The world’s a metabolic dance & early career scientists are leading the way!

Emerging perspectives in metabolism

This week, we explore the story of Dr. Luis Cedeno-Rosario, a postdoctoral researcher in the Rutter Lab at the University of Utah. Luis’s path into metabolism began with a biochemistry class—an early glimpse into how cells adapt, survive, and respond to their world. His work explores how cancer cells alter their internal wiring to support unchecked growth and resist treatment—uncovering how shifts in metabolism can give tumors a survival advantage. These insights may help identify new ways to target cancer by exploiting its metabolic dependencies. Continue reading to learn how Luis is driven by curiosity, scientific precision, and how having a supportive mentoring environment impacted his journey. Check out his thoughts on how he winds science and music together, and how he views metabolism more than just chemistry— but as a language through which disease reveals its secrets and a window into how life adapts under pressure. Give him a follow over twitter and bluesky.

What’s your first memory of the field of metabolism? Could you share your journey into studying metabolism in disease contexts like cancer and cardiac disorders?

I have always been passionate about understanding how cells adapt to different environments and challenges, with a focus on cancer cell signaling and mitochondrial metabolism. I was taking a biochemistry and cell and molecular biology class as an undergraduate student at the University of Puerto Rico – Humacao and became fascinated by how multiple pathways intersect to regulate this process and their impact on cell behavior. I also had the great opportunity to do summer research internships at UT MD Anderson Cancer Center and at Johns Hopkins University which allowed me to learn more about the cell signaling and metabolism field. This is what led me to pursue a PhD in cell signaling in Dr. Deborah Chadee’s lab at the University of Toledo and a postdoc in metabolism in Dr. Jared Rutter’s lab at the University of Utah.

Introduce us to the field of cancer metabolism – you have worked on different types of cancer cells like ovarian cancer cells and liver cancer cells – tell us about your experiences.

During my first year of graduate school, I knew that I wanted to study cell signaling but I wasn’t sure in what context. I remember listening to Dr. Chadee’s talk in the signal transduction class and I was very fascinated by the complexity of the MAP Kinase signaling pathways and their role in ovarian cancer progression. Therefore, I decided to complete my PhD under the mentoring of Dr. Chadee where I worked on the regulation of the MAP3K MLK3 by CDK1 and CDK2 and their role in controlling cell division and proliferation in ovarian cancer cells (Check out the paper here). For my postdoc in the Rutter lab, I wanted to apply what I learnt during graduate school in the context of mitochondrial metabolism and their signaling pathways that are involved in liver cancer cell proliferation and progression.

How are different cells metabolically heterogeneous within the same tumor? Why is it important to study metabolic heterogeneity in cancer occurrence/progression – in term of both the cells themselves and the microenvironment?

Cells can have different metabolic profiles depending on the metabolites they need or are available in their surroundings. That heterogeneity can also come from where these cells are localized, for example, cells that are in a more hypoxic environment will probably have other metabolic needs than cells that are in a less hypoxic or normal environment. So cells have evolved in a way that they are very smart in choosing or taking what they need to meet their metabolic demands.

Tell us about your current work on metabolic signaling in the context of Wnt/beta-catenin pathway activation in liver cancer cells. How do you link it to the mitochondrial functioning and what future questions are you most excited about?

Our lab has done extensive work in characterizing the importance of the Mitochondrial Pyruvate Carrier (MPC) and its role in proliferation and tumorigenesis. I discovered that activation of beta-catenin represses MPC expression in liver cancer cells, and that this regulation rewires mitochondrial metabolism from glucose oxidation towards fatty acid oxidation. This is particularly interesting in the context of cancers in which MPC is downregulated and fatty acid oxidation is increased. I am very excited for the future since my findings opens up new avenues to explore ways to increase MPC expression in these tumors and increase the quality of life and survival of cancer patients.

Tell us how difficult some of these experiments are – do you have to deal with midnight timepoints or require an army of undergrads/ long hours, has to use some un-conventional/creative tools to overcome experimental challenges etc.

Some of these experiments have been truly a challenge and I have definitely spent many many hours in the lab trying to solve multiple research questions and/or developing new techniques to study the regulation of MPC by beta-catenin. I mentored an amazing summer research student, Nimo Abdi, who helped me a lot in the beginning of this project. I also have excellent collaborators, inside and outside the lab, who have contributed to the development of new ideas and have given me new perspectives on this regulation. I am very grateful to have them as collaborators and truly believe that these efforts will make a great impact in the metabolism field.

Building upon your work in the context of liver cancer metabolism, what are your upcoming plans? What metabolic pathways do you aim to investigate further to understand cancer progression from a cell growth and signaling perspective?

This switch in metabolic profile from glucose towards fatty acid oxidation is very exciting. So we are definitely looking more in depth at the metabolic processes that are changing and at the proteins and enzymes behind that regulation. One of the big questions we are investigating right now is to understand what fatty acids these cells prefer to utilize and their implication in liver cancer progression.

Before this, you studied cell signaling in ovarian cancer cells. How was the transition between fields, and what do you carry over from your previous research? Could you shed some light on your results regarding how MLK3 (Mixed lineage kinase 3) regulates cell cycle of ovarian cancer cells and tell us about your cool findings?

I have always thought about metabolism as another way of cells to sense their environment and metabolites are signaling molecules. These are multiple signaling pathways that are interconnected, and this concept was very similar to what I studied during graduate school. During my PhD, I found that the MAP3K MLK3 (Mixed lineage kinase 3) becomes phosphorylated by CDK1 and CDK2 to control ovarian cancer cell cycle progression. This research was published in the Journal of Biological Chemistry (JBC) doi: 10.1016/j.jbc.2022.102263 and I would encourage everyone to read it. It is a very interesting story that shows how these phosphorylation events act as “on” and “off” switches to control ovarian cancer cell division and proliferation.

How do you think scientific paradigms in the field of cancer metabolism will evolve in the coming decades – in regard to the new upcoming tools? Are we moving toward a more nuanced understanding, or do you see potential pitfalls?

I feel like we have bright future in our metabolism community. We have seen the development of great techniques such as mass spectrometry integrated with equilibrium dialysis for the discovery of allostery systematically (MIDAS) that was developed in our lab to identify novel interactions between metabolites and proteins. This is a fast-growing field and we are opening more doors to understand the complexity of metabolic pathways in multiple contexts, including cancer, cardiac function and neurodegenerative diseases, and in development. I am very excited for our future findings and hope that I can contribute significantly and have a positive impact not only in the research field itself but also in training the next generation of scientists.

What role does curiosity play in your life, both within and outside of science? 

I believe that curiosity plays an important role in my scientific career. Understanding what is happening at the cellular level is pivotal in the development of new therapies, and that is what drives my passion for science. I want to be able to use my knowledge from cell and molecular mechanisms to develop new and better ways to treat multiple diseases or to at least increase the quality of life of the people affected by a particular disease.

What are the future research questions you are most excited to ask?

I am very excited about pursing metabolism in the context of cell biology and development. I think it is a field that is also growing very fast and I would like to contribute to it and make new discoveries.

Were there any pivotal moments that shaped your career path —and how have you found ways to build a supportive community in science?

I think that the most pivotal moment in my career path was creating a strong and supportive network of mentors within the cell metabolism and mitochondrial biology field. I have met many of these mentors in conferences and through the Burroughs Wellcome Fund Postdoctoral Diversity Enrichment Program (PDEP) that have been critical in my development as a future independent scientist. I am also very grateful to be part of the biochemistry department at the University of Utah and to receive a lot of internal support as a postdoctoral fellow.

How do you maintain a balance between your rigorous research activities and personal life? Are there hobbies or practices you find particularly rejuvenating?

Music! I have extensive training in classical music and I am actually a member of the Utah Medical Orchestra (UMO) where I play the flute and the piccolo. Music is definitely a big part of who I am.

If you hadn’t embarked on a career in biological research, what other profession might you have pursued, and why?

I would have pursued a law degree or a music degree in flute performance. In the law aspect, I like the complexity of finding new solutions to diverse problems. In the music aspect, I like how we can create art using a universal language and enjoy that art as a whole. Music can bring you different feelings and helps us express ourselves.

Last week we learnt about how viruses rewire and utilize host lipid metabolism using mosquitoes as a host model system with Wolbachia and dengue as viral players, check out the article – Lipids and Labyrinths (Cassandra Koh). Cassandra is a new PI, studying metabolic interactions of symbiosis and virus-virus host interactions. She is seeking motivated students and collaborators.

Check out the article All the world’s a metabolic dance, and how early career scientists are leading the way !!

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Madalena M. Reimão Pinto (Schier lab, University of Basel, Switzerland) and Sebastian Castillo Hair (Seelig lab, Washington University, Seattle, USA) joined forces to understand how zebrafish embryos orchestrate protein synthesis during early development. Through this collaboration, their recently published study in Developmental Cell identifies features in mRNA 5′ UTRs that act during early zebrafish development to regulate translation. 

Madalena, what brought you to Alex Schier’s lab and how did you embark on this project?

During my PhD at the Vienna BioCenter, I worked on understanding the molecular mechanisms regulating mRNA biogenesis and function in the fruit fly. It so happened that the exonucleolytic enzyme that I was working on at the time had a striking effect on spermatogenesis, and the data pointed to defects resulting from misregulated mRNA translation. By the end of my PhD, I was fascinated by mRNA translational control in the context of organismal development. I quickly realized that we lacked a comprehensive understanding of how mRNA translation initiation – which is rate limiting for protein production – is regulated during the very fast-paced and temporally coordinated stages of early embryogenesis. This motivated me to tackle this question in the context of early vertebrate development. I also realized that my background in RNA biochemistry gave me an edge to start studying developmental biology at a mechanistic level from a different perspective. I chose to address this question using the zebrafish model because it allows me to combine high-throughput approaches with biochemistry and powerful genetic tools in live embryos, as they develop.

