From Saturday 31.05.2025 to Friday 27.6.2025, an art gallery in Heidelberg, Germany, presents an interdisciplinary exhibition combining art and science. The exhibition features the work of Dr. Ayelen Valko, a visual artist and cell biologist who explores the cellular universe to express its beauty and mystery to the general public. Through a blend of artistic techniques, metaphor and symbolism, Ayelen makes complex biological concepts accessible and engaging. The Node previously featured Ayelen in our SciArt profile. Here, we caught up with Ayelen again to find out more about her art, motivations and experiences as a scientist in the art world.
Flyer for the exhibition at GEDOK Heidelberg, showing one of the works from the ‘Anthropo-Lysosomes’ series.
How did your interest in combining cell biology and visual art begin?
I have been painting and drawing my whole life. The natural world has always been my inspiration. My family often tells me that, as a child, I would spend hours drawing leaves and insects in my grandmother’s garden. However, it wasn’t until I began my Ph.D. program and was trained in various microscopy techniques that I realized how much artistic inspiration I could draw from microscopy images.
I have a dual background in art and science. I took several courses at the National University of Arts in Argentina, focusing on portrait and abstract painting and exploring traditional media, such as oil on canvas and acrylics. I then specialized in scientific and naturalistic illustration, developing skills in watercolor, scratchboard, graphite, and ink through courses and workshops at institutions such as the Ernst Haeckel Scientific Painting Lab, the Adumbratio Scientific Illustration Center, and Aves Argentinas.
Today, I use these and other techniques in mixed-media collages and paintings, which are mostly inspired by cell biology.
Vernissage of the exhibition.
Ayelen giving the opening speech.
Why is the microscopic universe an interesting subject for an art exhibition?
To me, understanding the biological processes that sustain life can help us to appreciate it more fully. The microscopic world holds a quiet, yet powerful kind of beauty—both artistic and philosophical. Although it is not a common theme in the arts, the complex and fragile systems that keep cells alive offer endless inspiration. This makes the microscopic universe a fascinating subject for an exhibition: it invites viewers to look closer, to discover an unseen dimension of life that is usually reserved for scientists. Through my work, I aim to capture the essence of these biological processes and bring them to life on canvas in a way that makes them more accessible to everyone. I try to show the hidden beauty of cellular landscapes as I see them, filtered through my own experiences and imagination. My paintings and collages blend scientific ideas with artistic expression, shaped by memories, emotions, and the subconscious. In essence, my work brings together biology, art, and psychology.
… it invites viewers to look closer, to discover an unseen dimension of life that is usually reserved for scientists.
Works depicting various organs, tissues, and biological processes.
What is the idea behind the exhibition?
The concept behind this exhibition is to take the viewer on a visual journey that begins with whole organisms and gradually descends into the inner world of organs, tissues, individual cells, and intracellular compartments—revealing the wonders hidden within a single cell.
To achieve this, I used a wide range of materials and techniques, including inks, colored pencils, fineliners, watercolors, oils, acrylics, and markers, working on paper, canvas, and fabric. The exhibition also features collages made from diverse materials such as thread, fabric, newspaper, tissue paper, cardboard, plastic beads, and sand—or combinations of these.
One section of the exhibition is dedicated to scientific journal covers. There, viewers can see how some of my artworks have been adapted into journal cover illustrations, and read a selection of art-and-science articles I have written for some of those publications.
As the exhibition moves into the realm of subcellular landscapes, I present two ongoing series: Anthropo-Lysosomes and Origins in Blue. These explore opposing biological phenomena—destruction and creation, respectively—through metaphor and symbolism. In both series, I incorporate anthropomorphic elements into the cellular environments. I believe this helps make complex biological concepts more accessible than they might be in more purely abstract representations.
In Anthropo-Lysosomes, I focus on the cell’s digestive compartment—the lysosome. Across the series, three anthropomorphic figures appear inside the lysosome and undergo a progressive visual degradation, symbolizing biological breakdown and psychological vulnerability. I use a variety of techniques to emphasize different facets of destruction in each piece.
The Anthropo-Lysosomes series.
In contrast, Origins in Blue zooms into the mammalian ovary, starting from the organ level and moving toward a single oocyte. Along the way, the imagery becomes increasingly fantastical, blending imagined cellular structures with emotional and symbolic layers. This series explores not only anabolism—biological synthesis—but also interpersonal relationships, particularly themes of otherness, judgment, and inherited conflict. It touches on early childhood and the entry of a new individual into a world shaped by unresolved tensions.
The Origins in Blue series.
How does your background in biology shape your artistic expression, and why do you bring personal experience into that mix?
While it is common to see art used as a tool for science outreach, such as on journal covers or in graphical abstracts, it is much less common to see the relationship reversed, with science becoming a source of inspiration for artistic creation. This inverse perspective is precisely where my work is rooted. As both an artist and a biologist, I strive to depict the beauty and mystery of the cellular universe through my own subjective lens and lived experience. Consider the Surrealists, such as Remedios Varo and Frida Kahlo: They drew inspiration from psychology and the unconscious, but they weren’t trying to educate their audience about Freud or Jung. I asked myself, “Why not use the cellular and subcellular worlds as artistic inspiration without always aiming to explain or teach science?” I believe there’s real artistic value in that approach—finding inspiration in science for expression, not just communication.
As both an artist and a biologist, I strive to depict the beauty and mystery of the cellular universe through my own subjective lens and lived experience.
What challenges have you encountered moving between the scientific and artistic worlds?
Overall, it has been a very positive experience for me. Creating cover illustrations for scientific journals and participating in science communication activities, such as giving talks in schools and running art-and-science workshops, have been deeply rewarding. I find that these kinds of projects offer clearer pathways: you can submit a cover proposal or apply to speak at an outreach event. They’re more structured and predictable ways of combining art with science.
However, finding my place in the art world has been more challenging, especially when trying to exhibit science-inspired work in galleries and museums. This path—less clearly defined—has brought me a great deal of satisfaction, but also some real obstacles.
While most people are curious and supportive, there’s still some confusion about my work. The scientific community sometimes asks me why I “paint” science instead of conducting bench research. In the art world, science is often seen as too rigid, even contradictory to artistic freedom. There’s a lingering assumption that scientists might not be flexible or imaginative enough to truly belong in the arts. The tension of working between disciplines is very real. I often feel like I belong to both artistic and scientific worlds, but also to neither.
Another challenge I face is my preference for creating handmade works rather than digital ones. This can be limiting when approaching certain institutions that focus on “sciart” but lean heavily toward digital aesthetics. They often seek pieces resembling glowing, rotating DNA holograms seen in science fiction films, not for their meaning, but for their visual effect. In those spaces, form tends to outweigh substance, and my more intimate, tactile approach doesn’t always align with the curatorial vision.
Additionally, most art residencies and exhibition programs at scientific or artistic institutions that intertwine art and science are designed for artists or scientists who want to collaborate with the other discipline, but rarely for individuals who belong to both fields.
The tension of working between disciplines is very real. I often feel like I belong to both artistic and scientific worlds, but also to neither.
The exhibition seen from the front of the gallery during a reading event by other GEDOK artists (and guest artists), as part of the organization’s ongoing cultural activities.
How did you find this art gallery and why you thought it was a good venue for your work?
I first came across the GEDOK Heidelberg gallery while walking through the city. I saw the exhibition they were showing at the time and thought it could be a good fit for my own work. So I waited for the next open call for new members, applied, and was accepted.
GEDOK is an artistic community in Germany — in fact, it’s the oldest and largest interdisciplinary network for female artists and art supporters in Europe. It brings together creators from the visual arts, music, literature, and beyond. Next year, the organization will celebrate its 100th anniversary, which speaks to its truly rich history. It has branches in 23 cities across the country, and I’m a member of GEDOK Heidelberg.
