With one week to go until Biologists @ 100, we can’t wait to see everyone there! Do you want to know more about the conference venue, the social events and where to find out more about the programme? Together with preLights and FocalPlane, we’ve recorded a video to walk you through the practicalities of the conference.
First-time conference attendee? Not sure what to prepare? Check out this ‘Beginners’ Guide to Scientific Conferences‘ from Jen Annoh, who will be attending the conference as a reporter for the Node, focusing on the cell and developmental biology scientific track of the programme.
Full transcript
Hi, I’m Helen, and I’m the Community Manager of FocalPlane.
Hello, I’m Joyce, I’m the Community Manager of the Node.
Hi. My name is Reinier, and I’m the preLights Community Manager.
We’ve made this short recording to tell you about our upcoming conference, Biologists @ 100. We’re really excited to have you join us for this special conference celebrating our 100th anniversary, and we hope that this recording helps you make the most of your experience. Let’s dive in.
So, starting with the venue. Biologists @ 100 will be at ACC Liverpool. On our conference website, you’ll be able to find all the information about travel and travelling to the conference venue. The ACC Liverpool entrance is actually not facing the river, so if you see the river, the entrance of the ACC Liverpool is on the other side. Hopefully this photo will help you to find how to get into the conference venue. There is an atrium where you enter and collect your badge.
The main auditorium is where most of the plenary talks will happen. Then the catering, exhibition and posters, will all happen in the big hall called hall two, which is in the basement. There will be lunchtime sessions held in a small theatre inside this hall. A little bit more about the exhibition hall; you will be able to find out more about the Company at our stand, and you’ll also be able to visit all the sponsor booths. Around the conference venue, you’ll find some discussion tables where you can tell us about your views on the future of publishing and help shape our journals. In the exhibition hall, there will be a sustainability area where you can find your tree in the Forest of Biologists, if you’ve ever published or reviewed for us, and you can chat to people and give suggestions about making science more sustainable. There will also be an image gallery, displaying images from the Node and FocalPlane image competition, and you’ll be able to vote for your favourite image.
As Joyce mentioned, there will be lunchtime lectures. The first one will be on Tuesday, called climate change challenges and solutions in biology. The panellists are passionate about this topic and will tell us a bit more on how to integrate sustainability in our day-to-day work. Do make sure to check it out. On Wednesday, we have a talk from Katherine Brown, Executive Editor of Development. She’ll talk about scientific publishing, and specifically, the future of scientific publishing. Then on Thursday, it will be the three of us talking about the community sites, what we do, and how you can get involved. So, please do drop by if you have any questions.
You can find us quite easily because we’ll be wearing these beautiful T-shirts. Also, we’ll have lime-green lanyards, as will our colleagues. So, you should be able to find those quite easily. Also, you’ll be able to see our conference reporters walking around the venue. They are representing the different community sites. There’s three of them, so it’s Jen, representing the Node, Jonathan for preLights and Margarida for FocalPlane.
To find out all you need to know about the conference, we’ll have a dedicated conference app, and this will have the full programme. You’ll also be able to access the abstracts for the poster sessions, find speaker information, and read about our sponsors. If there are any changes that happen during the conference, then this will be the place to find out. The conference app also has a chat function, which can be a great way to contact people and arrange to meet, so you can optimise your networking experience.
Going back to the programme, when you signed up, you’ll all have seen the wonderful diversity of speakers that we have through the sessions. The preliminary program is up on our website, and as I mentioned, the full program will be available on the app. Because this is a special conference incorporating all of the Company journals and all of the themes that link to the biology that we publish, there are a number of different strands. Importantly, we’ve made it possible for you to move between the strands. There’ll be signposts around the venue helping to direct you to the correct rooms. The sessions are running concurrently, and you will be able to move between lectures, but if you are moving in the middle of a session, we do recommend, that you sit towards the end of a row and try to minimise the disruption as you move around.
Now on to posters. All posters can be put up for the entire duration of the conference. If you have a poster, you should receive some communication about your number and when you’ll be presenting. This will tell you when you’ll need to stand by your poster during the two evening poster sessions. You’ll need to put your poster up before the morning break on Tuesday 25 March. The posters should be grouped together by topic, so if you’re interested in a specific topic, you can go and find all the related posters.
Something else that is important: food and drinks. Every day, tea and coffee will be served. There’ll be two refreshment breaks, and there will be hot food at lunch. This will all be vegetarian or vegan for sustainability reasons.
Onto other fun stuff. There will be two social events on Monday. First, there will be the welcome reception at the Museum of Liverpool, which is a 10-minute walk through the Albert Dock from the conference venue. This will be followed by the ECR dinner at Revolución de Cuba in the Albert Dock, which is a 10-minute walk from the welcome reception and a five-minute walk from the conference venue. Then on Wednesday, we’ll have the gala dinner, which is at St George’s Hall. There will be shuttle buses from the conference venue to take you to the dinner. These will start at 7pm and return shuttles will run from 10pm.
Are you attending a scientific conference for the first time? Well, we’re preparing a pre-conference 101 guide for you, together with Jen, the conference reporter for the Node. Jen has been collecting some tips from people who have been to conferences, and on the screen here, you can see some tips from our preLighters, including, ‘don’t be afraid to talk to you people’ and ‘introduce yourself and your research to others’. For the full 101 guide, check out Jen’s post on the Node. The link is in the video description below.
Okay, so that’s everything from us. Hopefully we’ve given you a little flavour of what to expect at the Biologists @ 100 conference. Please come and chat to us whilst you’re at the conference, we’ll be happy to hear from you. So, that’s everything and we’ll see you in Liverpool.
Attending your first scientific conference? In my experience, the weeks leading up to it can feel equal parts exciting and daunting. Whether you’re presenting a poster or just looking to network with fellow researchers, it is natural to feel overwhelmed if you don’t know where to start. But don’t worry! Conferences are learning experiences, not only about science but also about how to navigate these vibrant academic gatherings.