I had heard great things about the Schier lab from Andi Pauli (Schier lab Alumna, group leader at the Vienna BioCenter, Austria) and was inspired by Michal Rabani’s work on mRNA stability during zebrafish embryogenesis (Schier lab Alumna, group leader at the Hebrew University of Jerusalem, Israel). On one hand, I was looking to join a lab which had in depth knowledge about developmental biology and zebrafish genetics; on the other hand, I wanted to be part of a multidisciplinary and vibrant group of people who aspired to become group leaders, so the Schier lab was the perfect choice.

The main question motivating my postdoctoral work is: how do embryos know how much protein to make and when? To start dissecting this question systematically, I decided to focus on the 5′ UTR sequence, which is crucial for regulating translation initiation, and developed an approach to interrogate at transcriptome scale how the 5′ UTR contributes to regulating translational dynamics as embryos develop.

How did the collaboration with the Seelig lab start?

Well, it took more than two years to get to a stage when I had designed and generated the 5′ UTR massively parallel reporter assay (MPRA) library, validated it and acquired the in vivo data. To be honest, I also spent quite some time running data analyses before convincing myself that the assay had actually worked and was recovering biologically meaningful information! Once I realized that was the case, I was super excited to try and learn as much from the data as possible. I was familiar with Georg Seelig’s work and had actually met him in person when he gave a talk at the Biozentrum’s Discovery Seminar. At that time, I was still running experiments but I approached Georg and asked if he would be interested in collaborating to explore the data with deep-learning models. Georg was excited about my project and told me to reach out when the right time came, and so I did! He then paired me up with Sebastian, and we started a wonderful collaboration together. Honestly, it was so efficient and so much fun: we would meet every two weeks, and at each meeting discuss our progress, come to an agreement on next analyses and experiments and then execute them. It gave the project a really nice momentum and it was just great to feel part of a team working towards a common goal. At the same time, Georg joined the Schier lab for a sabbatical, so it was great to have the opportunity to discuss and get feedback on a regular basis from both PIs in person. The project would have not been the same without Sebastian’s contributions, who developed the Danio Optimus 5-Prime (DaniO5P) deep-learning model to evaluate and interpret the 5′ UTR MPRA data. And Georg was the one who came up with the model’s name!

What were for you the most exciting findings, or particular moments during the project that stuck with you?

The most exciting moment was running the Kozak sequence and uORF analyses and realizing that the assay had actually technically worked. It also meant that the data likely contained additional sequence information to be uncovered, which was a super exciting prospect. And then of course, seeing motifs emerging from the motif enrichment analysis and the DaniO5P model!

I’d also like to say that when I started this project, I had no experience performing polysome profiling. I was extremely fortunate to meet Sunil Shetty, at the time a postdoc in the Hall group at the Biozentrum (now leading his independent research group at the Tata Memorial Centre in Mumbai, India), who taught me how to prepare sucrose gradients and perform polysome profiling. His happiness and positivity are contagious, and some of the most fun moments of my postdoc were spent next to the polysome profiling machine learning from Sunil. I am deeply grateful to him, and also to Michael Hall for kindly welcoming me in his lab.

And what was most challenging?

For sure it was starting my postdoc and having the COVID-19 pandemic hit a few months later. At the time, my plan was to experimentally define zebrafish 5′ UTRs by long-read sequencing to design the MPRA. There was so much uncertainty about when we could be back in the lab full time, that I decided to instead use an alternative approach to computationally infer 5′ UTR sequences from a public dataset of cap analysis of gene expression data. I don’t have a background in computational biology, so it was definitely a slow and iterative learning process – but also very rewarding in the end, and most importantly it allowed me to move forward with the project.

What’s ahead for you?

I am currently applying for Group Leader positions. Going on interviews and getting to meet faculty members from different research institutions is really an amazing and rewarding experience, but also very time-consuming, so it’s hard to get any experiments done alongside applications and interviews. I am super excited to start my own independent research group soon, and I hope to continue to collaborate with Sebastian on future projects!

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At the end of each month, I pick the same month from a random year from the past 15 years of the Node, and take a look at what people were talking about back then.

Previously, I travelled back to February 2011, March 2013 and April 2014 to have a look around the Node. Luckily, I didn’t get lost along the timeline and managed to get back to the present day. But now I’m itching for another adventure. So this time, let’s fasten our seat belts and turn the dial to May 2016…

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It lives. It lives! What lives, you may ask? Well, somewhere in a lab at Yale University, one young scientist has stuck human brain cells and chimp brain cells together to make a chunk of hybrid brain. A few weeks ago, I met with her to ask more about this research. She admits that it all sounds like “mad science,” but this mad scientist might be taking a big step forward on our path to find out what really makes us human.

Chimpanzees are our closest relatives, and closer than most of us would probably like to think about. We share some 98.8% of our DNA with chimps.¹ This means only about 1.2% of our DNA accounts for the uncanny power of our species to build cities, write symphonies, split atoms, and do all the other things we alone do so well. We know that much of this uncanny power resides in our brain, which is massive compared to a chimp’s brain,² and has a much larger wrinkled region at its front³ that does most of our complex “higher” thinking. This wrinkled region at the front of our brains takes almost twice as long to finish developing in us as it does in chimps,⁴ and scientists have long thought that its slow development in humans helps to explain our subtle and adaptable “higher” thinking abilities.⁴ What we do not know is how that meager 1.2% of our DNA goes about making our wrinkly-fronted brains develop so slowly.

For the last two years, a young scientist named Reem Abu-Shamma has been trying to change that. Since graduating summa cum laude from UCLA, Reem has made a career of mutating genes, creating artificial 3D clusters of human intestinal cells (delightfully called “organoids”), and using computer programs to study vast amounts of DNA. These endeavors might sound eerily sci-fi, but have in fact taught us a lot about public health and disease. Her work mutating genes in parasites could shed light, down the line, on how we treat some particularly nasty strands of malaria,⁵ and her work with human intestinal organoids promises to tell us more about the cellular basis for inflammatory bowel disease. Now, as a PhD student at Yale University, Reem has set her sights on what makes our brains human.

” Slower development means more time to make a big brain…So where in the genetic code is it telling our brains to develop slower? “

To investigate what makes our brains unique, Reem has created something like a hybrid “half-human, half-chimp brain.” This phrase baffled me as much as it’s probably baffling you, so I sat down with Reem to ask her more about what inspired this research. And, as I listened to Reem’s enthusiastic, down-to-Earth explanation for her project, it began to seem less like mad science and more like vital research. “Large brains allowed us to dominate the world for better or for worse,” Reem explains. She wants to find “the underlying code in our cells that has allowed us to do that.” In searching for this code, Reem has focused on the speed at which that wrinkly portion at the front of our brains develops. “Slower development means more time to make a big brain…and we know that the human brain takes a really long time to develop.” This slow pace of human brain development manifests at the cellular level⁶—individual human brain cells take years to branch out and mature, whereas those of chimps develop much faster. Reem’s research question is simple, then: “Where in the genetic code is it telling our brain cells to develop slower?” 

To answer this question, Reem recently joined the Noonan Lab at Yale University, which has a long history of using the best-available gene-editing technology to study human brains. One particular focus of the Noonan Lab has been to find particular bits of DNA that distinguish humans from chimps and other animals. What exactly are these bits of human specific DNA? Well, as Reem explains, “they’re parts of the genome that are not genes,” but “dials” for genes, which make various brain-building genes more or less active as the brain develops.⁷ These bits of DNA are part of that 1.2% of our genetic code separating us from chimpanzees, and could tell us a lot about how that huge wrinkly portion at the front of our brains develops so slowly, gets so big and complex,⁵ and makes us so clever. Each one of these bits, once found, “gives us a hint that maybe this part of the genome helped us evolve big brains.” However, that hint alone doesn’t prove the bit’s role in making our brains bigger or tell us how it did. In order to actually verify what these human bits of DNA do, scientists have to mutate them, and see how those mutations affect the development and interaction of different human and chimp brain cells over time. Obviously, no one at any credible research institution wants to mess with the brain of an actual living human—institutional and federal guidelines fortunately forbid that kind of work. But scientists dowant to understand what these human-specific bits of DNA are doing. So how do you mutate realistic human brains without using actual real human brains?

Well, remember those “organoids” I mentioned before? Reem uses those. And they’re a lot less scary than they sound. “We’re not using real animals, or growing real brains” Reem assures me with a laugh. Instead, she’s using what amounts to just a few cells: To create brain “organoids”—again, 3D clusters of living brain cells—she uses cells that other labs have collected from human or chimp skin. These labs treated those skin cells with various molecules to “reprogram” them into stem cells, which can turn into almost any other kind of cell if given the right molecular cues. “In our case,” Reem explains, “we make them turn into neurons.”⁸ Reem uses this approach to create human and chimp brain cells, and then grows each reprogrammed brain cell into a different 3D cell cluster or “organoid.” The result in each case is a separate ball of brain cells⁹ for each species that develops much like they would in a real brain. 

A human brain organoid, 30 days old, made by combining two different human cell lines. Cells are labeled with two overlain molecular markers——a blue one marking all cell nuclei and a violet one that marks “forebrain cortical neuron progenitors” (the kind of cells that end up forming the wrinkly front of our brains). The cells in this organoid have spontaneously arranged themselves into “rosettes”, much like brain cells do in an embryonic brain. Image courtesy of Reem Abu-Shamma.