After becoming a member, I also applied for the opportunity to present a solo exhibition. A jury of artists and specialists accepted my proposal and gave me very encouraging feedback.
The exhibition was curated by Angelika Wild-Wagner and Anne Arend-Schulten, curators and artists from GEDOK, who accompanied me throughout the entire process. They helped me shape the exhibition concept and supported me during the installation. They also encouraged me to create a two-meter-long DNA sculpture that explores the theme of nature versus nurture, which is now part of the exhibition. It was a very enriching collaboration.
I also received support from Sabine Friebe-Minden, a graphic designer and fellow GEDOK artist. She developed the entire visual concept for the exhibition advertisement.
From left to right: Dr. Oliver Pajonk (a scientist and musician who provided the evening’s music), Dr. Ayelen Valko (the artist behind the exhibition), Sofie Morin (a GEDOK writer who also performed at the opening), and the curators Anne Arend-Schultenand Angelika Wild-Wagner (also GEDOK artists).
Oliver performing some of his original guitar compositions.
How has the public reacted to your work?
So far, the response has been very encouraging. The opening was well attended by a diverse audience.
Those with a scientific background often enjoy recognizing familiar cellular elements and biological processes. Some are drawn to scientific illustrations depicting different model organisms and organs, while others prefer more abstract cellular and molecular landscapes. Ultimately, it depends on each person’s interests and tastes.
Those without a scientific background tend to appreciate the works for their shapes, colors, and composition. Many engage with the idea of imagining the universe inside a cell, which opens the door to science communication and popularization.
Some visitors are also especially moved by the metaphors and symbolism. They connect with the psychological or emotional aspects of the work, demonstrating how the pieces can resonate on multiple levels.
Visitors discussing the artworks.
What’s next for you?
I’m currently looking for new venues to exhibit my work—such as scientific institutions, museums, and art galleries—and I hope to collaborate more closely with both artists and scientists.
I also plan to finish the two series I mentioned earlier and to continue exploring new biological themes in my artwork.
In addition, I’d like to engage more deeply in science outreach activities. I particularly enjoy working with schools: I’ve given virtual talks to students in Argentina, my home country, and those experiences have been especially rewarding.
As part of this outreach effort, Lis Albert, a science communicator and PhD student at Heidelberg University, and I will lead a science communication activity for high school students at the gallery. On June 23, ninth-grade students from Helmholtz-Gymnasium Heidelberg will participate in the session with their teacher, Silke Reinhardt. We will use my science-inspired art as a starting point to talk about cell biology and laboratory work.
At some point, I’d also love to connect with publishers to develop a book on art and science. It’s an idea I’ve been thinking about for a while, and one I’m eager to explore further.
Grasses play a crucial role in human food production and are primarily cultivated for their edible grains. The quantity of grain a grass species can produce is closely linked to the architecture of its inflorescence. Over the course of evolution, grasses have developed a wide variety of inflorescence architectures. From the complex branched inflorescences of the Oryzae tribe (e.g. rice), where multiple grains develop on primary and secondary branches, to the simple spike-type inflorescence of the Triticeae tribe (e.g barley and wheat), where single grains develop on short vestigial axes called rachillae1 (Fig.1 A).
These architectural differences are established during the early stages of the plant’s development by the activity of meristems, specialised structures leading organ growth. The size, position, and lifespan of these meristems determine the eventual shape of the inflorescence2. An example of how small differences in meristem activity can significantly impact the final inflorescence architecture is found within the Triticeae tribe. In barley, the rachilla primordium grows just enough to form a single floret and grain. In contrast, in wheat, its prolonged activity allows for the formation of multiple florets per spikelet, ultimately resulting in its characteristic multi-grain spikelet1 (Fig.1 B,C).
Figure 1: (A) Schematic representation of different grass inflorescence architectures. Main stem and branches in dark green, grains in light green and rachillae in red. (B,C) Scanning electron microscope images of barley and wheat inflorescences at early stages of development. Different organs comprising a spikelet are coloured (rachilla primordium in red, floret meristem in yellow and lemma primordium in green). Each spikelet develops into a single grain in barley and multiple grains in wheat.
When I joined Rüdiger Simon’s lab to begin my PhD, the group was primarily focused on understanding the role of CLE signalling pathways in regulating shape, size, and maintenance of shoot and root apical meristems in Arabidopsis thaliana. At that time, they had begun extending their research to the cereal plant barley. Gwendolyn Kirschner, a former PhD student in the lab, had started investigating the role of CLE-peptide signalling in barley by generating fluorescent reporter lines, including the barley orthologs of the Arabidopsis CLE40 peptide (HvFCP1) and CLV1 receptor (HvCLV1), which had previously been shown to regulate stem cell fate in Arabidopsis meristems3,4. While Gwendolyn primarily analysed barley roots, my project focused more on shoot apical meristem and inflorescence development.
In comparison to the simple inflorescence of Arabidopsis, grasses evolved a more complex organisation, with different meristem types leading to the formation of various organs comprising the spikelet, the basic unit responsible for the development of grains in cereals. This observation led us to the questions: “How is the shape and activity of all these different meristems regulated and coordinated to generate specific inflorescences in grasses? Did barley evolve specific CLE/CLAVATA signalling pathways to regulate the activity of different meristem types?”
HvCLV1 regulates meristem activity along the vertical and lateral axes of the barley inflorescence.
I began by mutating the closest ortholog of CLV1 in barley (HvCLV1) as well as other closely related receptors, which we are still investigating. In maize, as in Arabidopsis, mutation of CLV1 or its ortholog leads to a drastically enlarged inflorescence meristem, resulting in the disorganised formation of additional primordia4,5. In the barley Hvclv1 mutant, I initially observed occasional formation of extra grains within the inflorescence. However, detailed analysis by scanning electron microscopy revealed that an enlarged inflorescence meristem generated an additional row of spikelet primordia, organised in a spiral phyllotaxis rather than in a disorganised manner (Fig. 2A, B).
Moreover, I noticed that Hvclv1 inflorescences developed an elongated rachilla primordium, which produced additional florets per spikelet, an effect previously observed in barley mutants as multiflorus2.b and INTERMEDIUM-m6,7. These results led me to conclude that the ectopic grains generated by the Hvclv1 mutant were due to increased activity of the inflorescence meristem along the vertical axis and of the rachilla primordium along the lateral axis. To further support this, I imaged mature rachillae from WT and Hvclv1 plants and observed the formation of a meristem-like structure at the tip of the Hvclv1 rachilla, which developed into an actively growing small branch instead of the vestigial hairy structure seen in WT (Fig. 2C, D).
Figure 2: (A,B) Scanning electron microscope images displaying spikelet phyllotaxis (dashed lines) in WT (A) and Hvclv1 (B) early inflorescence tips, combined with photos of the respective final inflorescences. (C,D) Scanning electron microscope images of WT and Hvclv1 early inflorescences. Colours were used to highlight different meristems and primordia (inflorescence meristem in blue, spikelet meristem in violet, rachilla primordium in red, floret meristem in yellow, anther and carpel primordia in brown and pink). Red dashed lines indicate the mature rachilla, combined with zoom-in images where the white arrow indicates the meristem-like structure identified in Hvclv1. Figure modified from Vardanega et. al 2025.
The CLE peptide HvFCP1 acts with HvCLV1 to restrict rachilla primordium activity to the formation of a single floret.