As we are preparing for the Biologists @ 100 conference hosted by The Company of Biologists, we created a guide to help you feel prepared, confident, and ready to make the most of your time at any scientific convention. We’ve covered all the basics, from what to pack and wear to note-taking and networking, and even asked the scientific community to share some insider advice! And because everyone’s experience is different, we’ve included some tips for anyone who might feel insecure starting conversations in English or spending time in crowds.
So take a deep breath, grab a notebook, and let’s dive in! You’ve got this!
How to prepare
“To be prepared is half the victory”- and that’s especially true at a busy conference. Let’s look at a few simple ways you can ensure a smooth experience before you even leave home:
Get to know the location! – Find out where the conference centre is, how far it is from your accommodation, and the best way to get there and back. Pro tip: Look up a map of the venue in advance. Conferences usually have multiple sessions running in different rooms. Knowing the layout will help you navigate smoothly – and ensure you don’t miss lunch!
List your Must-See talks – Review the schedule in advance and highlight the talks you don’t want to miss. With multiple sessions running in parallel, you may have to prioritise – ah, the agony of Session Superposition! Look out for interesting poster abstracts, and make a note of the session and poster numbers. Bonus tip: Beyond the talks, keep an eye out for networking events, workshops, and socials happening during lunch, breaks, or in the evenings.
An Easy Way to Share Your Science – Even if you’re not presenting, it helps to have a quick way to introduce your research. Create a single slide summarising your work and generate a QR code to share it effortlessly – you can do this through your browser or using an online QR code generator. If English isn’t your first language, prepare 1-3 short sentences about your research in advance. That way, you’ll feel more confident when someone asks about your project.
Double check your morning alarms! – this one speaks for itself, and yes, I’ve learned it the hard way..
What to bring
Pack smart to make the most of the conference!
The poster (if) you will be presenting – this may seem obvious, but you’d be surprised how many of us have a story of a forgotten poster and last-minute replacements. If you want to avoid bulky poster tubes when travelling, try printing on canvas! This way, you can fold your poster and pack it in your bag.
Notebook and pen for taking notes (though you’ll likely get some freebies too ;) – if you prefer to take notes on a tablet or laptop, make sure you have your charger with you, but know that power outlets might be scarce!
Comfortable but smart-ish clothes – Academic conferences tend to have a relaxed dress code, so business casual is a safe choice. Jeans paired with a shirt or blouse work just as well. The key is to wear something that makes you feel comfortable and confident rather than self-conscious. Opt for comfortable shoes – you’ll be on your feet more than you think! And don’t forget a light layer, as an experienced attendee warns: “Conference venues are often (too) well-air-conditioned.”
A small snack – like a muesli bar or an apple. You might miss breakfast, or simply get hungry during a long session. It is better to have a discreet snack than to sit and starve!
What to do once you’re there
The big day has arrived! After registering and picking up your nametag at the entrance, you’re all set to explore. Dive into the sessions, check out the posters, and start making connections! Just don’t forget to silence your phone during the talks.
Be prepared for early starts and short breaks! – Conferences usually try to pack as much science into the day as possible. Try to get there at least 15 minutes before the first talk so you can find the right room and get a good seat. If you feel you may need to step outside during the sessions, sit near the back or at the end of a row. An experienced conference attendee suggested: “Go to the freebies booth!” And they are right! It is time to collect the mug/pen/notepad combo you’ll be using in the lab for the next year.
“Go to the freebies booth! also try to come up with questions after the talks. If you’re too shy to ask in the auditorium, at least write them down on your notebook. Practice your skills in coming up with good questions.”
Ethan Ewe
Take notes! – You’ll likely hear dozens of talks a day, and trust us, you will forget more than you remember. Make a note of the speakers’ names and their contacts. Don’t try to copy everything on the slides – use shorthand and focus on key phrases. Drawing a diagram might be quicker and more effective than writing down all details of an experiment.
Write down questions you want to ask. Even if you don’t get a chance to ask during the session, you may run into the speaker again. No better way to start up a conversation than with a burning question you had about their research.
“Don’t be afraid to talk to new people! Usually, one thinks that senior PIs or other researchers are not very approachable and that’s not the case most of the time.”
Felipe Del Valle Batalla
Ask questions! – Whether at a poster session or during breaks, don’t be afraid to ask people about their research, or their conference experience. It is a sure way to start conversations, and will allow you to connect with fellow researchers.
Go to poster sessions – You may have specific targets, but also spend time roaming around. Poster sessions are a great way to find fellow researchers in your area, and have been the birthplace of many collaborations. But try not to get stuck in one spot; you can always exchange contacts. Keep circulating!
Network with your fellow academics! – It may seem awkward at first, but the main point of conferences is to connect with researchers from all around the globe. If you’re unsure how to start, a smile and a friendly question works wonders. “Hi, I’m [Your Name]. What topic brought you to the conference?” or “What did you think of the last talk?” Don’t forget to exchange contact information so you can follow up on interesting conversations.
“Try to take the first step by introducing yourself and your research and benefit from this opportunity to make new connections that might be fruitful for your career.”
Jawdat Sandakly
If you’d like a bit more advice on networking, have a look at this brilliant article by Alex Eve, the Senior Editor of Development.
Bonus tips for a stress-free conference
You don’t have to do it all – It’s okay to take breaks or even skip a session to recharge. If you feel drained by crowds and small-talk, find a quiet corridor or terrace to ground yourself.
Ask for help – organisers and fellow attendees are usually happy to point you in the right direction if you are lost or have questions about the schedule.
Don’t be too self-conscious about using perfect English. Conferences are international gatherings, and people will be more interested in what you have to say than how, exactly, you say it.
Celebrate small wins – every conversation, new idea, or spark of inspiration is a success!