With each brain organoid, Reem plans to test what our human-specific bits of DNA are doing to make our brains grow slower and larger. She will do this by tweaking or changing¹⁰ various human-specific bits of DNA to make them act more like the corresponding regions of chimp DNA, and vice versa. Then she’ll see how these modifications affect the activity levels of various brain cell genes and the “speed” at which those brain cells ultimately develop. “By ‘speed’, we don’t mean absolute time; rather, we have the technology to look at a single cell and figure out how mature it is based on the molecules we observe in it,” Reem clarifies. Then, for each bit of human-specific DNA, she’ll see whether the humanized chimp cells appear to develop more slowly, while the “chimpanized” human cells develop more quickly. Then we would know that this specific bit of our 1.2% unique genetic code is partly responsible for making our brains so weirdly human. 

Reem finds the sheer size of this mystery fascinating. “The genome is a really big place,” she explains. “It’s so vast and we don’t know what most of it does. It kind of feels like detective work, because you’re trying to see where in this really big space it’s telling us to be human.” By tweaking little bits of human and chimp DNA so they behave more like their counterparts—a sort of genetic Freaky Friday—Reem can do just that, finding which bits of human-specific DNA tell our brain cells to grow in a human way. This in itself is the stuff of science fiction. However, Reem and her PhD advisor, Dr. James Noonan, are taking this approach one step further.

They aren’t just growing human brain-cell colonies and chimp brain-cell colonies. They’re mixing them together, to make something like a miniature hybrid brain. Despite their different origins, these cells branch out and interconnect much like the cells in our own brains, possibly creating a cellular communication network unseen in nature. “Why would you make a half-human, half-chimp brain?” Reem jokes that her mother and even her colleagues have often asked her this question. But Dr. Noonan initially suggested this approach, and Reem has pursued it, because we can learn a lot from it. 

” It kind of feels like detective work, because you’re trying to see where in this really big space it’s telling us to be human. “

Brain cells don’t usually grow on their own. They grow in response to cues from neighboring cells, and these hybrid brains can show us the extent to which human brain cell development is genetically encoded. How much of how our brain cells behave is written in their DNA, and how much is determined by interaction with their cellular neighbors? Specifically, Reem is curious whether the sum of brain cell interactions, and the presence of similar brain cells from other species, together affect how fast that wrinkly portion at the front of the brain develops. Previous studies have found that these external cues (the “cellular environment”) don’t matter much for the development speed of human brain cells.^11,12 However, few if any studies have used hybrid chimp-human brain organoids to study that big wrinkly-fronted part of the human brain. By creating hybrid chimp-human organoids with this specific type of brain cell, Reem will finally test whether environmental cues help it grow slower in humans. Reem gives me an example to help me wrap my head around this. So, suppose you “take a human cell and transplant it into a chimp brain organoid,” Reem explains. And then suppose you collect molecular data from human brain cells inside a purely human organoid and then do the same to human brain cells inside a human-chimp hybrid organoid. “If they’re exactly the same, then the environment the cell is in isn’t as important!”

Making and mutating hybrid brains is intense work. To do it right, Reem has to set up hundreds of different brain organoids, each in its own plastic well, and from a variety of different human and chimp donors. She goes into the lab every day. “I check on my cells immediately…first thing. I make sure they’re still alive.” She recounts instances where some of her organoids became cancerous, and others spontaneously collapsed and started dying—both unplanned events that threatened to skew her work and required hours of manual labor to remedy. “So many things can go wrong…it’s a lot of manual labor to make sure they’re alive and happy.” On a daily or weekly basis, she has to feed her many hundreds of brain organoids, and look at each one under a powerful microscope to make sure nothing has gone horribly wrong. She has to modify them all at just the right time, in just the right way. And then, when all of that is done, within the next few months, she’ll have to extract specific molecules from these organoids and analyze the resulting vast amounts of data to see how her mutations changed the approximate speed of brain cell development in her human brain, chimp brain, and hybrid brain organoids. 

Reem is eager to find “what inferences we can make about the speed of development using these models”—at what rate the brain cells are likely growing, dividing, branching out, and developing their various special functions. With this approach, Reem wants to pinpoint some of the intrinsic genetic factors responsible for speeding up and slowing down the “molecular rate” of human brain cell development.

A hybrid human-chimp brain organoid from Reem’s first experiment on this project. Molecular markers tag chimp brain cells red and human ones green. This hybrid chunk of brain is 17 days old. Image courtesy of Reem Abu-Shamma.

When I asked Reem about the benefits of this research, her answer surprised me. Of course, her work does have implications for treating and understanding psychiatric or developmental conditions—autism spectrum disorder, schizophrenia, and other cognitive differences that often relate to brain development. That was the answer I expected. But Reem went on to highlight something else. “This is a very exploratory study,” she explained. “It’s hypothesis-generating,” and “in the history of science, doing fundamental research can sometimes lead you down unexpected paths, just because you’re exploring your curiosity.” This “fundamental research” is done not for its direct societal benefits, but to better understand ourselves and our world, and often has unexpected humanitarian value. For example, Reem points out, CRISPR was discovered by fundamental research projects on a few seemingly random repetitive patterns in microbe DNA. And yet, CRISPR now forms the most promising avenue for therapeutic gene editing and has a variety of other applications for human health and disease worldwide.^13,14

Reem’s work on hybrid brains is fundamental research in the same way. Yes, it has biomedical implications. But its potential value is so much broader. It can shed light on the parts of our genetic code that separate us from chimps and other animals. As Dr. Noonan told her when he first suggested making human-chimp hybrids, “no one’s done it before,” and we can hardly begin to predict what it might tell us about what makes us human. 

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Caleb Gordon is a Postdoctoral Associate at Yale University, where he studies the evolution of reptiles during the time of the dinosaurs. Check out his website to follow his research and popular science writing.

Note from the author: This piece was written as part of a workshop series taught by Carl Zimmer, and organized by Yale’s Graduate Writing Lab, on science reporting intended for a general audience. This workshop challenged us to write a popular science article without any scientific jargon. However, for any scientists missing this jargon, I’ve included more scientific terminology in the References Cited below. This article benefited greatly from feedback by Lauren Gonzalez and Joseph Lee at the Graduate Writing Lab.

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References Cited

• [1] The figure of 98.8% is given in Smith, Shelley L. “Connecting with Our Ancestors: Human Evolution Museum Experiences.” Interdisciplinary Evolution Research 9, 1–528. https://doi.org/10.1007/978-3-031-69429-5. It is also often shown online: American Museum of Natural History, Hall of Human Origins. “DNA: Comparing Humans and Chimps.” Accessed online April 25, 2025. https://www.amnh.org/exhibitions/permanent/human-origins/understanding-our-past/dna-comparing-humans-and-chimps.

• [2] For more information about the evolution of human brain size, you can check out this research paper: Smaers, J. B., R. S. Rothman, D. R. Hudson, A. M. Balanoff, B. Beatty, D. K. N. Dechmann, D. De Vries, et al. “The Evolution of Mammalian Brain Size.” Science Advances 7, no. 18 (April 30, 2021): eabe2101. https://doi.org/10.1126/sciadv.abe2101.

• [3] This wrinkled region at the front of the brain is called the “prefrontal cortex.” For more information about this remarkable brain region and its implications for our higher executive functioning abilities, you can check out this research paper: Preuss, Todd M., and Steven P. Wise. “Evolution of Prefrontal Cortex.” Neuropsychopharmacology 47, no. 1 (January 2022): 3–19. https://doi.org/10.1038/s41386-021-01076-5.

• [4] Additional information on the prefrontal cortex is provided in this research paper from the same journal: Kolk, Sharon M., and Pasko Rakic. “Development of Prefrontal Cortex.” Neuropsychopharmacology 47, no. 1 (January 2022): 41–57. https://doi.org/10.1038/s41386-021-01137-9.

• [5] The following research paper summarizes the results from Reem’s collaborative gene-editing work with malarial disease vectors: Subudhi, Amit Kumar, Anne-Lise Bienvenu, Guillaume Bonnot, Reem Abu-Shamma, Faryal Khamis, Hussain Ali Abdulhussain Al Lawati, Stephane Picot, Eskild Petersen, and Arnab Pain. “The First Case of Artemisinin Treatment Failure of Plasmodium Falciparum Imported to Oman from Tanzania.” Journal of Travel Medicine 30, no. 3 (May 18, 2023): taac092. https://doi.org/10.1093/jtm/taac092.

• [6] The human brain matures more slowly in part because individual human brain cells take longer to develop. For a great review highlighting the uniquely protracted nature of human brain cell development, check out this recent paper: Lindhout, Feline W., Fenna M. Krienen, Katherine S. Pollard, and Madeline A. Lancaster. “A molecular and cellular perspective on human brain evolution and tempo.” Nature 630 (19 June 2024): 596–608. https://doi.org/10.1038/s41586-024-07521-x. 

• [7] For more information on what these human-specific bits of DNA are and what they do, check out this recent paper from the Noonan Lab: Pal, Atreyo, Mark A. Noble, Matheo Morales, Richik Pal, Marybeth Baumgartner, Je Won Yang, Kristina M. Yim, Severin Uebbing, and James P. Noonan. “Resolving the Three-Dimensional Interactome of Human Accelerated Regions during Human and Chimpanzee Neurodevelopment.” Cell 188, no. 6 (March 2025): 1504-1523.e27. https://doi.org/10.1016/j.cell.2025.01.007.

• [8] For additional information about how these scientists create brain cells from stem cells, check out the following paper: Mariani, Jessica, Maria Vittoria Simonini, Dean Palejev, Livia Tomasini, Gianfilippo Coppola, Anna M. Szekely, Tamas L. Horvath, and Flora M. Vaccarino. “Modeling Human Cortical Development in Vitro Using Induced Pluripotent Stem Cells.” Proceedings of the National Academy of Sciences 109, no. 31 (July 31, 2012): 12770–75. https://doi.org/10.1073/pnas.1202944109.