Once the function of the HvCLV1 receptor was characterised, I wondered whether the regulation of rachilla growth was determined by the binding of a specific CLE peptide. Barley possesses 28 different CLE peptides, but I was specifically seeking one that is strongly conserved among grasses and may have contributed to the drastic reduction of branch size in Triticeae. Upon reviewing the literature, I realised that only one peptide retained the same protein sequence across all studied grass species: FCP18. HvFCP1 is the closest ortholog to the Arabidopsis CLE40, for which we already had a fluorescent reporter line. When I examined the expression of HvFCP1 during barley inflorescence development, I noticed that it was not only co-expressed with HvCLV1 but also specifically expressed in the rachilla primordium (Fig. 3 A,B). The insensitivity of the Hvclv1 shoot apical meristem to HvFCP1 peptide treatment, along with the formation of an elongated rachilla producing additional florets even in Hvfcp1 mutants (Fig. 3 C), ultimately demonstrated that HvFCP1 interacts with HvCLV1 to regulate rachilla activity in barley, thereby determining its specific inflorescence architecture.
Figure 3: (A,B) Confocal microscope pictures of barley spikelets displaying HvCLV1 protein localisation (green) and HvFCP1 promoter activity (magenta). The white arrow indicates the rachilla primordium. (C) Hvfcp1 inflorescence displaying double florets (white arrow). (D) RNA seq results. The heatmap shows the z-score of median Transcripts Per Million (TPM) values for each of the Differently Expressed Genes (DEG) in Hvclv1 vs WT and Hvfcp1 vs WT. Black rectangles indicate similarly differentially expressed genes between Hvclv1 vs WT and Hvfcp1 vs WT, with the affected biological processes on the side. Figure modified from Vardanega et. al 2025.
I then investigated which genes are directly or indirectly regulated by HvFCP1/HvCLV1 by performing RNA sequencing on mutant inflorescences compared to wild type (WT). The transcriptome analysis revealed several similarly differentially expressed genes (DEG) between Hvclv1 vs WT and Hvfcp1 vs WT, involved in processes such as cell division, auxin signalling, and trehalose-6-phosphate signalling, providing possible target genes that we are currently investigating (Fig.3 D).
Translating knowledge and techniques from model plants to crops.
In addition to its biological novelty, this paper represents a successful example of translational research, bridging techniques and knowledge from model species to agronomically significant crops. We applied various microscopy techniques more commonly used in model plants, such as Arabidopsis thaliana, but less frequently employed in cereal biology. We developed reporter and complementation lines and quantified receptor cytoplasmic internalisation in rachilla and floret meristems. Furthermore, we utilised methods such as 3D reconstruction and smRNA-FISH for detailed phenotypic analysis of the inflorescence meristem and its expression patterns.
To build on this approach, we generated BARVISTA (http://purl.org/barvista/home), a dataset providing transcriptional information for each cell within the barley inflorescence by integrating single-cell RNA sequencing data with spatial transcriptomics results. Using this resource, we identified transcription factors involved in establishing the specific patterns of meristem ontogenesis necessary to shape the characteristic morphology of the barley spike9.
In conclusion, our work shed light on the signalling pathways that regulate the shape and behaviour of individual meristem types within the inflorescence, paving the way for future efforts to engineer inflorescence architecture through targeted regulation of distinct meristem activities.
REFERENCES:
Koppolu, R. & Schnurbusch, T. Developmental pathways for shaping spike inflorescence architecture in barley and wheat. Journal of Integrative Plant Biology61, 278–295 (2019).
Kyozuka, J., Tokunaga, H. & Yoshida, A. Control of grass inflorescence form by the fine-tuning of meristem phase change. Current Opinion in Plant Biology17, 110–115 (2014).
Schlegel, J. et al. Control of Arabidopsis shoot stem cell homeostasis by two antagonistic CLE peptide signalling pathways. eLife10, e70934 (2021).
Bommert, P. et al. thick tassel dwarf1 encodes a putative maize ortholog of the Arabidopsis CLAVATA1 leucine-rich repeat receptor-like kinase. Development132, 1235–1245 (2005).
Koppolu, R. et al. The barley mutant multiflorus2.b reveals quantitative genetic variation for new spikelet architecture. Theor Appl Genet135, 571–590 (2022).
Zhong, J. et al. INTERMEDIUM-M encodes an HvAP2L-H5 ortholog and is required for inflorescence indeterminacy and spikelet determinacy in barley. Proceedings of the National Academy of Sciences118, e2011779118 (2021).
Goad, D. M., Zhu, C. & Kellogg, E. A. Comprehensive identification and clustering of CLV3/ESR-related (CLE) genes in plants finds groups with potentially shared function. New Phytologist216, 605–616 (2017).
Demesa-Arevalo, E. et al. Imputation integrates single-cell and spatial gene expression data to resolve transcriptional networks in barley shoot meristem development. 2025.05.09.653223 Preprint at Biorxiv https://doi.org/10.1101/2025.05.09.653223 (2025).
We are pleased to support The Pavilion for People, running alongside the 2025 UN Ocean Conference. Explore the space to learn more and share your thoughts on saving our oceans.
As part of The Pavilion for People, we will host a webinar on Thursday 12 June at 11am (BST) on ‘How to organise events more sustainably’. The webinar is free to join. Access the schedule a few minutes before the event and follow the instructions on how to join it.
During the webinar, we will detail the latest best practice advice, as well as providing information on our available resources for creating sustainable events including our new carbon event calculator, coming soon. We look forward to meeting you.
The 28 May 2025 webinar was chaired by Development’s Executive Editor, Alex Eve and featured the first authors of the finalists of Development’s 2024 outstanding paper prize.
This week we’ll meet Dr Karin Van der Burg, a new faculty at Clemson University. Karin’s introduction to seasonal adaptation came during her undergrad first-year biology lecture, when she first heard about butterflies changing wing colors depending on temperature. “I thought that was SO COOL!” she recalls that moment. Her first encounter with phenotypic plasticity shifted how she saw development. Since then, Karin’s curiosity has led her deep into the physiological and genetic mechanisms that allow insects to tune their development to the seasons. From hormones and gene expression to chromatin and cold tolerance, her work spans multiple levels of biological organization. She’s studied butterflies that color-shift with the calendar, and budworms that shut down development to survive freezing winters. Now at her own lab, she’s combining genetics and physiology to explore how environmental cues like day length, temperature and seasons get integrated by hormonal systems to shape development using the Buckeye butterfly, Junonia coenia, and other incredible insect models. At heart, her science is driven by one thing: a need to know how it all works. Check out her lab page here. Give her a follow over Twitter and Bluesky. Keep an eye for announcements because she will soon be hiring postdocs and students in her lab !
What was your first introduction to the study of seasonal adaptation in insects? Tell us about that moment and how it shaped your scientific path?
I believe the first time I heard about this was in first year of college, in a lecture from Dr. Paul Brakefield. He told us about Bicyclus anynana, a small brown African butterfly species that changes its phenotype depending on rearing conditions. Exposure to cooler temperatures leads to a dull brown phenotype, which is adaptive in the dry season, while exposure to warmer temperatures results in the development of colorful wing eyespots, which are more adaptive in the wet season. At the time I thought that was SO COOL!
This was basically my first introduction to phenotypic plasticity: the phenomenon where multiple phenotypes could be created from one genotype. It really changed my perspective on how organisms develop and grow; I used to believe it was a very deterministic process, but instead it turned out to be very adaptable.
The Common Buckeye butterfly, Junonia coenia
Tell us what sparked your interest in the connection between endocrine signaling and seasonal adaptation? Walk us through your journey into studying the genetic and physiological basis of seasonal adaptation and introduce us to the field.
What really drew me in was the idea that phenotypes are plastic. At the time, work done in the evolution group at Leiden University did a lot of research in hormonal signaling underlying this plasticity, and I was fortunate enough to be able to do my undergraduate research project in that group. My project focused on genes associated with DNA methylation. It didn’t really go anywhere, but it was my first introduction to hormonal signaling and epigenetic signaling possibly working in concert.
As I continued my education, into my master’s and my PhD, I really started to think about how endocrine signaling affects epigenetic changes, which in turn results in changes in developmental pathways, resulting in different phenotypes. I realized to truly understand how organisms respond to seasonal changes, we need to look at the complete picture, and not one small aspect.
