concern was how to establish a dissection and culturing method for a piece of tissue that nobody has ever worked on. Third, labelling these myeloid cells requires microinjecting into two rather small, obscured-looking blastomeres in 16- or 32-cell-stage embryos. Luckily for us, the last concern did not need to start from scratch, as some early work on microinjection and labelling was done by the Enrique Amaya lab at the University of Manchester1,2 (https://research.manchester.ac.uk/en/persons/enrique.amaya/). I cannot recall how many microinjections I did or how long it took me to comfortably recognise the right blastomeres, but I do remember the day I saw those early myeloid cells glowing in one of the injected embryos. I ran to Roberto’s office and told him he needed to come take a look. These cells are difficult to target, but you would know in a heartbeat if you had labelled them correctly because they spread out individually and colonise the entire embryo. They also look beautiful under the microscope with their characteristic branches that closely resemble those seen in zebrafish and mice.
Embryonic myeloid cells (magenta) dispersing in a Xenopus embryo.
Now that we got them labelled, the real challenge was to culture them. Roberto taught me how to do my first dissection. He was always so enthusiastic about teaching. I remember those days when it was just the two of us sitting in the embryology room until 8 or 9 PM, testing different ways to cleanly dissect out the anterior ventral blood island, the tissue region where the myeloid cells come from. The original idea was to culture just the myeloid cells. However, we quickly realised that because these cells migrate individually, it would be impossible to separate them one by one into a pure population, as is often done for collectively migrating cells like the neural crest. It was also not possible to remove the top tissue layer of the explant – the ectoderm – without affecting the myeloid cells below. To add to the complication, this ectoderm layer causes the dissected explant to curl up quickly into a ball, even if the culturing dish is coated with fibronectin. After quite a bit of brainstorming, I came up with the idea of gently placing a small piece of glass on top of the explants to prevent them from curling up and promote their adhesion to the substrate. To ensure I did not compress the tissue too heavily, I added a small amount of vacuum grease to the two opposite edges of the glass piece, and this essentially was how the protocol for culturing the anterior ventral blood island was born. I still have goosebumps reminiscing about the day when I collected the time-lapse images and saw the explants spread on the surface; then came the waves of myeloid cells radiating out from the centre. The first major milestone was achieved!
An anterior ventral blood island explant spreading on a fibronectin-coated dish. Ectodermal cells in blue (GFP-membrane), embryonic myeloid cells in red (fluorescence dextran).
The quest to control tissue flow
It wouldn’t make a good story without the drama because a new problem quickly arose. Since we could not separate the mesoderm from the ectoderm, our explants would permanently be a co-culture of at least two different cell populations. This makes it incredibly challenging to image macropinocytosis because the surrounding ectodermal cells would also take up the fluorescent dextran, making it difficult to differentiate the signal from the myeloid cells. Secondly, because of this ectodermal layer, it was also impossible to culture the explants on softer hydrogels since they could not attach and spread. This makes studying the role of substrate stiffness on myeloid cells’ macropinocytosis almost impossible. After months of unsuccessful attempts, the philosophy of waterbending came to mind again: redirection. What if the co-culture aspect of our explant system wasn’t so bad after all? I noticed that myeloid cells outside the explant display a rounded-up morphology with an erratic migration behaviour, unlike their more streamlined morphology inside the explant. This suggested that even if I could separate these myeloid cells, their natural biology would be severely altered, which was not the best-case scenario. At the same time, the startling radial migration pattern that these cells display also became hard to ignore. A spark flashed in my mind: what if the direct interactions between these myeloid cells and the ectodermal cells weren’t just mere touching? What if the co-culture system reflected how these cells interact in vivo? What if being unable to separate these cells apart was a blessing in disguise? We subsequently showed that our explant system indeed preserved the natural development and cell-cell interactions of myeloid cells. We decided to leave macropinocytosis behind and refocus on the physical interactions between myeloid cells and the surrounding ectoderm. What if movement of the ectoderm could explain the striking radial movement of myeloid cells? What if this “tissue flow” could act as a guidance signal that myeloid cells could follow, much like a river could guide a moving boat? This question is exciting because much of cell migration research has been done on isolated cells moving on a matrix-coated dish. While this approach has revealed a lot about the fundamental mechanisms of cell migration, it lacks the physiological relevance found in vivo because it ignores a fundamental fact that in vivo cells are rarely, if ever, alone. These cells are always surrounded by other cells, yet the effect of cell-cell interactions on migration is often underappreciated. After manually tracking hundreds of myeloid cells, I noticed that their movement often followed that of the surrounding ectodermal cells. When the ectoderm retracted, the myeloid cells would often retract their protrusions. When the ectoderm jiggled, the embedded myeloid cells would jiggle in the same way. If we disrupted the movement of the ectoderm, this also impacted the movement of the myeloid cells. This observation was later supported by a correlation analysis and modelling by our in-house computational biologist Jonas Hartmann and an external collaborator, physicist Ricard Alert. However, to directly establish a causal relationship between the movement of these two cell populations, we needed a way to control ectoderm movement at will. This turned out to be the hardest but most crucial question to answer.