• [9] These colonies of brain cells are called “cortical organoids.” For more information about these remarkable 3D brain cultures, check out the following paper: Pollen, Alex A., Aparna Bhaduri, Madeline G. Andrews, Tomasz J. Nowakowski, Olivia S. Meyerson, Mohammed A. Mostajo-Radji, Elizabeth Di Lullo, et al. “Establishing Cerebral Organoids as Models of Human-Specific Brain Evolution.” Cell 176, no. 4 (February 2019): 743-756.e17. https://doi.org/10.1016/j.cell.2019.01.017.

• [10] Reem mutates brain cell colonies using “arrayed CRISPR screens,” which are described in more detail in the following research paper: Bock, Christoph, Paul Datlinger, Florence Chardon, Matthew A. Coelho, Matthew B. Dong, Keith A. Lawson, Tian Lu, et al. “High-Content CRISPR Screening.” Nature Reviews Methods Primers 2, no. 1 (February 10, 2022): 8. https://doi.org/10.1038/s43586-021-00093-4.

• [11] This research paper studied pure human and pure chimp brain cell organoids: Otani, Tomoki, Maria C. Marchetto, Fred H. Gage, Benjamin D. Simons, and Frederick J. Livesey. “2D and 3D Stem Cell Models of Primate Cortical Development Identify Species-Specific Differences in Progenitor Behavior Contributing to Brain Size.” Cell Stem Cell 18 (April 7, 2016): 467–480. http://dx.doi.org/10.1016/j.stem.2016.03.003. 

• [12] This research paper took human brain cells from that wrinkly region at the front of the brain and transplanted them into a live mouse brain: Linaro, Daniele, Ben Vermaercke, Ryohei Iwata, Arjun Ramaswamy, Baptise Libé-Philippot, Leila Boubakar, Brittany A. Davis, Keimpe Wierda, Kristofer Davie, Suresh Poovathingal, Pier-Andrée Penttila, Angéline Bilheu, Lore De Bruyne, David Gall, Karl-Klaus Conzelmann, and Vincent Bonin. Neuron 104 (December 4, 2019): 972–986. https://doi.org/10.1016/j.neuron.2019.10.002. 

• [13] Doudna, Jennifer A., and Emmanuelle Charpentier. “The New Frontier of Genome Engineering with CRISPR-Cas9.” Science 346, no. 6213 (November 28, 2014): 1258096. https://doi.org/10.1126/science.1258096.

• [14] Barrangou, Rodolphe, and Jennifer A Doudna. “Applications of CRISPR Technologies in Research and Beyond.” Nature Biotechnology 34, no. 9 (September 2016): 933–941. https://doi.org/10.1038/nbt.3659. 

(4 votes)
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The MRC National Mouse Genetics Network, in collaboration with the Cancer Research UK (CRUK) Scotland Institute, is organising Organoids Are Us 2025, a symposium that incorporates both basic and clinical/diagnostic research and will be a significant national and international forum for exchange of new data and a “progress report” on the application of organoid-based technologies. 

Disease Models & Mechanism is one of our partners, sponsoring one of our talks and ensuring an in-person representation for this hugely relevant journal and The Company of Biologists as a whole.

This year’s venue will be the CRUK Scotland Institute in Glasgow from Tuesday 23^rd to Friday 26^th of September and will be the 7^th since the meeting was first held at the Doherty Institute in Melbourne in 2018, the name having been coined by Prof Elizabeth Vincan at the time. The Glasgow meeting this September will be the first to be held in Europe!

Plenary, Keynote and Symposium sessions, including rapid-fire short talks and poster sessions, make up the programme, which includes many well-known international speakers.

Early bird registration closes on the 15^th of June and includes discounted rates for students.

Organisers are very excited to be hosting this meeting, where cutting-edge technologies meet unanswered biological and clinical questions.

Prof Elizabeth Vincan, Clinical Scientist and Medical Researcher in the Department of Infectious Diseases, Melbourne Medical School, University of Melbourne says: “Organoids Are Us brings together delegates from diverse fields and disciplines to show case and learn about the latest advances in organoid technology, and its application to fundamental and clinical research to fast track discovery and translation. This is the seventh conference in this highly successful series, and the first in the UK.”

Prof Ramanuj DasGupta, Professor of Cancer Systems Biology at the School of Cancer Science, University of Glasgow and CRUK Scotland Institute says: “The Organoids Are Us conference aims to bring together the key opinion leaders in the fields of cancer, infectious disease and regenerative biology, who utilise organoid models to address key questions in human disease biology and development of novel therapies.”

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All the world’s a metabolic dance, early career scientists are leading the way!

Emerging perspectives in metabolism

This week we will meet Dr Cassandra Koh, who is a new faculty at Institut Pasteur. Cassandra is driven by curiosity and is passionate about decoding the molecular choreography between viruses, their insect hosts, and the lipids that entwine them. Her research traces the intricate ways arboviruses hijack mosquito metabolism to fuel their replication and has delved deep into how symbionts like Wolbachia rewire these metabolic pathways. Her brand-new lab will focus on how virus–virus–host interactions offer a nuanced view of disease transmission and microbial co-evolution. But science for Cassandra is more than experiments — it’s a way of asking questions about the world. She credits strong mentors and surprising inspiration from artists and storytellers for shaping her journey. Whether she’s tracing lipid dynamics in mosquito cells or hosting a long lunch for friends, Cassandra believes in curiosity as a compass. She’s currently welcoming collaborators and postdocs interested in exploring the metabolic intersections of immunity, infection, and symbiosis. Check out her work here ! Give her a follow over Bluesky and Twitter.

What was your first introduction to the fields of metabolism and viral infections?

It started with cholesterol. The fruit fly Drosophila melanogaster carries a bacterial endosymbiont called Wolbachia that suppresses pathogenic viral infections in its host. This was a very exciting finding that resulted in a biological intervention strategy against mosquito-transmitted viral diseases based on the stable introduction of the Wolbachia wMelstraininto natural populations of a major mosquito vector species, Aedes aegypti. Eric Caragata had showed that Wolbachia-induced viral suppression became weaker when Drosophila flies had more cholesterol in their diets, leading to the conclusion that Wolbachia and Drosophila viruses were competing for host cholesterol (PMID: 24337107).

Naturally, this led to the question of whether Wolbachia and mosquito-transmitted viruses (also called arboviruses) also compete for host lipid resources. During this study, I learned a lot about the role of lipids in viral infections in mosquitoes from a key paper by Rushika Perera (PMID: 22457619). Her work had shown that dengue virus replication in mosquito cells relies on the activity of fatty acid synthase. In addition, as a flavivirus, dengue virus re-organizes the endoplasmic reticulum membranes to form replication complexes, and this is reflected in an enrichment of lipids that promote membrane curvature and permeability.

You use the term “virus-virus-host” interaction for describing the theme of your lab. Could you share your journey into studying this and using mosquitoes as one of your host model systems? Tell us how you got inspired to further branch out into metabolic aspects of viral infections?

The interaction between arboviruses with their mosquito host is a fascinating subject in itself. Mosquitoes have evolved interesting ways to fight off and tolerate viral infections and the virus seeks to complete its transmission cycle while minimizing virulence to its vector host. With the recent appreciation that mosquitoes harbor a multitude of other viruses that constitutes its resident microbiota, virus-mosquito interaction is no longer a two-player game. These resident viruses are called “mosquito-specific viruses” to distinguish them from the ones that infect and cause disease in humans and animals. They have entered the research spotlight as many studies have reported their ability to reduce or enhance arbovirus infection in mosquitoes, which implies that they have a role to play in disease transmission. Many questions have since sprung up about how they interact with arboviruses and the mosquito host. I am curious to see whether these interactions can be observed in the metabolic dimension.

Your work intersects virology, metabolism, immunology and RNA interference – tell us what studying immune-metabolism means for you. How do you integrate these disciplines in your research, and what unique insights have emerged from this approach?

Immune responses cost energy. Viral infections cost energy. A virus infection is therefore a disruption to immune and lipid homeostasis. There is already some evidence of crosstalk between immune signaling and lipid metabolism modulations in bacteria-infected Drosophila (PMID: 30902902, PMID: 33227003). On top of that, viruses hijack host lipid membranes and reconfigure phospholipids to form viral replication complexes (PMID: 33087565), adding to the toll on the metabolic burden of virus-infected cell. Immune and metabolic regulation therefore go hand in hand and would provide a more holistic view of cellular responses to viral infection.

How has Wolbachia evolved in Drosophila and mosquito species – are a lot of mechanisms of symbiosis evolutionarily conserved? How can studying Wolbachia-insect interactions help us understand symbiont-driven metabolic changes? Could you shed more light on these emerging areas of research.

Wolbachia is a common endosymbiont among arthropods including insects like Drosophila melanogaster and some mosquito species like Aedes albopictus. When it was observed that some Wolbachia strains protect their Drosophila host from viral infection, the notion that the endosymbiont could be introduced into Aedes aegypti mosquitoes, a non-native host, led to the development of Wolbachia-based intervention strategies to limit the spread of viruses transmitted by this major vector species. That Wolbachia is vertically transmitted through the maternal line was a very useful property for a sustainable and self-driving intervention.

Studying how Wolbachia interacts with its hosts would reveal its mechanisms of symbiosis, which would say something about the directions of evolutionary pressures in natural or introduced hosts. These mechanisms might take the shape of metabolic mutualism, immune priming, or something else entirely.

What are the key differences in how Wolbachia and DENV-3 (Dengue virus serotype 3) alter host lipid metabolism?