During my PhD I did mostly genetics research (with Dr. Reed at Cornell University), looking at genetic changes involved with changes in butterfly wing color plasticity. I also looked at changes to gene expression and chromatin accessibility, with a little bit of endocrine signaling, all to understand how seasonal plasticity in butterfly wing colors can evolve. While it was really interesting, I did feel like I was too focused on one aspect of a phenotype (in my case, butterfly wing color), and not the organism as a whole. I felt like there were many more changes involved in seasonal plasticity. Thus, for my postdoc I switched to a much more physiology focused lab (Dr. Marshall at UBC) to really get that more holistic perspective. To really understand how insects adapt to seasonal conditions, I believe we need to look at insect holistically, and not just one small aspect.
You have worked with different model systems including budworm Choristoneura fumiferana, and the common buckeye butterfly Junonia coenia. Tell us about your experience of working with these unique systems. What advantages do they offer in studying seasonal adaptations?
The biggest advantage is that these two organisms allow me to investigate two different types of seasonal adaptation; J. coenia has two flight seasons a year, an early and a late summer season. Each season has different conditions, such as temperature, rainfall, and food availability. We can use that to investigate how insects survive and reproduce in different conditions. Most notable about this butterfly is its change in wing coloration: butterflies emerge with a pale tan color when reared under warm, long-day conditions, and a dark red color when reared under cold, short-day conditions. Very likely there are other seasonal adaptations too, although they are not well known.
C. fumiferana, or the eastern spruce budworm, is really interesting in that it only has one lifecycle per year, and it is also stationary in the northern boreal forest. That means it needs to survive winter, with truly harsh conditions. Some very extreme changes in phenotype are necessary to survive under those conditions. My main interest is in the diapause phenotype, a prolonged period of arrested development during the early larval stages that allows for survival during harsh winters.
I like the combination of the two, because it allows me to study survival and reproduction in multiple different seasons, with very different survival strategies!
Tell us about your work on butterfly wing color plasticity. What were some of your key findings regarding the genetic factors controlling changes in wing color plasticity? Specifically, how does the upregulation of metabolites like trehalase contribute to the environmentally induced and genetically assimilated red phenotype?
During my PhD, I did a big research project on seasonal wing color plasticity in Junonia coenia. As I mentioned, in the wild this butterfly displays seasonal wing color plasticity, but we found we can easily manipulate this through artificial selection, such that plasticity was lost in only a few generations. We found three genes to be involved in this loss of plasticity, trehalase, herfst, and cortex. Later, my colleagues found that it probably wasn’t cortex regulating plasticity, but ivory, a long non-coding RNA. (Fandino et al., 2024; Livraghi et al., 2024; Tian et al., 2024).
Trehalase was indeed a very interesting find! The gene is upregulated under cold conditions in Junonia, and in other insects it is involved in cold-hardening. Trehalose (the sugar) can act as a cryoprotectant (prevents hemolymph freezing), and it is involved in metabolism.
We hypothesized that trehalase may be involved with the production of red pigments as well, because the ommochrome pigment that produces the red color contains a sugar molecule.
It’s really interesting to hypothesize on the multiple roles trehalase might play in seasonal plasticity. For example, it could be that the involvement in red pigmentation is a secondary effect; where trehalase was upregulated at first to manage cold conditions, and later was co-opted to produce red pigmentation as well! I will say that this is mostly speculation at this point, but it is definitely a research avenue worth pursuing.
Butterflies rely on endocrine cues to regulate metabolism and developmental timing. How does the ecdysone signaling pathway integrate environmental information to drive seasonal phenotypes?
These are really, really good questions! There is a lot of evidence that ecdysone signaling in butterflies is a universal regulator of seasonal plasticity (Bhardwaj et al., 2020). Given that ecdysone signaling is responsive to changes in day length, it is likely that circadian genes are involved, although that mechanism is not well worked out in insects.
Can small changes in endocrine signaling lead to tissue-specific adaptations without widespread disruptions. How does this level of regulation evolve, and what makes it so flexible?
Again, very good question. There are two things at play here: the seasonal responsiveness of ecdysone signaling, and the ability of seasonal plasticity to rapidly evolve. I believe overall development is very robust against predictable seasonal changes in ecdysone signaling. Tissue specific adaptations, such as wing color and wing shape in Junonia, or eyespot size in other nymphalid butterflies, can evolve rapidly to become more or less responsive to fluctuations in ecdysone. I suspect that outside of predictable seasonal changes, fluctuations in ecdysone signaling would be very problematic for normal development. I think (I may be wrong) the reason why plasticity can evolve so rapidly is because the seasonal responsiveness system (ecdysone signaling) is so robust and thus predictable, and so it makes for a reliable internal cue to adjust tissue specific developmental programs.
How does natural selection shape the regulation of hormonal pathways involved in adaptation? Are there evolutionary constraints that limit how endocrine signaling can be modified?
I think we know very little about the evolution of hormonal pathways itself! There are almost certainly many constraints on how endocrine signaling itself can evolve, because hormonal signaling is involved in so many different things. I believe that natural selection can readily act on downstream receivers of endocrine signals, but maybe not so much on the ecdysone signal itself. I’m happy to be proven wrong here though!
Speaking of your experimental approach – What have been the biggest challenges in studying endocrine regulation of seasonal adaptation? Are there specific experiments that were particularly difficult to execute? Did you have to deal with midnight timepoints or require an army of undergrads/ long hours etc.
Ecdysone measurements are a huge pain… Much harder than any of the genetic analysis I’ve done; ATAC-seq /RNA-seq / CRISPR/Cas9 were all a breeze compared to ecdysone measurements. It appears such a straightforward experiment, but I was constantly dealing with broken HPLC machines, degradation of ecdysone samples in the freezer… And yes, many late night or early morning sampling time points. I did all the sampling myself, but I did have an army of undergraduate students to help rear all the caterpillars!
Looking ahead, what are the next big questions in understanding how endocrine signaling and metabolism intersect with seasonal adaptation?
I’m very interested in exploring the interplay between circadian rhythms and ecdysone signaling! How/why is ecdysone signaling so responsive to external cues?
What role does curiosity play in your life, both within and outside of science? Why do you choose to work on insects?
Ultimately, I just want to know how stuff works… I enjoy thinking about biological research questions that integrate external and internal factors. I landed on gene regulatory mechanisms because for me, that’s where the bridge is between hard-coded DNA and the final phenotype which is very dependent on external conditions. I mostly work on insects because they are easier to work with than mammals, and because many insect species are very important to us.
Have you noticed a shift in how researchers approach insect biology?
Definitely have seen a shift to consider organisms more holistically, integrating factors at multiple levels of biological organization. I also feel like the scientific community is a lot more aware how important external conditions such as seasons are! So yes, I definitely think so.
Tell us about how you see the future of adaptative metabolism evolve with the new upcoming tools – what techniques have you used and which tools are you most excited about?
Single-cell RNA/ATAC-seq, and new CRISPR/Cas9 applications…
I haven’t worked with single cells yet, but I’d like to in the future! I’ve worked a lot with gene-editing through CRISPR/Cas9, but new techniques using CRISPR are coming out regularly and it is very exciting.
Were there any pivotal moments that shaped your career path? What’s an unexpected place you’ve found inspiration for your work? What advice would you offer to students and early-career scientists?
I was in a very genetics driven lab during my PhD, working with Bob Reed at Cornell. During my PostDoc, I shifted to a much more physiology-oriented lab, working with Katie Marshall at UBC. That shift really cemented that I wanted to integrate physiology and genetics research. I’m not sure this is ‘unexpected’ but I get most inspired from conversations with other folks, especially new students. The questions I get asked, especially ones that I don’t know the answer to, are really inspiring!
For advice, always be willing to consider new perspectives, and never be afraid to share your own thoughts, even if you’re not super confident. Science is a group effort!