The first idea was to create a flow of viscous liquid on top of isolated myeloid cells. The literature suggested using polyethene glycol (PEG), as this has been used to compress cells in culture3. However, Xenopus explants did not like PEG and would peel themselves off the dish. The thick and viscous liquid was also a nightmare to control. This was out of the window. The next idea was to stretch the explants cultured on a sheet of PDMS. But stretching generated tension and would cause the tissue to rip apart and detach. The stretching needed to be constant and continuous over time, which would require the automation and engineering we did not have the capacity or resources for at the time. Another idea bites the dust. Then I thought: “If explants are too difficult, why don’t I go back to my roots and try with cell culture? Afterall, I was great at cell culture!” What if we co-culture an epithelial-like cell line such as MDCK with a macrophage line such as RAW264.7, then scratch a wound in the monolayer and watch the MDCK cells flood in to fill the gap; perhaps then we would be able to observe the macrophages moving along? These cells are easy to grow, so this sounds like an easy experiment! Well… it was not! One thing I didn’t anticipate was that the junctions between MDCK cells and their substrate adhesions were incredibly strong, so as the monolayer grew, they pushed out all the co-cultured macrophages, which were much less adhesive! No matter what I did, I couldn’t get these macrophages to intercalate into the MDCK layer to mimic the explant system. I gave up! Well, almost!
I have had this one idea of using optogenetics to control cell movement for a while, but the reason I was hesitant to pursue it was that even in cell culture, optogenetics is not straightforward, and to use it in an even more complicated system like Xenopus tissue did not sound like an idea one could simply play around with over a weekend. I would also likely have to express multiple mRNAs, which the embryos might not tolerate well. However, since every idea I tried so far failed, I really had nothing to lose, so I tried out seven different optogenetic systems I found online. The initial idea was that if I could locally activate a major driver of lamellipodia and cell migration, such as Rac1, then perhaps I could control ectoderm movement. Sadly, neither Rac1 activation nor any of its upstream regulators, Ras, EGFR, and FGFR, resulted in any collective movement of the ectoderm in our explant system. Six out of seven options failed, then there was one! The last optogenetic system was not targeting Rac1 but its counterpart, the RhoA protein. I reasoned that if a local cellular contraction was created, it could pull on its neighbours, and like dominoes, this would create a collective movement toward the centre of the contracting cell. If myeloid cells could sense this movement, they should respond by changing their direction of migration toward the contracting cell. While browsing Bluesky, I came across a system that could potentially do this: an eLife paper from the Joachim Goedhart lab4 (https://joachimgoedhart.github.io/index.html). The system has two components, a membrane-binding iLID-SsrA protein and a cytoplasmic SspB-RhoA-GEF. When activated with blue light, the SsrA peptide is released and binds SspB, which brings the GEF protein to the plasma membrane and activates RhoA to induce cellular contraction. After a bunch of cloning and testing for the right expression dosage, it was finally the day I got to see if my idea worked! And… it didn’t! I was confused, annoyed, and excited at the same time. I was excited because I could clearly see my optogenetic constructs expressed and the change in signal localisation upon activation, which meant my cloning worked! But I was frustrated to see no movement of the ectodermal cells at all! I slept on it for a week, and then one day, an idea came to mind: What if strong adhesions between the ectoderm and the substrate underneath were preventing the contraction-induced flow? I got to work on the idea the next day, injecting embryos and holding my breath for the experiment in two days’ time! On the day of the experiment, instead of plating these explants on a normal concentration of fibronectin, I cultured them on a diluted fibronectin surface to reduce their substrate adhesion strength. I waited until 9 pm to image them because overnight culture is not ideal when explants are grown under low-adhesion conditions. I gently clicked the computer’s mouse to start the illumination. Click…! My eyes widened. I remember sitting in the imaging room staring at the computer screen with my heart rattling and butterflies in my stomach, knowing I might have just solved a major question in my project. Low adhesion allowed the cells to move more easily, and I could see them shift position upon light activation; a moment later, the nearby myeloid cell turned its protrusion toward the contracting cell. I finished the experiment at 1 AM that day, but it felt like only half an hour had passed by! That day now belongs to my (small) collection of eureka moments! I then went on to show that this effect is conserved in vivo, and that was how my postdoc paper came to be5. We showed that local tissue movements could bias the protrusion dynamics and directionality of nearby embedded immune cells through direct cell-cell interactions, a phenomenon we called “collective-assisted directional migration”. This experiment has that same defining effect as the moment I first observed the localisation of the protein CYRI-A on macropinosomes during my PhD6, but this can be a story for another time! Collective-assisted directional migration might have been observed in other systems too, including melanocytes spreading in mouse embryos (personal communication), and bipolar cell movement during eye development7. Beyond development, this phenomenon might be relevant during wound healing, when local tissue mechanics change, or during collective invasion in cancer.
A. The optogenetic system to activate RhoA. B. How contraction-induced tissue flow biases a nearby immune cell’s protrusion.
One final thought
To me, this project has been the definition of being curiosity-driven. There are many more moments that would make a good nerdy story time over drinks, but I want to give my biggest thanks to my boss, Roberto Mayor, who gave me complete freedom to explore and lead this project. From someone who had many big dreams but was always scared of never getting there (and was absolutely terrified of frogs) to someone who is much more confident to dare to dream bigger, that is how working in Roberto’s lab has changed me. I also want to thank each of my lab mates and all the friends I have made along the way, who have made my life in London much less lonely, being so far away from my family in Glasgow and Vietnam. They truly are the best bunch of people in life for free. And of course, if you know me well, you would know that it wouldn’t be my piece without me thanking Taylor Swift and her amazing music catalogue that pulls me through some of the hardest days! I also hope that I will be able to continue with this line of research into the biomechanics of immune cells within native tissue. Even just a simple video of immune cells migrating through ectodermal cells contains so much biology to be discovered, and I cannot wait to dive deeper into it, either through an organoid approach or another model system like the zebrafish!
And to the younger scientists who are still reading, if I have to give you a few pieces of advice: connect with people in your field, whether it’s online or in person; you never know when you’ll need their expertise; don’t be afraid to take the risk because you never know where it will lead you; learn to adapt, learn to change, let the science guide you; and finally, be like water!
References
1. Costa, R. M. B., Soto, X., Chen, Y., Zorn, A. M. & Amaya, E. spib is required for primitive myeloid development in Xenopus. Blood112, 2287–2296 (2008).