Attending your first scientific conference is a big milestone, and it’s completely normal to feel a little overwhelmed. Just remember – everyone you’ll meet was a first-timer once, and most people are happy to help if you need guidance. Whether your goal is to learn more about a topic, share your research, or connect with others in your field, the experience is what you make of it. Take it one session, one conversation, and one coffee break at a time.
Above all, don’t forget to enjoy yourself! Conferences aren’t just about discoveries – they’re a chance to meet the people behind the science and share experiences. You’ve worked hard to get here, and you have everything you need to make the most of it. Put your best foot forward and have a great time!
We’ll see you at Biologists @ 100!
If you want a practical guide to the Biologists @ 100 conference, from the venue, poster sessions to the social events, check out this pre-conference recording made by the Community Managers of the Node, preLights and FocalPlane.
An Editorial from the five Editors-in-Chief of The Company of Biologists’ journals
The Editors-in-Chief have written a joint Editorial, discussing the enormous challenges currently facing researchers in the US and how members of the community can support them through this difficult time.
“To our colleagues in the USA, we stand with you during this challenging period. The international scientific community recognises your contributions and the difficult circumstances you now face. Science is a global endeavour, and setbacks to research in one nation affect us all.
In these uncertain times, we must strengthen our international scientific networks. We must build new bridges of collaboration. We must speak with a unified voice in support of evidence-based policymaking and scientific freedom. Together, we can create a more resilient scientific community, with policies that strengthen rather than diminish research capacity. Science must transcend national boundaries and short-term political considerations.”
The response of the science community to the last month is not about one statement or action. It's about all of us with our different frames. For Science's part, we are doing what we have always done and have no plans to change. My thoughts on what we can do. www.science.org/doi/10.1126/…
US President Donald Trump is taking a wrecking ball to science and to international institutions. The global research community must take a stand against these attacks.https://go.nature.com/4kd1vIu
Although I originally set out to highlight the work of early career researchers at the symposium, Professor Vasso Episkopou’s overwhelmingly enthusiastic response coupled with my interest in anteroposterior patterning made her an obvious choice for an interview. At the end of the first day, although I was tired from a day packed full of interesting presentations and engaging conversations, I approached her poster – which was an unconventional, yet effective, series of laminated PowerPoint slides!
Vasso Episkopou presenting her poster.
Anteroposterior (AP) patterning in early vertebrate embryos is influenced by Nodal signalling – high levels promote anterior fates, while low levels drive posterior fates. You might therefore expect a gradient of Nodal along the primitive streak, but this is not the case; it is expressed ubiquitously in the streak. This discrepancy is the impetus of the research conducted by Vasso and her group at Imperial College London.
SnoN, a repressor of Nodal signalling, binds Smad4 to suppress anterior fate-promoting genes at Smad-binding elements (SBEs). Upon Nodal activation, phosphorylated Smad2/3 (pSmad) forms a complex with SnoN, which is recognized and degraded to its entirety by the ubiquitin ligase Arkadia (Rnf111). This surprising mechanism directly links pSmad levels to SnoN reduction, only forcing SnoN removal under high pSmad signaling. “The anterior target genes, they require Arkadia and high signalling, in order to degrade the repressor”, Vasso explained. The SBE is now clear, allowing pSmad-Smad4 to bind, and together with co-activators, initiate transcription of anterior genes. The necessity of Arkadia for anterior development is very clear in the headless phenotype of Arkadia-/- mice. In addition, head formation is rescued in Sno-/-;Ark-/- embryos, confirming that Arkadia is responsible for achieving the de-repression.
But Nodal signalling is abundant in the primitive streak – so how is AP patterning regulated? Vasso’s research group have identified that the dynamics of Nodal signalling control AP patterning in the primitive streak, rather than morphogen gradients. A TGF-B time course treatment of embryonic stem cells showed that, at high levels of signalling, there is a temporary decrease in SnoN at 1-2 hours due to its degradation by Arkadia, then SnoN levels increase again at 4-6 hours; this temporary reduction frees up space on the SBE for pSmad-Smad4 to activate transcription of anterior genes. The rising of SnoN levels at 4-6h is due to a negative feedback effect: one of pSmad’s early targets is SnoN itself, and the resulting increase in SnoN overwhelms Arkadia. This leads to a very transient activation of Arkadia-dependent anterior targets.
A sketch to show how, in the presence of high levels of Nodal signalling, Arkadia degrades the SnoN repressor complex, which allows the binding of pSmad at SBEs (Smad-binding elements) to activate transcription of anterior target genes.Sustained Nodal signalling causes anterior gene transcription to switch off, since pSmad activates SnoN transcription, leading to negative feedback.
On the other hand, in the presence of lower levels of Nodal, SnoN is not degraded by Arkadia, so there is competition between SnoN-Smad4 and pSmad-Smad4 for binding the SBE. Posterior Nodal targets do not require the SBE to be cleared completely – only a low level of Nodal signalling is required to relax the chromatin by pausing histone deacetylation, which permits co-regulators of posterior targets to bind (at other sites) and activate transcription. Since posterior genes are co-regulated by other transcription factors, they only need Nodal signalling for partial de-repression to become activated. This contrasts with the anterior targets, which can only be activated by pSmad-Smad4 after clearing of the SnoN from the SBE.
Altogether, this means that anterior identity in the primitive streak must be acquired in a very short time window, in response to acute, high levels of Nodal signalling, before any negative feedback can kick in. Vasso has put this together with what we know about cell migration in the streak – the first cells to exit, the fastest migrating cells, leave the streak via anterior migration and become the anterior endoderm. These cells also express Nodal antagonists, such as Lefty 1/2 and Cerberus, doubling down to ensure that their exposure to Nodal is very short-lived. “Cerberus is a triple attack,” Vasso explained, “a Nodal, Wnt, and BMP inhibitor. So, these cells express antagonists to shield themselves from sustained (posteriorising) signals”. These antagonists activate the transcription of immediate early genes, ensuring that anterior identity is swiftly acquired. In contrast, slower migrating cells acquire posterior identity, since remaining in the streak for longer exposes them to sustained Nodal signalling, leading to the repression of anterior genes and allowing co-regulators to impose a posterior fate.