How do you maintain a balance between your rigorous research activities and personal life? Are there hobbies or practices you find particularly rejuvenating?
These days I have a child, and that forces me to put down work when I’m at home! Otherwise, I love crafting! For example, making quilts or knitting.
If you hadn’t embarked on a career in biological research, what other profession might you have pursued, and why?
I truly don’t know – Before I found biology I tried engineering for a year and failed miserably. I feel like biology is the alternative career path for me and it has worked out well so far!
Anything you’d want to highlight for the future?
I’ll be looking for a postdoc this coming year! I’ll make a more formal announcement soon. I’m also rounding up a big project that I started in my postdoc on local adaptation in spruce budworm, I’m very excited for that!
Last week we learnt about how cancer cells rewire their metabolism to alter their cell fate and proliferate, check out –Switching Gears – Metabolic rewiring in cancer (Luis Cedeno-Rosario).
Spotted a preprint in this list that you love? If you’re keen to gain some science writing experience and be part of a friendly, diverse and international community, consider joining preLights and writing a preprint highlight article.
Hannah N. Gruner, C. J. Pickett, Jasmine Yimeng Bao, Richard Garcia, Akiko Hozumi, Tal Scully, Shaoyang Ning, Mavis Gao, Gia Bautista, Keren Maze, Karissa Lim, Tomohiro Osugi, Mae Collins-Doijode, Ofubofu Cairns, Gabriel Levis, Shu Yi Chen, TaiXi Gong, Honoo Satake, Allon Moshe-Klein, Eduardo D. Gigante, Yasunori Sasakura, Bradley Davidson
Alexandra E. Wehmeyer, Johanna K. Schmitt, Felix Eggersdorfer, Lea Zissel, Chiara M. Schröder, Mehmet Tekman, André Dias, Katrin M. Schüle, Simone Probst, Alfonso Martinez-Arias, Katie McDole, Sebastian J. Arnold
Wen Tian, Timothy Ting-Hsuan Wu, Shenbiao Gu, Jason L. Chang, Cerianne Huang, Ryan Vinh, Adam M. Andruska, Kyle K. Song, Dongeon Kim, Yu Zhu, Seunghee Lee, Junliang Pan, Peter N. Kao, Tushar Desai, Lawrence S. Prince, Lindsay D. Butcher, Xinguo Jiang, Marlene Rabinovitch, Kristy Red-Horse, Mark R. Nicolls
Alicia Lardennois, Chaitanya Dingare, Veronika Duda, Petra A Klemmt, Constanze Heinzen, David Kleinhans, Thorsten Falk, Carsten Schelmbauer, Olivia Mozolewska, Sofia Papadopoulou, Jason J K Lai, Didier Y R Stainier, Virginie Lecaudey
Chih-Wen Chu, Satheeja Velayudhan, Jakob H. Schauser, Sapna Krishnakumar, Stephanie Yang, Keiji Itoh, Dominique Alfandari, Ala Trusina, Sergei Y. Sokol
Soham Basu, Petrus Steenbergen, Florian Gabler, Alexandre Paix, Paolo Ronchi, Gleb Bourenkov, Thomas Schneider, Jonas Hellgoth, Anna Kreshuk, Suat Özbek, Aissam Ikmi
Konrad Chudzik, Isabel Guerreiro, Samy Kefalopoulou, Alex Abraham, Magdalena Schindler, Alessa Ringel, Mario Nicodemi, Irina Solovei, Andrea M. Chiariello, Stefan Mundlos, Jop Kind, Michael I. Robson
Alexandre Jourdon, Jessica Mariani, Abhiram Natu, Feinan Wu, Boxun Li, Davide Capauto, Kevin T. Hagy, Scott Norton, Livia Tomasini, Alexias Safi, Anahita Amiri, Jeremy Schreiner, Cindy Khanh Nguyen, Neal Nolan, Matthew P. Nelson, Daniel M. Ramos, Michael E. E. Ward, Anna Szekely, James C. McPartland, Kevin Pelphrey, Pamela Ventola, Katarzyna Chawarska, Charles A. Gersbach, Gregory E Crawford, Alexej Abyzov, Flora M. Vaccarino
Jason F. Cooper, Kim Nguyen, Darrick Gates, Emily Wolfrum, Colt Capan, Hyoungjoo Lee, Devia Williams, Chidozie Okoye, Kelsie Nauta, Ximena Sanchez-Avila, Ryan T. Kelly, Ryan Sheldon, Andrew P. Wojtovich, Nicholas O. Burton
Bernard K. van der Veer, Colin Custers, Wannes Brangers, Riet Cornelis, Spyridon Champeris Tsaniras, Kobe De Ridder, Bernard Thienpont, Huiyong Cheng, Qiuying Chen, Daniel Kraushaar, Richard H. Finnell, Steven S. Gross, Kian Peng Koh
Takashi Ishida, Juliane Mercoli, Adam M. Heck, Ian Phelps, Barbara Varnum-Finney, Stacey Dozono, Cynthia Nourigat-McKay, Katie Kraskouskas, Rachel Wellington, Olivia Waltner, Dana L Jackson, Colleen Delaney, Shahin Rafii, Irwin D. Bernstein, Kimberly A. Aldinger, Birth Defects Research Laboratory (BDRL), Cole Trapnell, Helong G. Zhao, Brandon Hadland
Cesi Deng (邓策思), Adedamola Elujoba-Bridenstine, Ai Tang Song, Rylie M. Ceplina, Casey J. Ostheimer, Molly C. Pellitteri Hahn, Cameron O. Scarlett, Owen J. Tamplin
Beverly A Rothermel, Malay Chaklader, Guilherme H Souza Bomfim, Neil Jeju, Yingli Duan, Brian F Niemeyer, Joaquín Maximiliano Espinosa, Edwin Rosado-Olivieri, Weichun Lin, Rodrigo S Lacruz
Akaljot Singh, Holly M. Poling, Jennifer Foulke-Abel, Nambirajan Sundaram, Abid A. Reza, Sarah Joseph, Abrahim ElSeht, Kalpana Srivasta, Maksym Krutko, Christopher N. Mayhew, David T. Breault, James M. Wells, Jay Thiagarajah, Amy E. O’Connell, Olga Kovbasnjuk, Michael A. Helmrath
Seungmi Ryu, Jason Inman, Hyenjong Hong, Vukasin M Jovanovic, Yeliz Gedik, Yogita Jethmalani, Inae Hur, Ty Voss, Justin Lack, Jack Collins, Pinar Ormanoglu, Anton Simeonov, Carlos A. Tristan, Ilyas Singeç
From Ryu et al. This image is made available for use under a CC0 license.