2. Costa, R., Chen, Y., Paredes, R. & Amaya, E. Labeling Primitive Myeloid Progenitor Cells in Xenopus. in Progenitor Cells: Methods and Protocols (eds Mace, K. A. & Braun, K. M.) 141–155 (Humana Press, Totowa, NJ, 2012). doi:10.1007/978-1-61779-980-8_11.
3. Bera, K. et al. Extracellular fluid viscosity enhances cell migration and cancer dissemination. Nature611, 365–373 (2022).
4. Mahlandt, E. K. et al. Opto-RhoGEFs, an optimized optogenetic toolbox to reversibly control Rho GTPase activity on a global to subcellular scale, enabling precise control over vascular endothelial barrier strength. Elife12, RP84364 (2023).
5. Le, H. A., Hartmann, J., Alert, R. & Mayor, R. Tissue flow acts as a guidance cue for immune cell polarization and directional migration. Nat Cell Biol28, 2008–2026 (2026).
6. Le, A. H. et al. CYRI-A limits invasive migration through macropinosome formation and integrin uptake regulation. Journal of Cell Biology220, e202012114 (2021).
7. Cruz, M. R., Paixão, T., Coelho, J. & Norden, C. Tissue lamination state switches neuronal translocation from active to passive in the vertebrate retina. Preprint at https://doi.org/10.64898/2026.07.02.736014 (2026).
We offer a YBDTP-funded PhD project (co-supervised Mehmet UCar) aiming to investigate how cells which differ in identity are able to move together. A very important process for both the development of an animal and cancer metastasis! This project is highly interdisciplinary and will combine multiphoton confocal imaging, quantitative image analysis, genetic and laser perturbation with mathematical modelling. Start=October 2027, deadline=6th January 2027). Find out more check out the Campbell lab and apply here.
PhD position available on cattle genetics in the Mort lab! Exciting collaboration with Davina Hill (University of Glasgow) and Barbara Shih (Lancaster University). Help us develop better approaches to understand pigmentation genetics in dairy cattle and build resilience to climate change.
Temporal cascades are conserved in different neuronal lineages in flies
Neural patterning is vital to ensure the correct birth order of neuron types during brain development. In Drosophila melanogaster, intermediate neural progenitors (INPs) and optic lobe neural stem cells (OL NSCs) give rise to the central brain and visual system, respectively. Despite their different origins and cell lineages, the temporal cascades of INPs and OL NSCs share similarities, there remain gaps in the INP temporal cascade. Jocelyn Tang, Alex Donovan, Andrea Brand and colleagues use Drosophila larval brains to show that the nuclear hormone receptor Tailless (Tll) has a conserved function as a terminal temporal factor across these two cell lineages. They use genetic approaches to show that Tll is expressed in late INPs and acts as a terminal temporal factor in the cascade, as in the optic lobe. They show that the preceding temporal factor Scarecrow (Scro) activates tll expression, and that Tll represses Scro, showing cross-regulation and defining a temporal window. Tll also represses lineage progression factors hamlet and odd-paired and promotes gliogenesis. Finally, genome-wide binding analysis shows that Tll plays a similar regulatory role during the temporal cascades of INPs and OL NSCs, but also context-specific roles across these neural lineages. Altogether, this study shows that temporal cascades are conserved in different neuronal lineages.
Here we talk with co-first authors Jocelyn Tang and Alex Donovan.
Jocelyn Tang (left) and Alex Donovan (right).
How did you come to work in the lab and what drives your research today?
Alex: During my PhD, I worked on the roles of chromatin remodelling factors in neurodevelopment, which sparked an interest in the epigenetic and gene-regulatory mechanisms that drive development. Towards the end of my studies, Andrea came to give a talk about new DamID methods that her lab had been developing. I was really drawn to these, as their modularity and flexibility could help me answer many of the questions around transcriptional and epigenetic regulation that I had found difficult to get at using the techniques I was working with at the time. I emailed Andrea and after a trip to Cambridge to meet the lab, she offered me a position. Alongside projects in flies, I went on to adapt many of these DamID technologies into systems compatible with human in vitro models, focusing broadly on questions relating to cellular competency and cell state transitions during development.
Jocelyn: I joined Andrea’s lab as a PhD student and was very interested in the topics of neural stem cell quiescence and temporal patterning. I was fascinated by the genetic versatility of Drosophila and the sophisticated experiments you could do with the model. Curiosity drives my research – since my PhD, my research interests have transitioned to studying non-autonomous signalling during neural stem cell quiescence and reactivation, as well as studying developmental mechanisms in the context of tumourigenesis (particularly in glioblastoma).
Can you tell us about the background of the field that inspired your work?
Over the past couple of decades, numerous labs have been steadily uncovering the complex gene-regulatory relationships that underlie the capacity of neural stem cells to change the identity of their neuronal or glial progeny over time. This process of temporal patterning has been particularly well studied in Drosophila neural stem cell lineages, which each have their own cascade of transcription factors that switch on and off over the course of neurodevelopment. In this study, we continue this long tradition of piecing together cross-regulatory relationships of temporal transcription factors, in a less well-defined neural stem cell lineage.
What are the key results of the paper?