In the early mouse embryo, slow migrating cells remain in the primitive streak for longer, so are exposed to sustained Nodal signalling, and acquire a more posterior mesoderm fate. Whereas fast migrating cells leave the primitive streak first, so are only exposed to Nodal signals for a short period. This allows them to acquire an anterior fate, such as anterior definitive endoderm.
Vasso suggests that this dynamic regulation of signalling may be a widespread mechanism in fate determination. A similar principle applies to T lymphocyte differentiation: high TGFβ levels drive Treg differentiation in an Arkadia-dependent manner, whereas low levels drive Th17 differentiation independently of Arkadia (Xu et al., 2021). This model may extend to other biological contexts yet to be explored.
You can read Vasso’s group’s preprint on Nodal dynamics here: Carthy, J.M., Ioannou, M. and Episkopou, V. (2019) ‘Arkadia via SNON enables NODAL-SMAD2/3 signaling effectors to transcribe different genes depending on their levels’. bioRxiv, p. 487371. Available at: https://doi.org/10.1101/487371.
Read about how the same system acts in T lymphocyte differentiation here: Xu, H. et al. (2021) ‘Arkadia-SKI/SnoN signaling differentially regulates TGF-β–induced iTreg and Th17 cell differentiation’, Journal of Experimental Medicine, 218(11), p. e20210777. Available at: https://doi.org/10.1084/jem.20210777.
Stay tuned for more poster interviews coming soon!
This series of interviews features principal investigators (PIs) within the first five or so years of establishing their own research group. Through these conversations, Development aims to illustrate that there is not a ‘one-size-fits-all’ approach to securing an independent position and setting up a research programme. Discussing the challenges and difficulties new PIs have overcome and highlighting the best moments will hopefully offer encouragement to other ECRs and stimulate discussion around the career path of a developmental biologist.
Click on the pins to read the interviews:
Collage of all 40 interviewees in the ‘Transition in development’ series. (No Ratings Yet) Loading...
An easily-consumable recap of the latest happenings in the #zebrafish community!
Special thanks to Maddie Ryan, Charli Corcoran & Michaela Noskova Fairley for putting this digest together! If you would like to thank the Zebrafish Rock! team for their time & effort, you can buy us a coffee at the link below. Every little bit keeps us caffeinated and motivated! We appreciate your support 🙂
Dr. Joaquín Navajas Acedo @mads100tist.bsky.social wins the Society for Developmental Biology Trainee Science Communication Award.
Dr. Navajas Acedo
Prof. Teresa Bowman receives inaugural Dr. Fernando Macian-Juan Award for Excellence in Graduate Student Mentoring at Albert Einstein College of Medicine.
Prof. Bowman (Image Credit to Albert Einstein SOM)
Prof. Robert Arlinghaus @rarlinghausfish.bsky.social honoured with Leibniz Research in Responsibility Award for his interdisciplinary work in fishery science.
Prof. Arlinghaus (Image Credit to Leibniz Institute)
The people behind the papers – Juan Yang and Xuanmao Chen
In mammalian embryos, brains develop from the inside out, with younger neurons moving to the outer layers in a process called radial migration. A new paper in Development finds that, during postnatal development, some of the neurons in the outer layers of the brain undergo a ‘reverse movement’, repositioning themselves by moving in the opposite direction to the initial radial migration. To learn more about the story behind the paper, we caught up with first author Juan Yang and corresponding author Xuanmao Chen, Associate Professor of Neurobiology at the University of New Hampshire (UNH), USA.
Xuanmao, what questions are your lab trying to answer?
Xuanmao: We pursue three major questions. First, we investigate how ciliary signalling modulates postnatal neurodevelopment and neuronal function, thereby influencing learning and memory formation. Second, we are intrigued by how a subset of excitatory neurons in the cerebral cortex are recruited to encode and store associative memory, and how a neuronal activity hierarchy in the brain is developed and maintained. Third, inspired by our recent progress, we seek to understand the evolutionary mechanisms, other than neurogenesis, that underly biological intelligence.
Juan, how did you come to work in the lab and what drives your research today?
Juan Yang: I first became interested in laboratory research during my undergraduate studies, particularly in my molecular biology class, where I was fascinated by how gene expression regulates organismal development and function. To pursue this interest, I joined the Hu lab at the Oilcrops Research Institute, Chinese Academy of Agricultural Sciences, to study how the LAZY gene regulates branching angle formation in rapeseed. I spent countless hours performing PCR for plant genotyping but genuinely enjoyed working in the lab and felt a thrill every time I saw DNA bands appear on an electrophoresis gel. After graduation, I was fortunate to obtain a technician position in the Shen lab at ShanghaiTech University, China, where I became fascinated by using cutting-edge tools such as optogenetics and fibre photometry to investigate how specific neural circuits control the body’s homeostasis. These combined experiences sparked my passion for neuroscience and guided me to pursue my PhD dissertation research in the Chen lab at UNH, where I study neuronal primary cilia and cellular mechanisms underlying postnatal brain development.
What was known about neurodevelopment before you started the project?
Juan Yang & Xuanmao: It is well-established that pyramidal neurons in the cerebral cortex migrate from the neurogenic regions toward the cortical or hippocampal plate an inside-out manner. Before we started the project, we had thought that pyramidal neurons only undergo unidirectional migration, and the “terminal translocation” of radial migration is viewed as the final step for neuronal placement.
Can you give us the key results of the paper in a paragraph?