In our work comparing how Wolbachia and DENV-3 modulate Aedes aegypti lipids, we found that the endosymbiont and the virus individually produce very different lipid alterations. While DENV-3 produced strong elevations, Wolbachia-infected mosquitoes exhibited much milder perturbations of different lipid species, which does not support the Wolbachia-virus competition hypothesis.

Tell us about your findings on association of DENV3 infection with lipid droplet growth and hyperglycemia in mosquitoes? Tell us about your exciting finding of how Cardiolipins are involved in DENV infection.

DENV-3 infection alone strongly elevated levels of triacylglycerols, glycerophospholipids high in polyunsaturated fatty acids, and Amadori-glycated phosphatidylethanolamines in Aedes aegypti mosquitoes. These lipid classes indicate lipid droplet accumulation, cellular membrane remodeling, and viral infection-induced hyperglycemia. The latter is especially interesting as it suggests that this cellular phenomenon, which has previously been observed in human cells infected by dengue viruses, could also occur in mosquito cells.

Cardiolipins were an interesting class of lipids to notice in our dataset because they have not been previously associated with infection. Given its role to maintain mitochondria function, and our finding that cardiolipin depletion disfavors virus replication, we surmised that cardiolipins help to buffer the effects of cellular stresses from viral infection that would otherwise lead to the triggering of the apoptosis regulation pathways.

Building upon your findings in lipid metabolism, what are your upcoming plans? Are there particular metabolic pathways or hormonal regulators you aim to investigate further?

It seems that viruses are strong remodelers of the lipid landscape in mosquitoes. I am keen to see how these modulations take place in different virome backgrounds. The crosstalk between immune and metabolic pathways is something I wish to dive into deeper. It would tell us something about the mechanisms through which host microbiota influence arbovirus infection and transmission.

What role does curiosity play in your life, both within and outside of science? How does studying viral manipulation of host lipid dynamics have implications on evolution of metabolism and its connection to therapies?

Interesting question, because I think I view and approach life in general with curiosity. The fact that I can make a living from finding out stuff is something I am very thankful for.

The insights from host lipids modulation could inform on long-term co-evolutionary dynamics between mosquitoes and their viruses. On the clinical side, understanding what host lipids and metabolites are co-opted by arboviruses, for both the arthropod and vertebrate side of the story, may lead to identification of disease severity risk factors or new therapeutic targets.

Tell us about how you see the future of immune-metabolism evolve with the new upcoming tools – what techniques have you used and which tools are you most excited about?

Single-cell transcriptomics and metabolomics are currently the ‘shiny new things’ in the omics space. As viruses don’t infect every single cell within a tissue, this unprecedented level of resolution would allow us to pinpoint cellular virus-modulated metabolism so much more accurately. I look forward to some paradigm shifting revelations that these techniques will bring about.

What advice would you offer to students and early-career scientists interested in exploring the intersections of metabolism and host-virus interaction? What’s an unexpected place you’ve found inspiration for your work?

Finding the right mentors who showed me what it means to be a scientist has been instrumental in my career path. I have also surprisingly found inspiration from actors and singers, like Hugh Jackman, who (according to a podcast interview I heard) gave himself five years after graduating from drama school to see where his career would take him, or Sabrina Carpenter, who debuted in 2014 and kept going until she produced chart-toppers ten years later.

Science-wise, I think more people should know about this thorough review about virus-vector metabolic interactions (PMID: 37360524).

How do you maintain a balance between your rigorous research activities and personal life? Are there hobbies or practices you find particularly rejuvenating?

Maintaining balance will be always a challenge for me but it helps greatly to know where I draw fulfillment and contentment from. I love my work as a researcher, but personal relationships are what brings me the most joy. I am the grandma friend, so I enjoy hosting long lunches and dinner parties.

If you hadn’t embarked on a career in biological research, what other profession might you have pursued, and why?

I think I would have been a food historian. I like learning about how cultures and geography influence the flavor profiles and methods of diverse cuisines. It is the intersection of anthropology and culinary science. I have questions like: Why do cuisines from warmer climates tend to be rich in spices? And what inspired someone to turn spent brewery yeast into a sandwich spread?

Anything else you’d want to highlight?

If immune-metabolism in vector mosquitoes sounds like your kind of vibe, please do get in touch. I would love to hear from postdoc candidates and/or grant co-writers.

Last week we learnt about treating rare metabolic disorders using Drosophila genetics and basic science research via precision medicine, check out the article – Finding Fruit in Flies (Holly Thorpe)

Check out the article All the world’s a metabolic dance, and how early career scientists are leading the way !!

(2 votes)
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An easily-consumable recap of the latest happenings in the #zebrafish community and beyond!

Use these links below to get to the section you want:

Community news

Zebrafish careers

Publications

Preprints

Reviews

Protocols and tools

Link to Bluesky post: https://bsky.app/profile/zebrafishrock.bsky.social/post/3lpxwto7crt2p

Community News:

Prof. Wendy Bickmore elected as an International Member of the US National Academy of Sciences (NAS).

Prof. Dr. Andrea Rentmeister receives 2024 Franco-German “Georg Wittig – Victor Grignard” Prize, awarded by the Société Chimique de France.

Prof. Edan Foley relocating her group from the University of Alberta to the Department of Life Sciences at University of Bath.

Prof. Dr. Ruben Portugues moving to the Department of Neurobiology and Behavior at Cornell University.

Dr. Sumeet Pal Singh joins the School of Natural Sciences at Shiv Nadar University as an Associate Professor.

Dr. Shawn Burgess named Associate Editor for GENETICS Journal.

Dr. Laurie Nemoz Billet awarded Accessit 2025 from SFBD for her thesis on the role of the ECM in motor nerve development and regeneration in zebrafish.

Zebrafish Rock! Slack tankspace surpassed 500 active monthly users. Register your interest, if you are keen to join at https://linktr.ee/zebrafishrock

IZFS publishes a new issue of the NewsSplash: https://www.izfs.org/newssplash/news-splash-issue-19-spring-2025 

ZHA is now on Bluesky: https://bsky.app/profile/zebrafishhusbandry.bsky.social 

The 11th Strategic Conference for Zebrafish Investigators (SCZI) will be held in Singapore on 14th-17th of January, 2026. More details to come.

The Killifish community is conducting an anonymous survey on husbandry of the African turquoise killifish (Nothobranchius furzeri) in hopes to standardize care & facilitate refinement. Link to help: https://survey.lamapoll.de/Global-Survey-on-Killifish-Husbandry-and-Care-2 

PhDs awarded to:

Dr. Luís Hernández-Huertas of Pablo de Olavide Lab

Drs. Briana Davis & Maggie Morash of John Rawls Lab

Now you can submit news, jobs and research to the #DanioDigest without a social media account! Get direct access to the #zebrafish community and beyond by filling out our Google Form with the details: https://forms.gle/H4nFUYqY5feMhBgQ8

#ZebrafishCareers posted by: 

‪@o-andersson-lab.bsky.social‬ 🇸🇪 (Lecturer)

https://uu.varbi.com/en/what:job/jobID:813452

@edanfoley.bsky.social‬ 🇬🇧 (All levels) – Contact directly

https://efoley4.wixsite.com/foleylab/personnel

@loicaroyer.bsky.social‬ 🇺🇸 (Scientist)

https://job-boards.greenhouse.io/chanzuckerbergbiohub/jobs/4553423005?gh_src=f5309c261us

‪@zfinmod.bsky.social‬ 🇫🇷 (PhD & PostDoc)

https://zfin.atlassian.net/wiki/spaces/jobs/blog/2025/03/31/6232375303/Postdoctoral+Scientist+PhD+Student+Neurofilaments+in+Health+and+Neurodegenerative+Diseases+Bomont+Lab+NeuroMyog+ne+Institute-PGNM+Lyon+France

@macdonaldlab.bsky.social‬ 🇬🇧 (Postdoc) #Killifish – Contact directly

https://zebrafishucl.org/macdonald-lab#macdonald-research

@zfinmod.bsky.social 🇩🇪 (Tech)

https://zfin.atlassian.net/wiki/spaces/jobs/blog/2025/04/28/6303383559/Molecular+Biology+Technician+ROLI+LAB+Max+Planck+Institute+for+Biological+Cybernetics+Tuebingen+Germany

Publications:

Reproductive Biology

Trudeau Lab at University of Ottawa (Secretoneurin/ Ovulation/ Pituitary)

doi.org/10.1093/pnasnexus/pgaf097 

@rohner.bsky.social (Astyanax/ Reproductive Biology/ Environment)

doi.org/10.1016/j.ydbio.2025.04.006 

Ming Shao Lab at Shandong University (Maternal rbm24a/ Germ cells/ Germ Granules)

doi.org/10.1038/s44318-025-00442-z 

Vasculature

Liangbiao Chen Lab at Shanghai Ocean University (Hepcidin/ Hematopoiesis/ Single-cell transcriptomics)

doi.org/10.1242/dev.204307 

@ssumanas.bsky.social‬ (Hemangioblast/ Macrophage/ Hematopoiesis)

doi.org/10.1242/bio.061948  

Notochord/ Spinal Cord

@slewzeus.bsky.social‬ (Notochord/ Hypertrophy/ Chondrocyte differentiation)

doi.org/10.1016/j.cub.2025.03.022 

Neuroscience

@piatkevich.bsky.social (SomaFRCaMPi/ Soma-localized red GECI/ In vivo neuronal imaging)

doi.org/10.1371/journal.pbio.3003048 

@alexbchen.bsky.social‬ & @mishaahrens.bsky.social (AQuA2/ Molecular spatiotemporal signals)

doi.org/10.1101/2024.05.02.592259 

@varshneylab.social‬ (Intellectual disability/ tRNA modification)

doi.org/10.1016/j.ajhg.2025.03.015 

@dkurrasch.bsky.social (Epilepsy/ CRISPR/Cas9/ NMDA receptor)