The main finding of this paper is that the nuclear orphan receptor Tailless (Tll), is expressed at the end of the intermediate neural progenitor (INP) temporal cascade, mirroring the optic lobe temporal cascade. Tll contributes to the regulation of INP proliferation, with partial effects on gliogenesis. It also functions as a canonical temporal factor, where it is activated by the preceding factor Scarecrow (Scro) and, in turn, represses scro expression. What is interesting is that Tll has diverging roles: it is expressed in the Type II neural stem cells (NSCs) which produce the INPs, where it maintains stemness and cell identity, but in INPs, Tll serves as a marker for the end of the temporal cascade and termination of proliferation. Using a combination of Targeted DamID and NanoDam, we profiled the genome-wide binding targets of Tll in different cell types (Type II NSCs, INPs and optic lobe NSCs), revealing that binding patterns were broadly similar. This suggested that the divergent role of Tll in different cell types may stem from additional cofactors or differences in chromatin accessibility. We also identified an interesting evolutionary observation, in which many of the mammalian orthologues of Drosophila temporal factors define spatial domains in the developing mouse cortex. While temporal patterning is not as readily observed in the developing mammalian brain, the same factors serve to establish spatial patterning instead.
When doing the research, did you have any particular result or eureka moment that has stuck with you?
The eureka moment was actually the start of this research project – we were planning on using tailless mRNA expression as a marker for the Type II NSCs for a different experiment at the time, but when we did the HCR, we noticed that there was always a bit of signal where the INPs were. We initially dismissed this, thinking that maybe the probe we were using was giving a bit of background signal, as all prior literature had reported that tailless was only expressed in Type II NSCs. However, as we were imaging brain after brain, the signal we saw was so clean and consistent, we began to think: “What if this is a real signal?” Once we managed to confirm its expression in the INPs, the project started taking shape quickly, as our previous paper on the INP temporal cascade noted there were actually a lot of similarities between the temporal cascades of the larval optic lobe and the central brain. Based on our observations, identifying the experiments that we wanted to do was swift. It was very satisfying to further add and expand on the observations of our previous work.
Why did you choose to submit this paper to Development?
Development has always been one of the best places to find papers in developmental biology, so the choice was easy!
What is next for you after this paper?
Alex: I am currently continuing on with my interest in gene-regulatory mechanisms in neurodevelopment with an evolutionary twist in Madeline Lancaster’s lab at the LMB in Cambridge.
Jocelyn: I will continue my postdoctoral work in Andrea Brand’s lab, shifting my focus to understanding niche interactions in neural stem cell behaviour during both development and tumourigenesis. I will continue working with Drosophila, but my research has also extended to using human organoid models and patient-derived tumour cell lines.
What do you enjoy most about research, and why?
Alex: I love picking things apart to understand the exact mechanisms of how they work, which probably comes from the massive amount of time I spent as a child taking electronics apart and putting them back together again (sometimes to the dismay of my parents).
Jocelyn: I think science is sometimes a bit like detective work – putting pieces of evidence or observations together, some seemingly unrelated and coming up with surprising findings is always very exciting. The most enjoyable part of research for me is also sometimes the most uncertain – you can start answering one question and by the end be reading about an entirely different field from your own – you’re constantly learning, and research keeps you on your toes.
Let’s move outside the lab – what do you like to do in your spare time?
Alex: I love to travel and spend time outdoors hiking, running and climbing. When indoors, I spend my time going to contemporary art exhibitions, reading sci-fi novels, playing probably too many games and most importantly, sleeping.
Jocelyn: I have recently developed an interest in pottery and have been honing my skills at the wheel. I used to go horse riding often but now since I have moved to America, I have combined this hobby with a fascination in cowboys and the Wild West. Yeehaw!
Tell us something interesting about yourself that wouldn’t be on your CV.
Alex: I used to be a competitive fencer and competed all over the world with the national team.
Jocelyn: I love reading about fashion history and know excessive details about 17th-century fabrics.
Job offer: Postdoc candidate (3 years) (deadline contact November 12th)
Cristian Cañestro’s lab at the University of Barcelona is seeking motivated postdoctoral candidates to apply for the Juan de la Cierva 2026 fellowship, funded by the Spanish Ministry of Science, Innovation and Universities, to join our newly granted project PID2025-170547NB-I00, “Gene loss impact: evolution of cardioparaxial-neuromesodermal development and genome scrambling in Oikopleura dioica as a case study” (OikoLoss).
REQUIREMENTS AND PROFILE OF CANDIDATES:
According to the Juan de la Cierva 2026 call:
Applicants must have obtained their PhD between 1 January 2024 and 31 December 2026, with specific extensions or exceptions under the official regulations.
Applicants of any nationality are welcome, provided they meet the eligibility requirements of the programme.
We particularly welcome candidates with research interests in evolutionary developmental biology, comparative genomics, genomic structural variation, bioinformatics, and population genetics. Expertise in single-cell omics will be considered an additional asset.
THE PROJECT:
OikoLoss investigates how gene loss can drive evolutionary innovation. Using the chordate Oikopleura dioica as a natural “evolutionary knockout” model, the project integrates EvoDevo, functional genomics, single-cell transcriptomics, population genomics and ecology through two complementary aims:
Aim 1. To determine how massive gene loss has reshaped heart, axial muscle and neuromesodermal development in chordates, using single-cell omics, gene-expression analyses and functional experiments.
Aim 2. To uncover how genome scrambling and chromosomal breakpoints generate gene-loss alleles, and to assess their potential adaptive impact under different ocean environmental conditions.
The successful candidate will contribute to the project according to their expertise and research interests, with opportunities to develop independent research directions within its scientific framework.
RESEARCH TECHNIQUES:
The project combines experimental and computational approaches, including embryo culture and manipulation, microinjection, CRISPR knockouts, interference-based knockdowns, HCR whole-mount in situ hybridization, confocal microscopy, single-cell RNA sequencing, PacBio HiFi long-read genomic sequencing, comparative and population genomics, and bioinformatics.
TRAINING AND INTERNATIONAL COLLABORATIONS:
The successful candidate will join a multidisciplinary research environment at the University of Barcelona, with opportunities to interact with international collaborators and undertake research stays, particularly at OIST in (Okinawa), IGFL (Lyon), SARS (Bergen), Imperial College (London) and CRG (Barcelona).