Anahí Binagui-Casas, Anna Granés, Alberto Ceccarelli, Eleni Karagianni, Daniel Lopez Ramajo, Rosa Portero, Matthew French, Jen Annoh, Frederick C.K. Wong, Sally Lowell, Osvaldo Chara, Valerie Wilson
Yiqian Li, Sean T.S. Law, Wenyan Nong, Wai Lok So, Yichun Xie, Thomas C.N. Leung, Tse Ho Li, Joyce Tse, Ho Yin Yip, Oli Jin, Jordan Zhang, Apple PY Chui, Kwok Fai Lau, Akbar John, Zhen-peng Kai, William G. Bendena, Alexander Hayward, Yingying Wei, Ting Fung Chan, Sai Ming Ngai, Jerome HL H
Ann K. Baako, Ragavi Vijayakumar, Daniel Medina-Cano, Zhaoquan Wang, Jesús Romero-Pichardo, Kelvin Fadojutimi, Stephanie C. Do, Yuan Lin, Mohammed Islam, Sanjana Dixit, Alissa J. Trzeciak, Justin S.A. Perry, Thomas Vierbuchen
Binayok Sharma, Xinyue Lu, Hamood Rehman, Vandré C. Figueiredo, Carol Davis, Holly Van Remmen, Shihuan Kuang, Susan V. Brooks, Krishna Rao Maddipati, James F. Markworth
Seda Akgün, Thomas Lenz, Annika Zink, Karina Stephanie Krings, Sebastian Wesselborg, María José Mendiburo, Alessandro Prigione, Kai Stühler, Björn Stork
Samuel G. Regalado, Chengxiang Qiu, Sanjay Kottapalli, Beth K. Martin, Wei Chen, Hanna Liao, Haedong Kim, Xiaoyi Li, Jean-Benoît Lalanne, Nobuhiko Hamazaki, Silvia Domcke, Junhong Choi, Jay Shendure
Cloe de Luxán-Hernández, Thomas J. Ammitsøe, Jakob V. Kanne, Sabrina Stanimirovic, Milena E. Roux, Zoe Weeks, Michael Schutzbier, Gerhard Dürnberger, Elisabeth Roitinger, Liechi Zhang, Oliver Spadiut, Masaki Ishikawa, Mitsuyasu Hasebe, Laura A. Moody, Yasin F. Dagdas, Eleazar Rodriguez, Morten Petersen
Edgar Demesa-Arevalo, Hannah Dorpholz, Isaia Vardanega, Jan Eric Maika, Itzel Pineda-Valentino, Stella Eggels, Tobias Lautwein, Karl Kohrer, Thorsten Schnurbusch, Maria von Korff, Bjorn Usadel, Rudiger Simon
Tasnim Zerin, Paola Ruiz-Duarte, Ann-Kathrin Schürholz, Theresa Schlamp, Yanfei Ma, Carlo Bevilacqua, Nabila El Arbi, Christian Wenzl, Andrej Miotk, Robert Prevedel, Thomas Greb, Jan Lohmann, Sebastian Wolf
Jie Fu, Brandon James, Madara Hetti-Arachchilage, Yingjie Lei, Brian McKinley, Evan Kurtz, Kerrie Barry, Stephen P. Moose, John E. Mullet, Kankshita Swaminathan, Amy Marshall-Colon
Callum V. Bucklow, Emanuell Duarte Ribeiro, Fabrizia Ronco, Nathan Vranken, Michael K. Oliver, Walter Salzburger, Melanie Stiassny, Roger Benson, Berta Verd
Allyson Caldwell, Liheng Yang, Rebecca L. Casazza, Rizban E. Worota, Cole McCutcheon, Patrick S. Creisher, Erika Zhan, Clara Reasoner, Ashley Higgins, Tony Schountz, Carolyn B. Coyne
Marie Lebel, Tiphaine Sancerini, Sharon Rabiteau, Solène Marchal, Pragati Sharma, Tal D. Scully, Estelle Balissat, Laurel S. Hiebert, Anthony W. De Tomaso, Allon M. Klein, Alexandre Alié, Stefano Tiozzo
Patrizia Pessina, Mika Nevo, Junchao Shi, Srikanth Kodali, Eduard Casas, Yingzhi Cui, Alicia L. Richards, Emily J. Park, Xi Chen, Florencia Levin-Ferreyra, Erica Stevenson, Nevan J. Krogan, Danielle L. Swaney, Qilong Ying, Qi Chen, Justin Brumbaugh, Bruno Di Stefano
Fangfei Jiang, Michael Boylan, Dale W. Maxwell, Wasay Mohiuddin Shaikh Qureshi, Charlie F. Rowlands, Gennadiy Tenin, Karen Mitchell, Louise A. Stephen, Elton J. R. Vasconcelos, Dapeng Wang, Tong Chen, Junzhe Zha, Jingshu Liu, Nouf Althali, Dragos V. Leordean, Meurig T. Gallagher, Basudha Basu, Katarzyna Szymanska, Advait Veeraghanta, Bernard Keavney, Martin J. Humphries, Jamie Ellingford, David Smith, Colin A. Johnson, Raymond T. O’Keefe, Sudipto Roy, Kathryn E. Hentges
Kristiina Uusi-Rauva, Anniina Pirttiniemi, Antti Hassinen, Ras Trokovic, Sanna Lehtonen, Jukka Kallijärvi, Markku Lehto, Vineta Fellman, Per-Henrik Groop
Atesh Kara Worthington, Beltran Borges, Tony Lum, Elisa Schrader Echeverri, Fareha Moulana Zada, Marco Cordero, Hyejin Kim, Ryan Zenhausern, Ozgenur Celik, Cindy Shaw, Paula Gutierrez-Martinez, Marzhana Omarova, Chris Blanchard, Sean Burns, Kyle Cromer, James Dahlman, Tippi MacKenzie
Quanyi Zhao, Albert Pedroza, Disha Sharma, Wenduo Gu, Alex Dalal, Chad Weldy, William Jackson, Daniel Yuhang Li, Yana Ryan, Trieu Nguyen, Rohan Shad, Brian T. Palmisano, João P. Monteiro, Matthew Worssam, Alexa Berezwitz, Meghana Iyer, Huitong Shi, Ramendra Kundu, Lasemahang Limbu, Juyong Brian Kim, Anshul Kundaje, Michael Fischbein, Robert Wirka, Thomas Quertermous, Paul Cheng
Annabelle Suter, Alison Graham, Jia Yi Kuah, Jason Crisologo, Chathuni Gunatilake, Koula Sourris, Michael See, Fernando J Rossello, Mirana Ramialison, Katerina Vlahos, Sara E Howden
Many times, the project or PhD is over, and the paper published, and yet the story unfinished. During the course of PhD, there arise many mysterious observations and unanswered questions.
My PhD work was published last year, where we describe the role of Cph (Chronophage) in locomotor behaviour of Drosophila. I report here an observation that isn’t completely explained by our present understanding of neural development in Drosophila.
Surprises on our path: When I started my PhD, with Prof. Upendra Nongthomba at the Indian Institute of Science, Bengaluru, this gene Cph was only a number (CG9650). Where to look for this unknown gene’s function? The project was a challenge, and it threw a couple of surprises in our path.
First, the only evidence that this gene might have a role in neural development (and hence our interest in it) came from a mis-expression screen. This screen showed that pan-neural expression of this gene i.e. in all neuroblasts and glia caused axon guidance defects. Was this due to its expression in neuroblasts/glia other than those in which it normally expressed? That’s what we thought – wrong cell, wrong time. The defects were grave enough to cause embryonic lethality.
However, upon knockdown of this gene in neuroblasts, or glia, or neurons, we didn’t see any axon guidance defect, or embryonic lethality. Knockdown in neurons resulted in flies that were constantly shaking, short-lived and failed to reproduce.
Normal fly movementMovement of Cph knockdown flies
The second challenge lay in understanding the behavioural defect. I first thought the constant shaking of these flies was due to seizures. I requested inputs from experts – the late Prof. K. S. Krishnan (National Centre for Biological Sciences, Bengaluru, India), and Prof. Dan Kuebler (Franciscan University of Steubenville, Ohio, USA). Prof. Krishnan asked me to take a video of higher magnification. (Unfortunately he passed away before we could reach a conclusion). Prof. Dan Kuebler, an expert in epilepsy in Drosophila, said the shaking didn’t look like seizures to him.
It occurred to me that the flies that lie on their back and keep shaking are perhaps trying to get back on their feet. Most of them were unable to stand up, and even if they did, they would fall down within seconds. So, the shaking was due to a motor defect, and not seizures. Electro physiological recordings also supported this – aberrant spontaneous spikes indicative of seizure were absent. (However, they did show bang sensitivity i.e. when subjected to a mechanical shock, they went into paralysis. This is mostly seen in seizure susceptible genotypes. So seizure susceptiblility cannot be ruled out in Cph knockdown animals.)