Juan Yang & Xuanmao: We discovered that primary cilia of early- and late-born principal neurons in compact layers in the mouse brain, such as the hippocampus CA1 region, display opposite orientations, while primary cilia of principal neurons in loose laminae, including the subiculum, entorhinal cortex, neocortex, and cingulate cortex, are predominantly oriented toward the pia. However, specific cilia directionality was not observed in astrocytes and interneurons in the cerebral cortex, or neurons in nucleated brain regions. Guided by this clue, we found that the cell bodies of principal neurons in inside-out laminated regions, including the hippocampal CA1 region and the neocortex, undergo a slow “reverse movement” for postnatal positioning. Our evidence indicates that it is the reverse movement during early postnatal development that leads to the primary cilia of pyramidal neurons to predominately orient toward the pia. Therefore, the “terminaltranslocation” of radial migration is not the last step, pyramidal neurons in the postnatal cerebral cortex continue to adjust their position and move inwards. The reverse movement must be important for constructing sparsely layered inside-out laminae and for forming sulci (grooves) in the mammalian brain.
Figure 1.(Top)The cilia/centrioles of late-born neurons cluster at the bottom of the CA1 SP before reversing. Image showing the distribution pattern of cilia (red) and centrioles (green) in the CA1 SP of Arl13b+ mice. (Bottom) Reverse movement of neurons helps to form a sulcus. Ift88 cKO mice exhibit a sulcus (white arrows) in the retrosplenial cortex, which is formed by reverse movement of the neurons during postnatal development. Green arrows denote a transition from a compact layer to a sparse and wide layer.
Why did you decide to focus on primary cilia?
Xuanmao: I initially studied type 3 adenylyl cyclase (AC3) during my postdoc training in the Storm Lab at the University of Washington, USA. AC3 is a cilia-specific cyclase originally identified in olfactory cilia. AC3 is known to be essential for olfactory perception in mammals. My first project was to study the role of AC3 in airflow-mediated mechanosensation of olfactory cilia (Chen et al., 2012). Cilia dysfunction is associated with numerous brain disorders in humans, and AC3 was found to be highly enriched in neuronal primary cilia throughout the brain (Bishop et al., 2007). However, the functions of AC3 and neuronal primary cilia in the brain are largely unknown (Guemez-Gamboa et al., 2014). The significance of these unanswered questions prompted me to study neuronal primary cilia in the central nervous system. Years later, it is the intriguing cilia directionality of pyramidal neurons marked by an AC3 antibody that guided the lab to make a breakthrough in the context of postnatal neurodevelopment.
What implications does your work have for understanding human brain evolution?
Xuanmao: In my opinion,the mammalian cerebral cortex, particularly the primate neocortex, can be likened to a “library” consisting of numerous shelves and layers of “books” (excitatory principal neurons). The development of such a sparsely layered, matrix-like architecture and its evolution from the allocortices of lower vertebrates (amphibians or reptiles) to the neocortex of humans not only involves increased neurogenesis (Florio and Huttner, 2014; Rakic, 2009; Taverna et al., 2014) and sufficient accommodating space but also requires fast, long-distance neuronal migration (Nadarajah et al., 2001) and slow, fine-tuned repositioning for final neuronal placement. These processes, particularly the slow repositioning step, permit orderly neuronal maturation and progressive circuit formation, and allow the brain to acquire external information during postnatal development to gradually construct well-organized neural circuitry to enable efficient information processing, storage and retrieval.
Upon the completion of fast radial migration, the outer layer in the cerebral cortex is highly condensed. It is unclear how the mammalian neocortical structures gradually become loosely layered, while allocortical regions remain highly compact. I believe that an additional step of reverse movement is needed for constructing the sparse 6-layered neocortex. Without reverse movement, only tightly compact 3-layered laminae can be made. Without reverse movement, neuronal maturation in the hippocampal CA1 and neocortex might occur simultaneously (as occurs in the CA3 region)(Yang et al., 2024), rather than following a sequential pattern. Therefore, the reverse movement of pyramidal neurons must be crucial for the evolutionary transition from the 3-layer allocortex to 6-layer neocortex. It is also linked to the gyrification process in gyrencephalic animals, because we discovered that a sulcus is formed, at least in part, via reverse movement.
When doing the research, did you have any particular result or eureka moment that has stuck with you?
Juan Yang & Xuanmao: The Chen lab has been intrigued by the directionality of primary cilia for many years, having observed interesting cilia orientation patterns in multiple peripheral tissues and many cortical regions. We noticed a striking alignment of cilia in the mouse hippocampus at postnatal day 14 (P14), with most pointing in the same direction. However, within the thin stratum pyramidale (SP) of the CA1 region, we observed a small subset of cilia oriented in the opposite direction. This orientation pattern was absent at other developmental stages. We did not know how to interpret this phenomenon, and the question lingered in our minds for several years. One day at home, while casually browsing hippocampus-related articles, Juan Yang came across a review article by Soltesz and Losonczy (Soltesz and Losonczy, 2018), from which she learned that the hippocampal SP contains two distinct neuronal populations: early-born and late-born neurons. This paper inspired her to speculate that the opposing cilia orientations in the CA1 SP likely belong to two distinct groups of neurons. Yang then sent the review paper to Chen in an email explaining her hypothesis. After reading the review paper a few days later, Chen responded: “That makes sense and let’s verify it”. This was the first eureka moment in advancing our understanding on cilia directionality.