Funding: €35,700 per year to co-finance gross salary and employer Social Security contributions. The final salary and ent conditions will follow the applicable University of Barcelona regulations.
Additional research funding: €15,000 for research-related expenses over the fellowship.
Selection: Competitive national evaluation based on the candidate’s scientific track record and the quality of the host team.
DEADLINES AND APPLICATION TIMELINE
Expressions of interest and pre-selection are NOW OPEN. Early contact is strongly encouraged.
12 November 2026: Official application period opens.
26 November 2026, 14:00 CET: Deadline for candidates to complete their application forms.
Because of the short application window, interested candidates are strongly encouraged to contact us as soon as possible (before November 12th) to allow sufficient time for evaluation and preparation of the application.
CONTACT and PRE-SELECTION:
Interested candidates should email Cristian Cañestro at canestro@ub.edu, attaching a single PDF containing:
A motivation letter describing their research interests, relevant experience and reasons for joining our laboratory.
An updated academic CV, including date of their PhD award or expected PhD defense, publication record, research experience and technical expertise.
Shortlisted candidates will be invited to an online interview. Pre-selection process will follow principles of equal opportunity and non-discrimination, with particular attention to promoting gender balance.
Further information, related publications and updates:
Inspiration for scientific research projects can come from many unexpected places. With the publication of my second PhD research paper [1], I am looking back at my sources of inspiration as well as some hurdles I had to overcome to see this work come to fruition.
As a PhD student at the Stowers Institute for Medical Research in Kansas City, I was going through the first semester trying to absorb as much information as possible while deciding on my rotation labs. I had decided on my first rotation in the lab of Dr. Scott Hawley very quickly after joining the program. The esteemed Drosophila geneticist was particularly enthralled by the synaptonemal complex, a multi-protein structure that assembles between the maternal and paternal copy of each chromosome in early meiosis (Fig. 1). This structure is crucial for the formation of crossovers between these homologous chromosomes and thereby ensures proper chromosome segregation and fertiltiy (Fig. 1). Apart from this fundamental function, I was fascinated by the fact that this massive proteinaceous structure is able to assemble across the entire length of chromosomes.
As is common at many research institutes, we regularly heard seminar talks from researchers coming to us from all over the world. One of these presentations was given by Dr. Catriona Munro, a scientist who studies meiosis in the jellyfish Clytia hemisphaerica [2]. Previously, I hadn’t really considered the possibility of doing research with unusual organisms like jellyfish. For my bachelor’s thesis in Germany, I did strictly in vitro work. For my year-long research stint at Purdue University in the US, I worked with Drosophila melanogaster. All fairly standard research systems. Seeing that someone performed systematic studies using a jellyifsh was truly fascinating and unexpectdely paved the way for my own future research.
Shortly after this talk, I heard from Dr. Matt Gibson at the Stowers Institute about his lab’s research using the sea anemone Nematostella vectensis. His research team investigates various kinds of fundamental biological questions ranging from how stinging cells in cnidarian species function [3] to neuroscience [4] and Hox-mediated segmentation during embryogenesis [5]. What particularly caught my attention was the fact the Nematostella is relatively large and that each adult has eight gonads that took up the majority of the animal’s body mass. Immediately, I thought that this would make a pretty good meiosis model organism. Scott had previously told me that most meiosis models come with the difficulty that meiotic material is fairly limited. This certainly wouldn’t be a problem with Nematostella.
After I went home for the day, I googled whether anyone was doing research on Nematostella meiosis and its synaptonemal complex. I was surprised to find that research on cnidarian meiosis in general was quite sparse. When it came to the synaptonemal complex, almost 10 years ago a research team in Germany had identified specific protein homologs in the related cnidarian species Hydra vulgaris [6]. In addition, Catriona had looked at the synaptonemal complex in Clytia briefly as part of her research [2]. Other than that, there was no systematic research being done in this area. Considering the importance of the synaptonemal complex for the maintenance of an organisms’ fertility, I was convinced that we needed to understand how it functions in cnidarians. Particularly, as cnidarians like corals are facing tremendous challenges to their fertility. I gathered my scientific curiosity and courage to email Scott and Matt, proposing a research project on studying the conservation of synaptonemal complex proteins in Nematostella. The answers came quickly: Scott absolutely loved the idea. Considering his lab’s newest research with the silk moth Bombyx mori [7] which had quite an unusual synaptonemal complex, he practically couldn’t wait to learn about what novelties the Nematostella equivalent could reveal. Matt was similarly intrigued by this new research direction and my enthusiasm for cnidarian research.
Once I completed my three lab rotations, I decided to pursue my PhD thesis research co-mentored by Scott and Matt. My particular focus was to study whether the architectural functions of Nematostella synaptonemal complex proteins were conserved. Curiously, synaptonemal complex proteins exhibit rapid sequence divergence, despite their crucial function in ensuring meiotic success throughout eukaryotes [8]. As a result of this divergence, it was actually surprising how easy the identification of protein homologs of vertebrate synaptonemal complex proteins in Nematostella was. Most protein homologs were already identified by other researchers but I was able to expand these findings [1]. Now we needed to try and figure out whether these proteins actually function in the same way as they did in other organisms. Considering that the synaptonemal complex consists of three distinct structural elements (Fig. 2), I wanted to generate three individual mutants each disrupting one of these elements. This would allow us to understand the functional importance of each element as well.