The baffling observation: We asked – at what stage of development was this gene necessary? Surprisingly, knockdown of this gene in adults didn’t have any effect! Knockdown during the larval stage reduced locomotor activity at that stage, but abolished locomotor activity in adults.
Effect of Cph knockdown at different stages of development: Cph was knocked down during different stages, and the resulting flies were assessed for their time spent upright.
Animals were initially reared at 18°C, and then shifted to 29°C at different stages of development. Shifting Cph knockdown animals at embryonic or L1 stage results in flies with locomotor defects. Shifting the animals post L3 stage results in flies with normal locomotor activity.
E, Embryo; L1, first larval instar; L3, third larval instar; P1, early pupa (less than 30hrs); P2, late pupa (70-90 hrs); A, adult
Animals were initially reared at 29°C and then shifted to 18°C at different stages of development. Shifting Cph knockdown animals at embryonic or L1 stage results in flies with normal locomotor activity. Shifting post L3 stage results in flies with locomotor defects.
How could this be explained? Were this protein expressed in larval neural stem cells, a possible explanation could be arrived at. But our observation was the result of knockdown in neurons! How could neuronal activity during development or the lack thereof affect their function in adults?
I outline two hypotheses:
Effect on re-specification of primary neurons.
Primary neurons are those born during the first phase of neuroblast divisions in the embryo. These neurons function during the larval stage and are reconfigured to connect to new targets to function during the adult stage. During neuronal remodelling that occurs during metamorphosis, neuronal processes are withdrawn from the larval targets and new axons and dendrites form towards adult specific targets. This re-specification of primary neurons could be affected if their functioning during the larval stage caused irreversible changes in them.
In case of motor neurons, activity dependent plastic changes during the larval stage could affect neuromuscular junction morphology, and this effect could persist during the remodelling stage.
Effect of energy state on formation/function of secondary neurons
Quiescent embryonic neuroblasts, post activation in first instar larvae, undergo another round of proliferation. This phase of neuroblast divisions produces the secondary neuronal lineages that function in the adult brain. Reactivation and subsequent division of these quiescent neuroblasts depends upon a signal from the fat body, which in turn depends upon the nutritional state of the animal (Chell and Brand 2010; Sousa-Nunes et al. 2011). Whether nutritional state also affects differentiation of neurons is not known.
Synapse function is an energy intensive process. ATP is required for axonal transport, vesicle fusion, neurotransmitter uptake etc. Animals with reduced PGK (PhosoGlycerateKynase), an enzyme required for ATP generation, show locomotor defects at larval and adult stage (Wang et al. 2004). PGK deficiency in humans has been shown to cause seizures, myopathy and muscle fatigue (Tsujino, et al. 1995), (DiMauro, Dalakas et al. 1983). The metamorphosis that follows the larval stage occurs using the energy stored during this stage. Metamorphosis is triggered by ecdysone release, which happens only after sufficient nutrients to survive metamorphosis have been acquired (Di Cara and King-Jones 2013). Though Cph knockdown animals probably acquire sufficient energy to survive metamorphosis, their neuronal development during this phase might be compromised.
I would welcome other ideas or suggestions.
References:
Chell, J. M. and A. H. Brand (2010). “Nutrition-responsive glia control exit of neural stem cells from quiescence.” Cell 143(7): 1161-1173.
Sousa-Nunes, R., L. L. Yee, et al. (2011). “Fat cells reactivate quiescent neuroblasts via TOR and glial insulin relays in Drosophila.” Nature 471(7339): 508-512.
Wang, P., S. Saraswati, et al. (2004). “A Drosophila temperature-sensitive seizure mutant in phosphoglycerate kinase disrupts ATP generation and alters synaptic function.” J Neurosci 24(19): 4518-4529.
Tsujino, S., S. Shanske, et al. (1995). “Molecular genetic heterogeneity of phosphoglycerate kinase (PGK) deficiency.” Muscle Nerve Suppl 3: S45-49.
DiMauro, S., M. Dalakas, et al. (1983). “Phosphoglycerate kinase deficiency: another cause of recurrent myoglobinuria.” Ann Neurol 13(1): 11-19.
Di Cara, F. and K. King-Jones (2013). “How clocks and hormones act in concert to control the timing of insect development.” Curr Top Dev Biol 105: 1-36.
The Center for Scientific Collaboration and Community Engagement (CSCCE) has announced its next offering of Scientific Community Engagement Fundamentals (CEF25F), which will run on Mondays and Thursdays beginning Thursday, 4 September until Thursday, 23 October.
The key dates are:
Social hour: Thursday, 4 September at 10am – 11am EDT / 2pm – 3pm UTC
Monday lessons: 8, 15, 22, 29 September; 6*, 20 October at 10am – 11:30am EDT / 2pm – 3:30pm UTC
Thursday Co-Labs: 11, 18, 25 September; 2, 9, 16 October at 10am – 11:30am EDT / 2pm – 3:30pm UTC
Graduation: 23 October at 10am – 12pm EDT / 2pm – 4pm UTC
*CSCCE will be closed on Monday, 13 October 2025 in observance of Indigenous Peoples’ Day. To accommodate this, we have slightly adjusted the schedule for this CEF cohort. “Reading Week” will now only take place during one session, on 2 October 2025, and the Week 7 lesson that would have taken place on Monday, 13 October will be held on Thursday, 9 October.
Scientific Community Engagement Fundamentals is an eight-week course designed to offer new or existing community managers core frameworks and vocabulary to describe their community’s purpose, refine or create strategic programming to engage community members around their shared goals, and identify ways to lower barriers to member participation. While the content is designed for any level of learner, it should not be thought of as a “beginner” course. Rather, it is intended to create common ground so that scientific community managers can converse across disciplines, more efficiently learn from one another, and build successful engagement strategies that are grounded in theory.
Each week, participants will meet virtually (using Zoom) for a 90 minute lesson and a 90 minute Co-Lab. While lessons will involve structured presentations and activities, Co-Lab time is for discussion, reporting out, and seeking feedback from instructors and fellow learners.
Each week will also include approximately 90 minutes of homework, for a total time commitment of 4.5 hours per week.
Pricing
Our pricing structure for CEF reflects the different organizations that community managers work for and the range of available budgets.
Discounted rate: Depending on participants paying the supporting rate, we may be able offer a limited number of discounted tickets for this cohort. If you would like to participate but your organization is unable to cover the whole cost, please complete this course discount request form.
Long range order and topological defects as tissue shapers
My PhD focused on studying the role of CDC42 isoforms during cell polarization and migration1. As CDC42 is a well-known regulator of actin polymerization, I developed extensive training in understanding actin regulation and dynamics in the context of cell polarization and migration.
Towards the final year of my PhD, during my time at the Institut Curie in Paris, I encountered the captivating field of biological active matter. There, I was introduced to the works of several renowned biophysicists working at the intersection of physics and biology. I became deeply intrigued by the emerging studies in this field, which is largely driven by biophysicists exploring long-range order in biological systems and investigating whether singularities in this order—known as topological defects—act as organizational centers that facilitate key biological processes.
Figure 1 Skeleton schematic showing actin long-range order on the Hydra’s body plan
One striking example came from Benoit Ladoux, who demonstrated that cell extrusion events can occur at sites of topological defects in epithelial monolayers2. This was followed by two compelling preprints. The first, from the Roux Lab at UNIGE, showed that myoblasts confined to circular patches organize into nematic order (i.e., long-range, thread-like alignment). At aster-like topological defects, they observed cellular tornado-like 3D bulk cell extrusions, mimicking an in vitro reconstitution of muscle morphogenesis-like events3. The second preprint, from the Keren Lab in 2020, revealed that Hydra exhibits long-range nematic ordering in its supracellular actin organization, with topological defects correlating with head and foot morphogenesis4 (Fig. 1). Circling back to my PhD and my training in actin biology, seeing such single-cell-like highly organized actin structures in a tissue-scale regeneration in Hydra was fascinating and puzzling at the same time. I had so many agitating questions.