The concept of reverse movement could not have been developed if the lab had only used wild-type (WT) mice to assess cilia orientations. In the WT hippocampal CA1 region, the primary cilia of pyramidal neurons are not very long (5-8 µm), and they protrude out of the plasma membrane within a short two-day window (P9–P11), by which point centrioles are no longer clustered at the bottom edge of the SP. Fortunately, the lab also maintained Arl13b-mCherry, Centrin2-GFP double transgenic (Arl13b+) mice (Bangs et al., 2015; Higginbotham et al., 2004), which mark primary cilia and centrioles, respectively. The transgenic mice have much longer cilia (~16 µm) in the CA1 region than the WT mice. They also express cilia a few days earlier than WTs and have a prolonged ciliation time-window spanning from P3 to P14. This extended period provided us with more snapshots to track the cilia and centriole positioning process as well as cell body movement during early postnatal development. For example, at P7 in Arl13b+ mice, early-born neurons have already emanated long cilia, which are largely oriented toward the stratum oriens (SO), whereas late-born neurons are only just beginning to protrude cilia, which are enriched in the bottom edge of the SP and orient toward the stratum radiatum (SR) (Figure 1, top panel). This striking contrast instantly led Chen to formulate a concept of reverse movement, in which late-born neurons first migrate to the bottom edge of the SP before moving back to the main part of the SP. Recognizing the existence of this reverse process was the second key step in advancing this research. Subsequently, we found that slow reverse movement is a common positioning step for most of pyramidal neurons in the cerebral cortex.
The lab also housed a Ift88 conditional knockout (KO) mouse strain (Haycraft et al., 2007), which lacks primary cilia on the excitatory neurons and astrocytes in the forebrain. Notably, Ift88 cKO mice produce a lot more late-born neurons than WTs. The overcrowding of late-born neurons in the outermost cortical layer of Ift88 cKOs gradually leads to the formation of a sulcus via a reverse movement (Figure 1, bottom panel). This observation indicates that principal neurons are subject to backward movement for postnatal repositioning, sometimes individually if the outermost layer is not very crowded, and sometimes collectively if too crowded.
And what about the flipside: any moments of frustration or despair?
Juan Yang: The challenges of scientific research are numerous, but for me, they gradually fade away – either forgotten over time or overshadowed by new research progress and gaining recognition from my peers.
Why did you choose to submit this paper to Development?
Juan Yang & Xuanmao: Development has a long-standing reputation as a leading peer-reviewed scientific journal focused on developmental biology. We rely on the editorial board’s expertise in neurodevelopment and professionalism to evaluate the significance of our discoveries.
Where will this story take your lab next?
Xuanmao: This story opens multiple new avenues to explore. The lab is well positioned to address the following questions: (1) what key factors control cilia directionality and the reverse movement of principal neurons, and consequently neuronal maturation; (2) how primary cilia regulate or stabilize neuronal positioning; (3) how reverse movement impacts the cortical evolution of mammals; and (4) how neuronal primary cilia modulate neuronal function, contributing to associative learning and memory formation.
Finally, let’s move outside the lab – what do you like to do in your spare time?
Juan Yang: I enjoy playing table games, exploring new cuisines and traveling.
Xuanmao: In the summer, I enjoy spending time with friends and family, swimming and paddling on lakes and beaches. Fall is my favourite time for hiking and admiring the vibrant maple leaves in the mountains. In winter, I love skiing with the kids. The most rewarding activity in my spare time is thinking freely without set objectives and sketching on whiteboards – a hobby that I call “whiteboard fun”.
Juan Yang (left) and Xuanmao Chen (right)
References:
Bangs, F.K., N. Schrode, A.K. Hadjantonakis, and K.V. Anderson. 2015. Lineage specificity of primary cilia in the mouse embryo. Nat Cell Biol. 17:113-122.
Bishop, G.A., N.F. Berbari, J. Lewis, and K. Mykytyn. 2007. Type III adenylyl cyclase localizes to primary cilia throughout the adult mouse brain. J Comp Neurol. 505:562-571.
Chen, X., Z. Xia, and D.R. Storm. 2012. Stimulation of electro-olfactogram responses in the main olfactory epithelia by airflow depends on the type 3 adenylyl cyclase. J Neurosci. 32:15769-15778.
Florio, M., and W.B. Huttner. 2014. Neural progenitors, neurogenesis and the evolution of the neocortex. Development. 141:2182-2194.
Guemez-Gamboa, A., N.G. Coufal, and J.G. Gleeson. 2014. Primary cilia in the developing and mature brain. Neuron. 82:511-521.
Haycraft, C.J., Q. Zhang, B. Song, W.S. Jackson, P.J. Detloff, R. Serra, and B.K. Yoder. 2007. Intraflagellar transport is essential for endochondral bone formation. Development. 134:307-316.
Higginbotham, H., S. Bielas, T. Tanaka, and J.G. Gleeson. 2004. Transgenic mouse line with green-fluorescent protein-labeled Centrin 2 allows visualization of the centrosome in living cells. Transgenic Res. 13:155-164.
Nadarajah, B., J.E. Brunstrom, J. Grutzendler, R.O. Wong, and A.L. Pearlman. 2001. Two modes of radial migration in early development of the cerebral cortex. Nat Neurosci. 4:143-150.
Rakic, P. 2009. Evolution of the neocortex: a perspective from developmental biology. Nat Rev Neurosci. 10:724-735.
Soltesz, I., and A. Losonczy. 2018. CA1 pyramidal cell diversity enabling parallel information processing in the hippocampus. Nat Neurosci. 21:484-493.
Taverna, E., M. Gotz, and W.B. Huttner. 2014. The cell biology of neurogenesis: toward an understanding of the development and evolution of the neocortex. Annu Rev Cell Dev Biol. 30:465-502.
Yang, J., S. Mirhosseiniardakani, L. Qiu, K. Bicja, A. Del Greco, K. Lin, M. Lyon, and X. Chen. 2024. Cilia Directionality Reveals a Slow Reverse Movement of Principal Neurons for Postnatal Positioning and Lamina Refinement in the Cerebral Cortex. BioRxiv 473383v7.
We have now shortlisted 15 images, which will be presented in our gallery at Biologists @ 100 at ACC Liverpool, 24-27 March 2025, and online on the Node and FocalPlane.
Conference attendees will be able to see the images in our gallery and vote in person; for those online, you can browse through the gallery below and vote for your favourite in the poll at the bottom of this post. We’ll add up the votes from the Node, FocalPlane and our conference delegates, and the winner will be announced on Thursday 27 March.
Please vote for your favourite image at the bottom of the page. The voting will close on Wednesday 26 March 11:59pm GMT.