doi.org/10.1371/journal.pbio.3002499

@eveseuntjens.bsky.social (Killifish/ Telencephalon/ Development)

doi.org/10.1242/bio.061984 

@zerotonin.bsky.social (Mitochondria/ Neurodegeneration/ Dendrites)

doi.org/10.1242/dmm.052029 

Cancer

@katkajerabkova.bsky.social (Lysosomes/ Melanoma) 

doi.org/10.1038/s41467-025-58528-5

@nasimsabouri.bsky.social (Photodynamic therapy/ Rhabdomyosarcoma/ ROS)

doi.org/10.1021/acsptsci.5c00061 

Evolution

‪@mollyschumer.bsky.social‬ @hybridzones.bsky.social (Hybrid dysfunction/ Speciation genes/ Evolution)

doi.org/10.1038/nrg2718

@rohner.bsky.social‬ (miRNA/ Cave adaptation/ Astyanax)

doi.org/10.1111/nyas.15300

Behavior

Palagi Lab at University of Pisa (Yawning/ Contagion/ Synchronization)

doi.org/10.1038/s42003-025-08004-z

‪@johannakowalko.bsky.social (Astyanax/ Hunting/ Blindness)

doi.org/10.1242/jeb.250633

Cell Biology

@munromit.bsky.social‬ (Deoxynucleosides/ RRM2B/ Supplementation)

doi.org/10.1093/hmg/ddaf047

DeSantis Lab @umich.edu (Dynein/ Centrosome/ Endosome trafficking)

doi.org/10.1083/jcb.202406153 

Infection/Immunology

@ortizdeora.bsky.social‬ (Bacteriophages/ Live imaging/ Transmission dynamics)

doi.org/10.1038/s41564-025-01981-1

Huttenlocher Lab @uwmadison.bsky.social @kellerlab.bsky.social‬ (Burn/ Wound infection/ Innate immunity)

doi.org/10.1128/mbio.03480-24

Huttenlocher Lab @uwmadison.bsky.social (Live imaging/ Amoeboid migration)

doi.org/10.1242/dev.204351 

@cgmargarida.bsky.social & @sergemostowylab.bsky.social (Shigella/ Macrophages/ Inflammation)

doi.org/10.1016/j.celrep.2025.115601 

@zebrafish007.bsky.social‬ & #WeinsteinLab (Axillary lymphoid organ/ Immune surveillance)

doi.org/10.1084/jem.20241435 

@iic-umu-imib.bsky.social (Samhd1 deficiency/ Macrophages/ Salmonella)

doi.org/10.3389/fimmu.2025.1509725 

Lateral line

‪@vdisanto.bsky.social‬ (Astyanax/ Lateral line/ Sensory compensation)

doi.org/10.1016/j.cbpa.2025.111863

Disease models

@iic-umu-imib.bsky.social (Diamond-Blackfan anemia/ Spironolactone)

doi.org/10.1002/hem3.70131 

Bone/Cartilage

@kanaimichi.bsky.social & @clouthierlab.bsky.social (Gq/11 Family/ Lower Jaw Development)

doi.org/10.1242/dev.204396 

Regeneration

Ying Su Lab at Ocean University of China (scRNAseq/ Heart regeneration)

doi.org/10.1038/s41467-025-59070-0 

@abeisaw.bsky.social (Heart regeneration/ Cardiomyocytes/ Macrophages)

doi.org/10.1038/s41467-025-59169-4 

Toxicity/ Stress

@santastic-k.bsky.social (Toxicity/ Tire tread leachates)

doi.org/10.1016/j.envpol.2025.126286 

@odysyslab.bsky.social (Heat stress/ DNA repair/ Social metabolites)

doi.org/10.1002/1873-3468.70047 

Muscle

Fumihito Ono Lab at Osaka Medical and Pharmaceutical University (Action potentials/ Muscle/ Sodium channels)

doi.org/10.1371/journal.pbio.3003137 

Development

@cedricfeschotte.bsky.social (Gag proteins/ Retroviruses/ Development)

doi.org/10.1073/pnas.2411446122 

Preprints:

Regeneration

@sengulesra.bsky.social, @beckrichardson.bsky.social & @tillymommersteeg.bsky.social (Cavefish/ Macrophages/ B cells/ Heart regeneration)

https://www.biorxiv.org/content/10.1101/2025.04.24.650152v1

Gross Lab at University of Texas at Austin (Optic nerve injury/ Retinal ganglion cells/ Glaucoma)

doi.org/10.1101/2025.04.09.646875

@burgesslab.bsky.social (Lateral line/ Hair cell regeneration)

https://www.biorxiv.org/content/10.1101/2025.04.18.649014v1

Knight Lab at King’s College London (Muscle regeneration/ Ageing/ MMPs)

https://www.biorxiv.org/content/10.1101/2025.04.25.650659v1

Toxicity

@andrewwhitehead.bsky.social‬ (Killifish/ Environmental toxicants)

https://www.biorxiv.org/content/10.1101/2025.02.10.637481v1

Neuroscience

@erikacalvophd.bsky.social  (Olfactory dysfunction/ Parkinson’s disease/ Neuroinflammation)

https://www.biorxiv.org/content/10.1101/2025.03.29.645796v1

@rashi-agarwal.bsky.social & @wittbrodtlab.bsky.social‬ (Medaka/ Retinal stem cell/ Microglia)

https://www.biorxiv.org/content/10.1101/2025.04.01.646524v1

@zilova.bsky.social & @wittbrodtlab.bsky.social (Lens morphogenesis/ Ocular organoids)

https://www.biorxiv.org/content/10.1101/2025.04.17.649366v1

Hideaki Takeuchi Lab at Tohoku University (Calcium imaging/ Brain/ Medaka fish)

doi.org/10.1101/2025.04.09.647916

@rastapopolus.bsky.social‬ (Neural stem cells/ Cis-regulatory elements/ Transcriptional regulation)

doi.org/10.1101/2025.04.09.647643

@rodrigomorec.bsky.social & @uribelab.bsky.social (Enteric nervous system/ Gene networks)

https://www.biorxiv.org/content/10.1101/2025.04.17.649413v1

@tahneema.bsky.social & @mirimiam.bsky.social (Neural microexons/ Neuronal signaling)

https://www.biorxiv.org/content/10.1101/2025.04.24.650407v1

Evolution

@marcrr.bsky.social‬ (Molecular convergence/ Teleost fish)

https://www.biorxiv.org/content/10.1101/2024.06.24.600426v2

Cancer

@goetzjacky.bsky.social‬ (Renal cell carcinoma)

https://www.biorxiv.org/content/10.1101/2025.04.07.647527v1

#WeinsteinLab at NIH

‪@biomarina-vg.bsky.social & #WeinsteinLab (Meninges/ Single-cell transcriptomics)

doi.org/10.1101/2025.04.09.646894

@jimmykjm.bsky.social, @isabellaclsci.bsky.social & #WeisteinLab (Epigenetics/ Fin regeneration)

https://www.biorxiv.org/content/10.1101/2025.04.21.649771v1

@mmarvel.bsky.social & #WeinsteinLab (Epigenetics reporter/ Fatty liver disease)

https://www.biorxiv.org/content/10.1101/2025.04.21.649821v1

#WeinsteinLab (Novel imaging technique/ LUCID/ 3D structures)

https://www.biorxiv.org/content/10.1101/2025.04.04.647305v1

Somites/ Muscle

Davidson Lab at University of Auckland (Somites/ GESTALT/ Kidney)

https://www.biorxiv.org/content/10.1101/2025.04.15.649022v1

Behavior

@ryosuketanaka.bsky.social & @portugueslab.bsky.social (Optic flow/ Memory/ Behavior)

https://www.biorxiv.org/content/10.1101/2025.04.15.648832v1

Evolution

Woltering Lab at University of Konstanz (Dorsoventral limb patterning/ Cichlids/ Sturgeons/ Catsharks)

https://www.biorxiv.org/content/10.1101/2025.04.16.648507v1

Development

Minchin Lab at University of Edinburgh (Adipose remodeling/ Development)

https://www.biorxiv.org/content/10.1101/2025.04.20.649706v1

Chitnis Lab at NICHD (Lateral Line/ Wnt/ FGFR)

https://www.biorxiv.org/content/10.1101/2025.04.23.650055v1

Back to top

Reviews:

@jiaxingli.bsky.social‬ (Calcium/ Microdomain, Neuronal activity)

doi.org/10.1016/j.tins.2025.02.010 

‪@ishitani-lab.bsky.social (Morphogen/ Mechano-gradients/ Cell competition)

doi.org/10.1016/j.semcdb.2025.103607

‪Rebeca Bosso Dos Santos Luz & Braga Lab at Federal University of Paraná (Macrophages/ single-cell RNAseq/ Cardiac insult)

doi.org/10.3389/fcvm.2025.1570582

Protocols and Tools:

‪@mcgraillab.bsky.social‬ Zebrafish Community cre/lox Resource

https://zebrafishccr.org

#RaabeLab (Diffuse midline glioma, Transplantation protocol)

https://www.biorxiv.org/content/10.1101/2025.03.31.646163v1

@sethblackshaw.bsky.social‬ (Sleep deprivation/ JACUZI-SD,)

https://www.biorxiv.org/content/10.1101/2025.04.03.647099v1

@erezraz.bsky.social‬ (mRNA/ Optochemical control/ UV irradiation)

doi.org/10.1038/s41467-025-58207-5

@scholpplab.bsky.social (Prime editing/ Nickase- & Nuclease-based editors)

https://www.biorxiv.org/content/10.1101/2025.04.23.650248v1

@leanneiannucci.bsky.social & @katwrog.bsky.social (Optogenetics/ FGF/ BMP/ Nodal)

https://www.biorxiv.org/content/10.1101/2025.04.17.649426v1

@vishnums007.bsky.social‬ (Husbandry management/ Open-source)

doi.org/10.1089/zeb.2024.0183

‪@zfinmod.bsky.social‬ (New mutants/ Transgenic lines registering)

https://zfin.org/action/nomenclature/line-name

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 strong cuppa at the link below. Every little bit keeps us caffeinated and motivated! We appreciate your support 🙂

Link to donate: https://buymeacoffee.com/zebrafishrock 

Fin!