Beginning the postdoc: are topological defects shapers of in vivo morphogenesis?
I started in Aurélien Roux’s Roux Lab in September 2021—it was a rocky start, as I was still wrapping up my PhD manuscript and applying for postdoctoral fellowships, with deadlines fast approaching. I was also recovering from medical conditions that had worsened due to the sedentary lifestyle imposed on us during COVID.
In spite of these bottlenecks, I was genuinely excited to take on a new project to study the role of active matter in morphogenesis, especially in light of the recent breakthroughs in the field. Aurélien and I decided to explore the hypothesis of whether—and how—topological defects are required for shaping biological tissues, using various model organisms. We ventured into root morphogenesis in Arabidopsis (in collaboration with Luis Lopez Molina), slug morphogenesis in Dictyostelium (in collaboration with Thierry Soldati), and specifically, head regeneration in Hydra multi-headed mutants (in collaboration with Brigitte Galliot).
While I was juggling these different organisms and studying their fascinating morphogenetic events, I encountered a practical issue: my Hydra were constantly moving during imaging. I was performing these experiments with the help of Matthias Vogg, then a senior postdoc in the Galliot lab. To address the movement issue, I decided to image them using an agarose slab confinement method typically used for imaging plants—and Matthias agreed. Little did I know that this would compress the animal, leading to a mechanical induction of two-headed morphogenesis in Hydra.
Riding on this serendipitous discovery, I began following the phenomenon of mechanically induced morphogenesis in Hydra. During regeneration under compression, I tracked the emergence of new topological defects in the actin organization of the animal, which correlated with the formation of new heads. This observation confirmed the hypothesis proposed by the Keren lab, which suggested that aster topological defects are associated with new head formation during Hydra regeneration.
Topological defects shape animal tissues in a curvature dependent manner
Following this, Aurélien was thrilled and suggested I reach out to a theoretical physicist to explore the physical mechanisms behind how these additional topological defects could influence tissue shaping. He connected me with Daniel Pearce, an active matter theoretical physicist (then a postdoc in Karsten Kruse’s lab), who had already developed a mathematical model describing how long-range organization in Hydra could shape tissue5.
When I showed Daniel my findings, he was extremely excited and immediately came on board to help develop theoretical simulations of tissues under compression. Using his elastic nematic model, he described how +1 aster topological defects organize stresses and generate positive curvature (dome shapes), which is reminiscent of the shape of the Hydra head. In simulations under lateral compression, we observed that placing topological defects at the extremities, as seen in our regeneration experiments, led to the evolution of two dome-shaped structures.
Furthermore, it was Dan who predicted that the orientation of tissue compression could dictate the fate of regeneration. The direction of compression influences how the long-range actin orientation experiences and responds to stress. As he suggested, we observed that when the tissue was oriented parallel to the compressive agarose slab, the sites of +1 aster defects buckled (inverted dome shapes) and underwent tearing, which then healed to form a defect-less toroid (Fig. 2).
This was a ground-breaking observation—it was the first time we observed the abolishment of body axis in an animal tissue that remained viable. I followed the defect-less torus over several days and observed that it failed to regenerate, as it maintained a perfectly symmetric actin configuration in which de novo +1 asters never arose. The tissue continuously attempted to regenerate a head but failed, due to the absence of a +1-aster topological defect.
Lastly, we all collectively thought however we should still be able to generate toroid with a +1 aster. By then we were also in touch with the Kerren lab and she invited me to Israel for a stay in her lab. Everyone suggested that theoretically a torus with defects could be generated. Then I hypothesized that if the compression occurred in a tissue with disordered actin to start with and a simultaneous tear occurred, then while the wound heals to create a 3D hole for the torus the disordered actin will order around it while generating a +1 aster required for a head. That is precisely what happened when we compressed the spheroid tissue that undergoes initial actin disorder and then ordering. This way we generated a torus with a +1 aster therefore a toroidal adult Hydra animal. This was really the cherry on top to see an animal with such a twisted muscle organization and topology.
In conclusion, these experiments established the need for +1 aster actin topological defects as head shapers in the animal. Their presence shapes the head and their absence give rise to no head formation, as observed in the defectless torus. The prospective research is to try to identify such long-range physical morphogens in other organisms, and strengthen the understanding of biological active matter.
Figure 2 Spinning disk microscopy images of fluorescent actin expressing (GFP-Ecto-LifeAct) Hydra at Day 6 of head regeneration. The three mechanically induced Hydra phenotypes, two-headed, actin-defectless toroid and toroidal Hydra. (2 votes) Loading...
Anyone—regardless of coding skills—should be able to generate a publication-quality plot of their data in minutes. That was the main motivation to develop a series of web apps to make state-of-the-art data visualization more accessible (huygens.science.uva.nl). But who cares, the same result can be achieved with generative AI (genAI) based tools, right?
Before discussing what genAI can bring us for coding a plot, I briefly explain how the web apps work, so we can compare it with genAI later on. The data visualisation produced by the web app (the output) is coded in R and uses the {ggplot2} package. Another R-package, {shiny}, is used to create a graphical user interface (GUI). This GUI enables the user to optimize the data visualization by modifying the (invisible) code, through sliders, buttons, drop-down menus, and text fields. The process of creating a data visualization in a web app is highly interactive. By using a web app, the user can focus on what the data visualization should look like, without dealing with the code.
A screenshot of the web app SuperPlotsOfData. Users can optimize the data visualization with sliders, buttons, drop-down menus, and text fields.
By design, the web apps are somewhat limited in their options, so I started an online resource with dataViz protocols as well. My hope was that this resource would lower the barrier for people that wanted more control than what is possible in the web app and therefore would be motivated to learn R&ggplot2. But now, there is genAI. Coding can be done, rapidly and interactively, with websites that spit out code based on Large Language Models. Instead of focusing on the code and the technicalities that are required to build a data visualization, the user can focus on what the data visualization should look like (do you see the parallels with web apps?). This approach is aptly called vibe coding.
One of the prompts that was used in ChatGPT for vibe coding the data visualization of the output of a 96-wells plate that is shown below.
In a previous blog, I described that vibe coding “felt like I gained some kind of superpower”. But not everything is hunky-dory. It has been nicely documented by Mine Çetinkaya-Rundel that the AI-tool, besides the required changes, makes changes that are not explained and may be difficult to understand. I had exactly the same experience when I tried to vibe code a data valisualization that I had previously manually crafted (protocol 8 in the dataViz protocols book). In the end, the result (see below) is pretty neat, but it took several iterations (prompts), including some debugging of errors. I also noticed that understanding some of the basics (loading packages, knowing where to place the input data, how a plot is built using the {ggplot2} package) is needed to get the code to work. Worse yet, if the code seems to work but actually makes mistakes that are hard to spot things can go really wrong. For instance when doing some calculation for statistics that are difficult to understand or verify.
Graphical representation of readings from a 96-wells plate. The data visualization on the left was manually coded as detailed here and the data visualization on the right was generated by vibe coding in ChatGPT.
Are web apps still relevant when the same result can be obtained with vibe coding? Both the web apps and the genAI tools can be considered as a black box and allow the use to focus on the output. The genAI based tools offer great flexibility, but a strong point of the web apps is their predictable outcome, delivering a fully reproducible data visualization. The underlying code is available and the web apps are documented in (peer-reviewed) papers that can be cited. A practical advantage of web apps is that there is no need to install software or specific packages to run them. So I think there is still a future for the web apps. At the same time, I encourage experimenting with genAI as vibe coding offers new and exciting opportunities for data analysis and visualization. This will require at least a basic understanding of the coding language and sanity checks. Altogether, these are exciting times as the options for generating publication-quality data visualizations are expanding!
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