Thank you and good luck to the following researchers for their contributions:
Aaron Scott, Allan Carrillo-Baltodano, Andrew Octavian Sasmita, Camila Weiss, José Palma, Marina Cuenca, Çağrı Çevrim, David Grainger, Ioakeim (Makis) Ampartzidis, Julia Peloggia de Castro, Krystyna Gieniec, Lea Berg, Michael Raissig, Ludovica Altieri, Maik Bischoff, Mathieu Preußner, Min Ya and Özge Özgüç.
And a big thank you to everyone who submitted their images to the competition. There were many good quality submissions that it was very difficult to narrow down the selection!
Browse through the gallery (click to expand the images)
1. A song of ice and fire Aaron Scott The plasma membrane of every cell in these 2-day-old larval zebrafish is fluorescently labelled and shown in grey. The endothelial cells and the blood vessels they form are shown in cyan or red. Imaged on a Leica SP8 AOBS confocal laser scanning microscope and reconstructed using ImageJ.
2. Dancing actinotroch Allan Carrillo-Baltodano Actinotroch larva of a phoronid worm with phalloidin shown in yellow and acetylated tubulin in magenta. Imaged with a Zeiss LSM 800 at 10 x magnification.3. The glial response to amyloid skies Andrew Octavian Sasmita Confocal maximum projection image of several amyloid-β plaques (blue, 6E10) surrounded by microglia (gold, Iba1) and astrocytes (white, GFAP) in the cerebral cortex of a 6-month-old female APPNLGF mouse model of amyloidosis. Imaging was done with a Zeiss LSM 800 Airyscan confocal microscope and processed with the Zen imaging software.4. A mystery amphipod Camila Weiss, José Palma and Marina Cuenca Lateral view of an unknown species of chilean amphipod labelled with DAPI (cyan) and phalloidin (magenta). Imaged using light-sheet imaging at the Quintay developmental biology course in 2023 and processed with Fiji. 5. A beautiful contamination Çağrı Çevrim A scanning electron micrograph (SEM) of a Parhyale hawaiensis limb, showing an external mechanosensory organ – a plumose seta – in the background. In the foreground, a pollen grain, possibly from a Platanus tree, has contaminated the sample. 6. Thymus in the spotlight David Grainger A colour-coded depth projection of the blood endothelial cells of the E14.5 mouse embryonic thymus and surrounding structures. A 200 μm thick vibratome section was immunostained for endomucin and imaged on a Zeiss LSM980 confocal microscope and depth-encoded using a rainbow LUT before performing a maximum intensity projection. 7. Beat Ioakeim (Makis) Ampartzidis Mature beating cardiomyocyte cell cluster from human induced pluripotent stem cells. Cells were grown for a total of 20 days and stained positive for cardiac troponin (Hot Blue) and actinin (Hot Red) markers. The image was acquired at the Veneto Institute of Molecular Medicine (VIMM), in Nicola Elvassore’s lab, using an upright LSM900 ZEISS microscope and LUTs adjusted using Fiji software. 8. Who’s active? Julia Peloggia de Castro The image depicts a zebrafish embryo at 9 hours post-fertilisation on a lateral view. Cells are stained with MitoTracker, which labels active mitochondria, and cell membranes are labelled in cyan with a EGFP transgenic membrane tag. Image was taken using a 20x objective on a spinning disk confocal microscope.9. Unexpected guests Krystyna Gieniec 2D culture of mouse mammary fibroblasts stained for Acta2 (magenta) and Vimentin (gold), with some contaminating epithelial cells stained for pan-Cytokeratin (cyan). Image acquired using a Leica Stellaris 8 confocal microscope.
10. The plant-atmosphere interface that feeds the world Lea Berg and Michael Raissig Mature epidermal cell types in a grass leaf of the emerging developmental model system Brachypodium distachyon. Cell outlines are blue, which is plant cell wall UV-autofluorescence. In yellow is stained lignin, a secondary cell wall modification that can be found in the hair cells (‘shark-tooth’-shaped) and the stomatal guard cells (‘dumbbell’-shaped). Imaged by confocal microscopy and processed in Fiji.
11. Plenty of fish in the sea Ludovica Altieri Murine primary cortical neurons developing interconnections, stained with neuronal tubulin (cyan) and DAPI (blue). Imaged on a Nikon microscope implemented with a CrestOptics confocal spinning disk module with post-processing using NIS Elements AR by Nikon.Acquired at the IBPM Institute of Molecular Biology and Pathology – CNR National Research Council of Italy, c/o Department of Biology and Biotechnology “Charles Darwin” – Sapienza University of Rome.
12. Invisible architects Maik Bischoff Drosophila hydei testis musculature stained with phalloidin to label F-actin (blue), anti-N-Cadherin (orange/gold) to mark cell-cell junctions between muscle cells and DAPI to stain nuclei (purple). Autofluorescence (orange/gold) makes the trachea visible. Imaged with a Zeiss 980 confocal microscope with Airyscan 2. The image was processed in Zen Blue, and LUTs (by KTZ) applied in Fiji with further modifications in Photoshop.13. Breath of the water Mathieu Preußner Lateral view of the overlying gill arches in 1-month-old Danio rerio expressing endothelial kdrl:mCherry. Clarity-based tissue clearing of the sample enabled comprehensive image acquisition using a Nikon Ti spinning disk system. In ImageJ, the hyperstack was modified using a temporally colour-coded lookup table.14. Pin shoot Min Ya Maximum projection of confocal stacks of a mutant Mimulus parishii shoot apex with cells labelled with a plasma membrane marker. The shoot apices of this plant can grow but are unable to produce any organs, resulting in a phenotype that resembles a pin. 15. Cell-estial bloom Özge Özgüç A ‘Cell-estial bloom’ of human induced pluripotent stem cells (hiPSCs) flourishes on a micropatterned island. This image presents a colony of live hiPSCs, with fluorescently labelled Lamin B delineating the nuclear lamina within each cell. Acquired with a Zeiss LSM 880 Airyscan microscope, this maximum intensity projection is enhanced with depth-coded coloring to reveal the captivating three-dimensional landscape.