Fig. 2: The synaptonemal complex consists of distinct structural compartments. The lateral elements are connected to the chromosomes respectively. In the central region, a central element with distinct structural components is found. The transverse filaments span the entire width of the synaptonemal complex. Adapted from [1]
While Nematostella has quickly become my favorite laboratory model, one of the major downsides of working with it is the relatively long generation time of roughly 3 months. This meant that I was raising animals and making crosses for over a year with mutants I had no idea would show any interesting phenotypes. In the meantime, I established necessary tools to study meiosis and the synaptonemal complex in this model, allowing me to investigate the wild-type structure. Some techniques that I had to adapt was preparing chromosome spreads of meiotic and mitotic stages (Fig. 3). During this time, I also worked on a second project investigating the synaptonemal complex in Drosophila species, which you may learn more about here.
Fig. 3: Chromosome spreads enable to visualization of chromosomes and synaptonemal complexes in meiosis (A) – (B) and mitosis (C). (A) Chromosome spread from a male Nematostella individual at pachytene of meiosis I. The stained synaptonemal complexes are shown with SYCP3 (lateral element) in magenta and SYCP1 (transverse filament) in yellow. (B) Chromosome spread from a female Nematostella individual. (A’) and (B’) are schematic representations of what can be seen in the above image. (C) Mitotic chromosome spread at metaphase of a 64-/128-cell stage embryo with DNA visualized in grey. Adapted from [1].
Unfortunately, in my case, this long waiting period also meant that my co-supervisor Scott passed away only one month before I was able to start working with the homozygous mutant adults I had established and raised. His death was not only felt deeply because of the sudden loss of scientific support but also because he was so much more than just a scientific supervisor to so many people – including me.
Once I was able to exit the sudden stupor that Scott’s death led me into, I began investigating my homozygous mutants. The three Nematostella proteins I mutated shared approximately 30% of sequence identity with their vertebrate orthologs. While this may seem very low, it is worth emphasizing that orthologous proteins between vertebrates and Drosophila, for example, share no identifiable sequence homology. Thus, I hypothesized that the Nematostella synaptonemal complex proteins and their architectural functions are fully conserved in comparison to vertebrates. First and foremost, this meant that each individual protein component is essential for the successfull assembly of the synaptonemal complex. Thus, I definitely thought I must have made a huge mistake when my first microscopy session on one of my mutants’ chromosome spreads showed no significant assembly defects (Fig. 4). As it turns out, it was not a mistake but the fact that this particular protein is not essential for synaptonemal complex assembly in Nematostella males. Looking at all three of my synaptonemal complex mutants, I was able to reveal that some architectural functions of synaptonemal complex proteins in Nematostella are distinct from those found in vertebrates and, additionally, exhibit dramatic sexual dimorphisms.
Fig. 4: Example image of meiotic pachytene-like chromosome spreads from syce2 mutant Nematostella individuals. (A) synaptonemal complexes from a syce2 mutant male. SYCP3 (lateral element) is shown in magenta, SYCP1 (transverse filament) is shown in yellow. (B) synaptonemal complexes from a syce2 mutant female. (A’) and (B’) are schematic representations of what can be seen in the microscopy images. Adapted from [1].
While these findings by themselves were deeply fascinating, I also wanted to understand the functional relevance of the synaptonemal complex and its protein components on overall fertility and chromosome segregation. While a TUNEL assay was supposed to provide me with a quick answer to the question whether spermatocytes were undergoing increased rates of cell death (hinting at meiotic checkpoint activation), this experiment turned into a 6-months long ordeal of troubleshooting and protocol optimizations. Nonetheless, I persevered and was able to confirm that even those proteins that appeared to be non-essential for synaptonemal complex assembly were necessary to ensure proper meiotic progression. Taken together, it became clear that the synaptonemal complex in Nematostella was quite distinct in its architectural composition when compared to vertebrates. The sexual dimorphisms I observed further complicated this picture but made it all the more intriguing.
When I envisioned this research project, I could have never foreseen where this work would go. Practically all my hypotheses were proven wrong. In addition, I discovered a research interest that follows me into my current postdoc and likely beyond. By establishing Nematostella vectensis as a model for investigating meiosis, this work now opens the door to exploring how the mechanisms that ensure reproductive success have evolved across animals. As this work is the first systematic investigation into how cnidarian synaptonemal complexes funciton mechanistically, this also paves the road to understand how fertiltiy is ensured in these basal metazoans. Considering that Nematostella is closely related to corals, this work further has important implications for coral sexual reproduction. Altogether, this research paper is the product of a lot of sweat and tears but I could not be prouder and happier to see its publication and I cannot wait to see what else I will learn about cnidarian reproduction.