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No such thing as a standard career path – an interview with Eve Seuntjens

You were originally trained as a pharmacist. What made you decide to pursue an academic career?

We had a pharmacy at home, and out of the 8 siblings, I was the only one who studied pharmacy, so my mother was expecting me to take over her pharmacy. But during my studies, I got more interested in doing science, so I wanted to do a PhD first to know whether academia was for me. I always had this backup plan that I could go back and take over the pharmacy business. In that sense, I think I was a bit naive, because I wasn’t really very purposeful when I entered academia. My training had been very focused on running a pharmacy and not really doing science. I didn’t know the academic world when I started. It was a big jump into the unknown.

How did you end up doing a PhD in developmental biology?

For my PhD, I just picked a lab that somebody told me might have had an open position. It was a pharmacology lab, but in reality, they weren’t doing much pharmacology anymore. They were more into understanding paracrine signalling in pituitary function. My project was different, as I got to study how paracrine factors affected embryonic development of the pituitary. When I started by PhD, I was the first batch of students in our university’s formal doctoral training programme. They organised a few specific courses – one of them was on developmental biology. The professor of that course, Danny Huylebroeck, was super enthusiastic, and he really lit the fire of developmental biology in me. Even though he wasn’t my PhD supervisor, he later supported me to go for a postdoc.

How was your career path after your PhD?

By the end of my PhD, I’ve let go of the pharmacy idea, and I really wanted to go for an academic career. For my postdoc, I was more purposeful, and I went for EMBL in Heidelberg. By that time, I already had my first kid. I thought that raising a family and doing an academic career had to be combinable. It shouldn’t be because you’re raising a family that you’re a worse scientist. In Belgium, there already was a lot of support for women that wanted to pursue careers – universities had daycare and there were schemes for both parents to stay at home for your kids part time. But when I went to EMBL in 2001, I realised that people looked at having a family differently. EMBL was really great as a community with exciting science, but my PI didn’t really understand my viewpoint of having kids and an academic career. When I became pregnant again, he openly questioned why I bothered to have kids if I was putting them in daycare instead of taking care of them myself. I was shocked, because I came from a very different environment during my PhD. After two years, we decided to move back to Belgium; a bit earlier than anticipated, because of a job offer my husband had. I extended my postdoc in Belgium with Danny Huylebroeck and I continued working on developmental biology. He was very supportive of me while I was establishing my career. He also had the financial means to support me for a longer period of time. His lab was like a bio-incubator for postdocs who wanted to start their independent line of research.

You had three children during your postdoctoral period. How was your experience managing the various career breaks?

I didn’t really feel like, scientifically, there was that much impact. Of course, I lost time, because I was a postdoc running my own projects and had to pause them. I also stayed at home for one day a week for a long period. This impacted the speed of my publications, that’s for sure, but my publications were of high impact, and that was why I eventually landed my independent position. It just took me more time. More importantly, at key moments in my career, there were people that stood up for me and pushed me forward. They were not necessarily always the PI that I was working for, but influential people that would write reference letters for me and prepare me for an academic interview.

In the current academic system, where there’s often a time limit to how long a person can be a postdoc, what advice would you give to postdocs who are uncertain and anxious about their next career step?

I think how academia works is that there are windows of opportunity, and these windows open and close. For example, you just published a key paper, then a window opens for you to go to the next step of your career. But if you don’t manage to land a job in that window, maybe you have to go and get another experience somewhere else, make another contribution, and then a new window opens. Institutes are hiring at different levels and looking for different people at different times. I was super slow in figuring out what I wanted to do for my research. I didn’t have a plan to start with, so having more time to develop my plan was useful. Because I had so much incubation time, and worked in different environments and circumstances, I’m a bit more resilient to the stress that comes with an academic career.

During my longest postdoc period in Danny Huylebroeck’s lab, I was really given the freedom to build my own research line and network. I went to conferences and started collaborations on my own as a postdoc. And it was with this network where I shared my anxiety of this endless postdoc period. These people from that network would stand up and support me.

I was super slow in figuring out what I wanted to do for my research. I didn’t have a plan to start with, so having more time to develop my plan was useful. Because I had so much incubation time, and worked in different environments and circumstances, I’m a bit more resilient to the stress that comes with an academic career.

How was your experience applying for an independent position?

I applied to many open positions within and beyond our university in the broader area, because it was difficult to move away from Belgium with my family. I didn’t have many options, and everything failed. I was quite independent already, because of the leadership style of my PI. People in the hiring committees couldn’t really see that, as formal options to show independence, like obtaining grant funding, were not accessible to postdocs. When my contract ended, I didn’t know what to do, so I consulted my network, by sending an email to every PI that I knew, asking if anybody had any bridging money. Luckily, Laurent Nguyen from GIGA/University of Liège said he could pay me for a year. He was one of the key people who were there for me at the right time, at the right place. He helped me prepare for my final academic interview in which I landed the position that I have now.

After almost 16 years as a postdoc, you finally got a PI position at the University of Leuven (KU Leuven). How did you find the first few years as a PI?

The Department of Biology at KU Leuven was the perfect place for me to start my own group, because it was close to home, but in a new environment within a different group of people who saw me as somebody that brought something new. They also welcomed somebody who is Dutch speaking, because of the teaching language of our university in the Bachelor’s programme. I arrived in an environment that was very friendly, welcoming and sharing. It was an eye opener to me, because I was in a more competitive environment before. Having a close group of people that support you is so important at the beginning. Throughout the years I have been in different labs, institutes and universities, and these experiences have given me the impression that in times and places where there is not a lot of money, everyone collaborates more, shares more, and makes things work with the limited funding. That sense of solidarity I also experienced in my current environment, and it gave me peace of mind to endure times when grants wouldn’t come through easily.

Can you briefly talk about what your research is about? How did you find your niche?

I was always very interested in how nervous systems are built. For a long time, I collaborated with centres for human genetics. We would get genotype phenotype correlations and then build mouse models for human disorders. But when I started my lab, I had this crazy idea of going more in the evolutionary direction. Instead of using mice to study the mammalian brain, I got interested in cephalopods, which have a very unique and independent way of building a large nervous system. I didn’t have funding for it, but I thought it was fun and found somebody who got very excited very quickly. That was Graziano Fiorito (Stazione Zoologica Anton Dohrn in Napoli, Italy) but he was working on adult cephalopods, whereas I wanted to look at how the brain is built. Through a COST action network I met Eduardo Almansa (IEO, CSIC), who had access to octopus embryos. It took me a while to get funded for the octopus work, but I convinced collaborators and took bits and pieces from my other funding to start it up. Now, I almost only have money to do octopus research. I completely stopped working on mice because it was too much to keep the colonies running at the same time in my relatively small group.

How did you convince your institute to provide the space for raising octopus??

In my department, I can just ask, and we will get together and try to find a solution. My colleagues did ask if I was really sure to make that investment, but otherwise everyone was just helpful and excited for me. They were fine as long as I would pay my bills, and I wasn’t really asking for tons of space. A professor who worked on chicken just retired, so the chicken room became free. I asked whether I could put my system there. It was very small. I’ve always taken baby steps – nothing too radical or drastic. Gradually we started getting grants and papers on our cephalopod work.

You seem to be very good at reaching out to people and finding a supportive network. How do you manage that?

What I think saved me a lot of times, is my naivety and optimism. I always try to see the good in people, and in return, I feel like people are also more supportive of me. For example, during my inaugural lecture, I laid out my plan to study protocadherins in brain development in mice. Then as a sidenote, I said, but weirdly, there is also this protocadherin family expanded in cephalopod, so maybe it’d be nice to look at this in cephalopods as well. During the drinks after my lecture, a colleague from ecology (ecology evolution wasn’t really on my radar at the time) asked whether I was serious about working on cephalopods. He said he could introduce me to Graziano Fiorito. So, I got in touch with him, who invited me to join the COST network CephsInAction, a network of people interested in the research on cephalopod biology.

Have you ever revisited topics from your pharmacist background? Did you take anything away from your pharmacist training?

I moved away from pharmacy completely. The only thing I got from it is the way I work in the lab. As a pharmacist, you have to be super attentive. You cannot make any mistakes, because you could kill someone, so I’ve learned to be very precise. Coming from a pharmacist background into the developmental biology field, I was not too bothered by the dogmas of the field and that made me see different perspectives that other people don’t see, which I see as an advantage.

What’s the most memorable piece of career advice that you’ve heard/received?

I have spent a long time in this postdoc anxiety phase, where you have no idea where you’re going to land, and people keep asking whether you have a plan B, C, D and E. This anxiety is so draining. At some point someone asked me: “Where do you get your energy?” It’s a simple question, but to me it was an eye-opener, so my advice would be: try to identify what gives you energy and where your intrinsic motivation can be found. I tried plan B and C and D as well, but I kept failing in my applications for non-academic jobs, because during the job interviews, it would turn out that my heart was in academia. I think identifying the source of your energy is very important throughout all the steps of your career.

I kept failing in my applications for non-academic jobs, because during the job interviews, it would turn out that my heart was in academia.

What were your plan B and C? What other jobs did you explore?