Voting is now closed. Thank you to everyone who voted!
The 3rd Crick-Beddington Symposium, in memory of Rosa Beddington FRS (1956-2001), took place on 10th-11th February at the Francis Crick Institute, London. Rather than providing a broad summary of the event, I decided to embody the ‘Node correspondent’ persona and approach poster presenters to interview them about their research.
The symposium was very well attended, and as a result the posters were distributed across two different areas. On the lunch break of the first day, I made my way over to the quieter poster area, hoping to find a scientist willing to take part in a recorded conversation without too much background noise. Alas, enthusiasm for science was all around in the form of loud, animated discussion, which made my mission challenging!
The first poster to catch my eye was presented by Dr Hocine Rekaik, who was luckily more than happy to take part. Hocine is a postdoc in the lab of Denis Duboule at College de France, Paris. The lab is interested in the function of Hox genes in vertebrate body axis development, of which the sequential activation provides the axial and paraxial tissues with positional information along the anteroposterior axis. Hox genes exhibit temporal and spatial collinearity, which means that for each gene, the timing of expression and the anteroposterior expression domain is linked to its location on the chromosome. This sequential activation, often referred to as the Hox timer, has been extensively studied in vertebrate model systems. However, the precise mechanisms linking gene expression onset with axis elongation remain elusive.
Mice, along with humans and chickens, possess four Hox gene clusters. Hocine explained that, due to the high degree of redundancy, the ideal experiment would involve deleting all of them, yet this is not possible in the mouse. Instead, they turn to the gastruloid, an embryonic stem cell (ESC)-derived model that recapitulates many aspects of gastrulation and axis elongation. Hocine explained, “These gastruloids, when they elongate, they implement the collinear expression of Hox genes, so these are really nice models to study their function and temporal expression”, which is mirrored in the gastruloid as in the embryo. Conveniently, the mouse ESCs used to create them can be modified beforehand to create a mutant line that lacks all four Hox clusters – the Hox-less clone.
Dr Hocine Rekaik presenting his poster “Genetic ablation of Hox function in mammalian pseudo-embryos reveals major rewiring in the early developmental program”.
Surprisingly, the Hox-less gastruloids elongate and exhibit the same anteroposterior patterning as normal, so to delve deeper into the differences between mutant and wild-type, Hocine and his colleagues performed a single cell RNA-Seq experiment. They found that at 96h and 120h of development, the Hox-less gastruloids were lacking two cell types: definitive endoderm and pharyngeal mesoderm, both of which arise from the anterior primitive streak. Yet the expression of anterior primitive streak genes was unaffected, suggesting that the streak forms as normal but its anterior derivatives are dependent on Hox expression. In accordance with this, CER1 – a crucial gene for anterior development – was significantly downregulated in the mutants. CER1 is expressed in the anterior endoderm, but also as a characteristic stripe in the newly-formed somites.
While gastruloids do express somite marker genes, they don’t exhibit the segmentation that is characteristic of somitogenesis – unless they are placed in Matrigel. “Normal gastruloids have this smooth elongation, but in Matrigel, they start to form this segmented structure” he described, and later went on to explain that this is because the Matrigel provides an extracellular matrix, which allows the cells to polarise, causing the somites to condense and epithelialise. I was surprised to learn that gene expression with and without Matrigel is the same, but Matrigel drastically changes the morphology. Hocine found that the Hox-less gastruloids tended to have fewer somites than wild-type controls, because most of them would form temporarily, then disaggregate. This was accompanied by extrusions developing at the posterior end. A pseudo-time analysis showed that the posterior somite-forming cells – derived from neuromesodermal progenitors (NMPs) – didn’t pass through all the usual cell states on their way to becoming somites, leading to the development of posterior extrusions. Hocine puts this down to the absence of the Hox clock, suggesting “there is no control over the differentiation process, so the cells start to differentiate directly – there is no gatekeeper”. However, no markers of mature, epithelialised somites were ever found in these Hox-less gastruloids.
One explanation Hocine proposed relies on the observation in the embryo that the first, most anterior somites do not give rise to segmented structures and instead, contribute to the muscles of the head, rather than the vertebrae. This region corresponds to the most anterior limit of Hox gene expression, explaining why the anterior somitic tissue is produced as normal – through disaggregation, it is simply undergoing its natural lifecycle. On the other hand, the more posterior, NMP-derived somitic tissues in altered gastruloids may have an altered trajectory and do not develop into the trunk-like mature somites seen in the control.
What’s next for Hocine’s research? He stressed that there is more work to do to understand the changes in gene expression brought about by the absence of the Hox timer. But he is excited for future experiments involving the Hox-less cell line and knows it will be very useful for the lab. They plan to do further experiments to find out how other tissues are affected, especially those involved in axial elongation, like the neural tube.
You can read Hocine’s latest article here:
Rekaik, H. et al. (2023) ‘Sequential and directional insulation by conserved CTCF sites underlies the Hox timer in stembryos’, Nature Genetics, 55(7), pp. 1164–1175. Available at: https://doi.org/10.1038/s41588-023-01426-7.
Stay tuned for more poster interviews coming soon!
Join us in Athens 3-4 April 2025 for an unforgettable symposium, as global leaders in stem cell research come together to explore groundbreaking advancements in neural stem cells. From development to aging, disease, and repair, this event will dive deep into the complexities of stem cell plasticity, epigenetics, metabolism, and more. With a focus on neuron-glia interactions and brain disease modeling, this symposium offers a unique opportunity to connect, learn, and push the boundaries of science. Don’t miss out on this exciting event that promises to shape the future of neural research!
Visit our webpage to learn more and register today!
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