References
[1] Stefanie Williams, Jennifer Gardner, Stephanie H. Nowotarski, Matthew C. Gibson. The Nematostella synaptonemal complex mediates divergent and sexually dimorphic meiotic programs. Science Advances Volume 12, Isse 43, eaei0758 (2026). https://doi.org/10.1126/sciadv.aei0758
[2] Catriona Munro, Hugo Cadis, Sophie Pagnotta, Evelyn Houliston, Jean-René Huynh. Conserved meiotic mechanisms in the cnidarian Clytia hemisphaerica revealed by Spo11 knockout. Science Advances Volume 9, Issue 4, eadd2873(2023). https://doi.org/10.1126/sciadv.add2873
[3] Ahmet Karabulut, Melainia McClain, Boris Rubenstein, Keith Z. Sabin, Sean A. McKinney, Matthew C. Gibson. The architecture and operating mechanism of a cnidarian stinging organelle. Nature Communications Volume 13, 3494 (2022). https://doi.org/10.1038/s41467-022-31090-0
[4] Ruohan Zhong, Chris W. Seidel, Anna M. L. Klompen, Matthew C. Gibson. Morphological, molecular, and functional evidence for a CNS-like oral nerve ring in the sea anemone Nematostella vectensis. bioRxiv 2026.01.28.701697; doi: https://doi.org/10.64898/2026.01.28.701697
[5] Shuonan He, Florencia Del Viso, Cheng-Yi Chen, Aissam Ikmi, Amanda E. Kroesen, Matt Gibson. An axial Hox code controls tissue segmentation and body patterning in Nematostella vectensis. Science 361,1377-1380 (2018). https://doi.org/10.1126/science.aar8384
[7] Youbin Xiang, Dai Tsuchiya, Zulin Yu, Xia Zhao, Sean McKinney, Jay Unruh, Brian Slaughter, Cathleen M. Lake, R. Scott Hawley. Multiple reorganizations of the lateral elements of the synaptonemal complex facilitate homolog segregation in Bombyx mori oocytes. Current Biology, Volume 34, Issue 2, p352-360. (2024). https://doi.org/[10.1016/j.cub.2023.12.018](https://doi.org/10.1016/j.cub.2023.12.018)
This post is co-authored by Dante Albino Idesti and Larissa de Moraes Chiarelli
One hundred years ago, in 1926, Thomas Hunt Morgan published The Theory of the Gene, a landmark work that consolidated the physical basis of heredity and forever changed the landscape of modern biology. To celebrate this centenary, researchers and students gathered with the public on the evening of October 22, 2026, at the Exploratory Science Museum of the University of Campinas (UNICAMP), in Campinas, Brazil, for a special outreach event combining science, history, and cinema. Designed as an open and free Cine-Debate for the general public, the initiative built a bridge across three core pillars: the historical centenary of the gene concept, the enduring legacy of Drosophila melanogaster as a model organism, and the role of science museums as democratic spaces for public engagement. Bringing the “Fly Room” to the Science Museum For many outside academia, genetics can feel abstract and distant from everyday life. Hosting the event at UNICAMP’s Exploratory Science Museum allowed us to step outside the traditional walls of our research laboratories and invite the local community into an interactive, welcoming environment and open conversation (UNICAMP news). The evening began at 7:00 PM with a brief historical contextualization introducing Thomas Hunt Morgan, the early days of chromosomal research, and the tiny fruit fly that became one of biology’s most powerful allies. This set the stage for the screening of Alexis Gambis’s feature film The Fly Room (2014). Told through the eyes of ten-year-old Betsey as she spends a day in the genetics laboratory of her father, Calvin Bridges (one of the key pioneers in Morgan’s group at Columbia University) the film offered the audience an intimate look into both the scientific breakthroughs and the complex human dynamics behind the birth of modern genetics. Throughout the screening, the sensory imagery of the flies and the delicate father-daughter narrative captivated attendees, bridging the gap between historical science and everyday emotion.
Exhibit poster of the movie night showing the The Fly Room at the Exploratory Science Museum, in celebrationg of 100 years of “The Theory of Gene” by Thomas H. Morgan.
“From Flies to Genes: 100 Years of a History That Transformed Biology”
Following the screening, the evening transitioned into a lively roundtable discussion. The panel was intentionally assembled to reflect how the foundations laid in Morgan’s fly room have branched out across generations, model organisms, and biological scales at UNICAMP: Prof. Dr. Guilherme Oliveira Barbosa, a researcher in the Fly Lab at UNICAMP’s Institute of Biology. Holding a PhD in Cell Biology, Guilherme investigates morphogenesis using Drosophila melanogaster and actively works in science education and public outreach. He anchored the discussion in the day-to-day reality of working with fruit flies today and how basic developmental questions continue to drive discovery. Prof. Dr. Vera Nisaka Solferini, a leading reference in genetics and evolutionary biology in Brazil. Whose research explores the historical biogeography of Neotropical biomes and the adaptive processes driving biological diversification, Vera expanded the conversation from the classic laboratory bottle to natural populations and evolutionary history. Gustavo Seguchi, a Master in Genetics and Molecular Biology from UNICAMP and current PhD candidate at the Laboratory of Genomics and bioEnergy (LGE), where he studies the potential of non-conventional yeasts for biofuel production from diverse biomasses. Gustavo brought the perspective of early-career researchers applying century-old genetic principles to modern genomic and biotechnological challenges.
Prof. Vera N. Solferini, Gustavo Seguchi and Prof. Guilherme O. Barbosa sharing their perseption of classic genetics to modern perspectives based on their current research. Dante Albino Idesti (in the back) was the host of the night.
Bridging Past and Present: The Human Side of Science
During the conversation, the speakers unpacked the scientific and historical nuances portrayed in The Fly Room, sharing behind-the-scenes curiosities of working with Drosophila and tracing how the concept of the gene evolved over the last century — from classical linkage maps to modern developmental biology, evolutionary ecology, and synthetic genomics. The dialogue with the audience flowed naturally, sparked by curiosity about how routine work with tiny model organisms translates into major biological concepts. Towards the end of the discussion, Dr. Guilherme Barbosa offered a poignant reflection that captured the spirit of the entire evening. He highlighted how powerfully the film portrays the human side of scientists, reminding everyone that researchers are not detached figures isolated in lab coats, but ordinary people driven by the same wishes, passions, insecurities, and desires as anyone else, and that these personal realities inevitably intertwine with and shape their scientific work. Looking back on the evening, celebrating the centenary of The Theory of the Gene through cinema proved to be an inspiring way to demystify academic research. By bringing Drosophila out of the lab and onto the big screen at the Exploratory Science Museum, the event reminded both seasoned researchers and first-time visitors that the history of genetics is not just a collection of textbook facts, but an ongoing, deeply human story fueled by curiosity.
The Fly Room, movie night at the Exploratory Museum of Science (PROEEC-UNICAMP), Campinas-Brazil (1 votes)
To mark International Open Access Week 2026, The Company of Biologists has been reflecting on this year’s theme: ‘The Cost of Knowledge’.