They were all science related. I applied for a role as a grant advisor in a funding institution. There was another opportunity in the university for a role that scouts for international funding opportunities. I also interviewed for a company that was doing probiotics, because of my pharmacy background. After all those interviews, I figured out I was very poor in those things. I also found that going through the job application process is super draining for me, because you have to envision yourself in another job that might be very different from what you’re doing now. I massively underestimated the energy and time it took to apply for those jobs. In the end, the academic interviews were much easier for me.

Finally, what do you like to do in your spare time?

I like to swim and snorkel. I also like gardening and being outside. But in general, I don’t have any regular hobbies really! There is so much planned in my agenda during the day that I really like to have the freedom of doing just nothing.

(5 votes)
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In this SciArt profile, we meet Queralt Tolosa, who has a background in biochemistry and developmental biology. After her PhD, she transitioned into being a freelance scientific illustrator and animator. Check out this interview where we find out more about her scientific and artistic influences.

Can you tell us about your background and what you work on now?

I have a background in Biochemistry and earned both a Master’s and a PhD in Biomedicine. My doctoral research focused on how mechanical forces influence the formation and function of epithelial tissues during early development, using zebrafish embryos as a model.

Throughout my academic journey, I developed a growing interest in visual communication. As a visual learner, I found that graphical representations helped me focus and retain information more effectively from a young age. This realization led me to value the visualization of complex concepts, not only for my own understanding but also as a tool to communicate information and ideas to others. I quickly recognized how impactful clear, engaging visuals could be in simplifying difficult concepts. People appreciated them, and during my PhD was when some colleagues started to reach out to me for help or feedback on creating their own.

Encouraged by my colleagues, I began to explore scientific illustration more seriously as a potential career, rather than just as a tool I used in my research. After completing my PhD, I transitioned into freelance work as a scientific illustrator and animator, largely through self-teaching. Today, I create both 2D and 3D illustrations and animations, combining my scientific expertise with visual storytelling to make science more accessible and engaging.

If you need help transforming complex science into compelling visuals, feel free to reach out. I’m just an email away! :)

Were you always going to be a scientist?

In many ways, yes. As a kid and teenager, I was completely captivated by medicine, especially surgery. The idea of understanding what was happening inside the human body and being able to repair something so complex really intrigued me. TV shows like House, Grey’s Anatomy, and Bones definitely fueled that fascination, although I’ll admit I may have started watching them a little earlier than I probably should have.

By the time I reached the later years of high school, my interests shifted towards genetics and epigenetics, which ultimately led me toward a research career. It felt like the natural progression, combining my love for science with a deep curiosity about how the body works at a molecular level.

Of course, I had other strong interests, like cinema, literature, and drawing. However, when it came time to choose a career, none of them felt like something I would want to pursue professionally. There’s a clear difference between enjoying something as a hobby and envisioning it as a career.

And what about art—have you always enjoyed it?

Absolutely. Art has always been a part of my life. I’ve been passionate about it for as long as I can remember, exploring every form I could, from pottery to drawing to acrylic painting. I took classes throughout school and high school, constantly doodling or sketching whenever I had the chance. It became my go-to way to relax, reflect, and express myself.

At the time, though, I never considered art as a career. The idea of having to create for a living felt overwhelming, almost like it would take the joy out of it. I wanted to keep art as a personal, stress-free outlet and do it when inspiration struck, not because it was expected of me.

But over time, things changed. Now, I’ve found a way to blend my love for science with my creative side. I’ve also learned how to maintain a healthy balance between professional work and personal art. Keeping a clear distinction between the two has allowed me to preserve the joy and freedom in both aspects, making sure that each one remains fulfilling in its own way.

What or who are your most important artistic influences?

My artistic influences have changed a lot over time and are still evolving. They span all sorts of things, from painters and sculptors to cinema and other visual arts.

When it comes to scientific illustration, my early influences were a bit limited, but I’ve always admired the work of people like Leonardo da Vinci and Ramón y Cajal, who managed to combine science and art so well. It’s a pretty basic answer, I’ll admit, but they were huge for me. Growing up, most of the scientific visuals I came across were focused on wildlife and plants, which I didn’t really connect with. It wasn’t until my PhD that I discovered David Goodsell’s work in molecular biology, and that completely opened my eyes to the world of scientific illustration in that area. These days, I’m lucky enough to be influenced by a lot of my colleagues in the field, and being able to interact with them is pretty amazing.

When it comes to broader influences, I’d say my inspirations are eclectic. The first drawings I loved and tried to replicate in order to learn how to draw were the works of Hayao Miyazaki, Tim Burton, and Disney classics. I’ve also been a lifelong fan of manga and anime, which have greatly influenced both my aesthetic and storytelling instincts.

I’m also a huge admirer of classical art, some of my favorite pieces of artwork are from artists like Toulouse-Lautrec, Francisco Goya, Sandro Botticelli, or Artemisia Gentileschi. Nowadays, I follow closely artist such as Laura H. Rubin, Miles Johnston, Zipcy, Lucas David, Kildren, or Guillermo Lorca García.

How do you make your art?

For my personal work, I’m drawn to traditional media, particularly graphite and ink. There’s something about the tactile nature of these materials that make the process feel more intimate and fulfilling. I often incorporate a touch of color, but it’s the slower pace and hands-on approach that allow me to truly reconnect with the creative process on a deeper level.

When working professionally, though, my approach shifts entirely to digital. I use Procreate and Photoshop for illustration, which give me the flexibility to experiment and refine ideas quickly. For animation and post-production, I rely on Procreate Dreams, After Effects, and Premiere Pro, which provide all the tools I need to bring my work to life in dynamic ways. For 3D projects, I turn to Blender, which offers the versatility to create detailed, immersive environments.

I believe in always evolving as an artist, so I make it a point to stay curious and open to new techniques. Whenever I can, I dive into new tools, software, or courses that expand my skill set and challenge me to approach my work from fresh perspectives.

Does your science influence your art at all, or vice versa? Or are they separate worlds?

They’re definitely distinct in terms of content, but they absolutely influence each other in surprising ways. My personal art is often more introspective—an outlet for my own thoughts and feelings, where I can step back from the scientific side of things. It’s a space for creativity and self-expression that’s more abstract.

But in my professional work, the two worlds are tightly intertwined. My scientific background gives me the ability to break down complex ideas and understand them in depth. That foundation allows me to create accurate representations of those concepts. On the flip side, my artistic skills help me present these ideas in a way that’s visually engaging and easy to understand, making complex science more approachable and relatable.

It’s all about balance—honoring the rigor of science while using the creativity of art to communicate it in a way that resonates with people. I love how they complement each other, and it’s that intersection that keeps me motivated and inspired.

What are you thinking of working on next?

I’m still in the early stages of my freelance career, so right now I am really focused on building a solid foundation for my scientific illustration and animation business. I am working on reaching more potential clients, building strong relationships, delivering thoughtful work on every project, and fine-tuning my workflow so I can keep getting better and growing.

I am also very committed to continuous learning. I am always looking for ways to improve, whether through online courses or personal projects. I am putting a lot of time into sharpening my techniques and finding the best ways to visually communicate different scientific topics, making sure my work stays accurate, engaging, and high quality.

Looking ahead, I am excited to take on more challenging projects that will push me to grow professionally and help me build a reputation as someone people can trust for beautiful, accurate scientific visuals.

How/where can people find more about you?

(1 votes)
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The Art-Science Symbiosis. Marcelo Velasco – Ignacio Nieto. Springer Nature. 2024.

The increasing influence of science on contemporary art (often referred to as art-science) prompted us to explore a central working question: could contemporary art, in turn, significantly influence scientific activity?

We observed that contemporary art possessed distinctive attributes, absent in more traditional artistic forms, that enabled it to interact fruitfully with the creativity inherent in the scientific process. Our own dual background –Velasco is a Biologist, Nieto a PhD in Aesthetics– provides us with an informed perspective in both fields, and places us in a relatively comfortable position to analyze the inherent strengths and weaknesses of both.

This interest culminated in the publication of a book by the prominent scientific publisher Springer-Verlag, which inevitably leans the work towards a scientific audience. However, precisely because of this orientation, we anticipate that the book will also pique the curiosity of artists and the general public interested in interdisciplinarity. Throughout our research, we discovered notable examples of practicing scientists who have produced significant artistic works, including Manuel Théry (France. PhD. Cytomorpholab Research director @ CEA, EMBO Member); David Goodsell (USA. PhD in DNA X-ray crystallography, illustrator and Professor of Computational Biology at the Scripps Research Institute and a Research Professor at Rutgers University); Jimena Royo-Letelier (Chile. Artist and researcher, PhD in applied mathematics at Université de Versailles Saint-Quentin-en-Yvelines; and François-Joseph Lapointe (Canada. Artist and scientist at the University of Montreal. PhD in evolutionary biology (1992) and a PhD in dance and performance), among many others.

In our approach, we made a conscious effort to avoid the commonplaces that often accompany these discussions. We aimed to integrate theoretical elements to better understand the broad scope of the practice; a curatorial process (reasoned selection) of artworks; relevant historical references; and qualitative research through interviews with the unique artist-scientists included. The curatorial process involved an exhaustive review of the vast art-science-technology landscape, selecting those works that we considered of particular interest to both the scientific and artistic communities.

We are confident that the publication of this book represents a valuable opportunity for establishing collaborative networks, through other platforms for dissemination and debate. The trust placed in our work by Springer allowed us to receive an enthusiastic response from the artist-scientists participating in the project, all developed from Santiago, Chile, and without external funding.

We hope that this exploration will contribute to fostering a deeper dialogue and reveal the symbiotic potential between the analytical rigor of science and the evocative and conceptual capacity of contemporary art.

Find front matters here:

https://link.springer.com/content/pdf/bfm:978-3-031-47404-0/1

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