In our latest blog post, ‘The true cost of knowledge: exploring value in publishing‘, we reflect on what researchers value in publishing and who bears the cost of creating that value. We also discuss how, through initiatives like Biology Open’s Fast & Fair peer review, we are continuing to innovate to improve the author experience.
During August, we ran a writing challenge, giving contributors to the Node a chance to win £200 for publishing a blog post on our website. We really appreciate the effort that all of our contributors put into sharing posts on the site, and we hoped that the challenge would help motivate and encourage writers to share their ideas. The Node is a community for all, regardless of experience, background, skills or career stage. For this reason, we decided to award the prize by randomly selecting the winner rather than a competitive format. We hope this approach reassured authors to share on the Node without apprehension that their work would be judged.
The winner of our writing challenge was Bill Hinchen with the post ‘The little beach hopper that could’. This entry explores the story of the unsung hero, the beach hopper. Check out our interview with Bill.
Bill Hinchen
Tell us about yourself.
I’m a freelance science writer and copywriter, working mostly for those in the biotech industry. They have cool science but struggle to get that across to clients or the public, and I can understand the science well enough, and write well enough, that I can bridge that gap. I’m a wordy bridge, essentially. I started writing back in 2011, and went freelance in 2019, but before all that I was in a lab at Cambridge poking crustacean embryos to see what on earth cells are doing in the stages leading up to gastrulation.
Can you describe your research journey?
My first taste of proper research was at the University of Plymouth, where I was looking at copper-induced neurotoxicity in catfish. I’d always loved ecotoxicology, and with a marine biology background, it was a perfect step into research. I quickly realised that having the lab to myself, with experiments to plan, failures to recover from and just a whole world of independence afforded to me, research was the one.
From there I started a PhD at Cambridge with Cassandra Extavour in the lab of Michael Akam. Bit of a subject shift, for sure, but dev bio was another thing I was always in awe of (after looking at On Growth and Form, by D’arcy Wentworth Thompson – go read it!) and I’m not a fan of limiting myself to one topic forever.
Starting out felt like the very deepest of deep ends and I had lead weights made of solid imposter syndrome tied around my ankles. But, I eventually settled and got into the swing of things, from peeling Parhyale embryos with tungsten needles under the microscope, to running endless antibody stains on the hunt for beta-catenin and finally into making lots, and lots and lots of 4D time-lapse movies of these embryos. By the end, I felt fully confident about how research works, and, like anyone studying something long enough, just how little I knew in the grand scheme of things!
After that, I spent a short spell in a biophysics lab with Susan Cox at King’s College London. They needed someone who could work with embryos for a microscopy experiment they were running (controlled light exposure microscopy), so I jumped in. Absolutely incredible! I had to pick up C. elegans embryology super quick and work alongside some brilliant physicists. It’s rather impressive how much our academic backgrounds didn’t overlap! But interdisciplinary research is a true joy, and I encourage everyone to get out of their comfort zone and go get cosy with other scientists from other fields.
What does Parhyale hawaiensis mean to you on a personal level? What inspired you to write this story?
I’ve been a science writer for a long time now, and a common theme in what a lot of folks are saying is just how much their work is going to “accelerate innovation”, cause a “paradigm shift” or some other hyperbolic marketing sentiment. 99% of the time it’s not true, but the emphasis on practical, tangible outputs that will have a huge impact is consistently (over)stated.
Parhyale for me is plain old humble. It’s a tiny little crustacean that looks a bit like a shrimp and at the time, was worked on by just a handful of people who all knew each other on a first-name basis. It wasn’t claiming to change the field or revolutionise medicine; it just had some cool embryos that were amenable to experimental manipulation. But because of its flexibility, it was slowly adopted by a new lab, then another, then another, and then it suddenly crossed disciplines. Such an innocuous little critter, making no grand claims, but being used to develop new tools and answer new questions by new scientists from new fields – like a tiny little baton of research. And all without the fanfare that usually accompanies this sort of thing. I like that.
How did you pivot from research to science writing?
Honestly, it was an accident. Academia was the only career I ever wanted, but that all went a little awry and I needed work. Someone suggested medical writing, which I’d never heard of, and the rest is history.
What are your favourite things about your career as a scientific writer?
As a freelance writer, it’s freedom. I don’t have to waste time in meetings or fill my time with pointless jobs just to keep busy during the day. I take on clients I like, I write in bursts, take my son to and from school and go surfing when the waves look good. Being able to choose my own schedule and my own clients has been my favourite aspect of this by far.
But in general, I’d say it’s dipping my toes in all the different fields of biology. Admittedly, sometimes it feels a little shallow because it’s always someone else’s research, and I don’t think I’ll ever not want to be at the bench, but it can be fascinating to read and write about something you’d never even considered up until you start researching it!
Do you have any advice for researchers who are interested in a career in science writing?
Figure out the type of writing you want to do. Do you want to translate science for the public, or do you want to help companies articulate the benefits of something? Do you want to do journalism or editing? Once you’ve got an idea, start doing it. Start on a blog or LinkedIn and start putting your writing goal into practice. Show people your voice – don’t waste your time trying to sound professional, just be honest. Also, read the terrible things people write across their webpages and write about why they’re wrong and what you’d do differently! I kid you not, in no time at all you’ll have a better understanding of what not to do when it comes to science writing.
Where can people find other pieces written by you?
Want to take Bill’s advice about writing? The Node, as well as our other community sites, preLights and FocalPlane, give you a place to share your writing and provide a network that supports you through the writing process. With this in mind, please reach out to any of our Community Managers if you would like to discuss any ideas or drafts for the sites, or if you would like to join the preLights community team. In addition to written posts, the Node welcomes other types of audio or visual communication, including images, illustrations and videos. With challenges such as this one, we also want to remind our readers and authors that anyone can write and publish a blog, and you don’t need an invitation to do so.
