The Worm Podcast

Dr Veeren Chauhan

The Worm Podcast explores the latest research using worms to understand biology. Hosted by Dr Veeren Chauhan (University of Nottingham), each episode takes a recent paper and breaks down what was discovered, how it was done and why it matters. From C. elegans and Pristionchus pacificus to ageing, metabolism, neuroscience, behaviour, host–microbe interactions and analytical tools, the podcast follows new discoveries across biology. This podcast is generated with artificial intelligence and curated by Veeren. www.veerenchauhan.com veeren.chauhan@nottingham.ac.uk

  1. 2d ago

    EPISODE 55: The Worm’s Stress Network

    Welcome to the next episode of the WOrM Podcast 🪱⚡ Today we are looking at how one stress-response protein helps a worm adapt to changing conditions. At the centre of the story is PMK-1, the C. elegans equivalent of p38 MAP kinase. Rather than acting through one fixed pathway, PMK-1 changes its molecular partners across development, tissues and environmental stress. The result is a flexible network that helps generate phenotypic plasticity. ⸻ 🧬 Meet ContinuumID The researchers developed ContinuumID, an in vivo proximity-labelling method combining TurboID with an auxin-induced degron. This allowed them to control when and where proteins near PMK-1 were labelled and identified by mass spectrometry. They mapped PMK-1 interactions across: • four developmental windows• five tissues• osmotic stress• ultraviolet stress• oxidative stress Together, this created 26 datasets and a spatiotemporal atlas of the PMK-1 interactome. ⸻ 🕸️ A huge interaction network The atlas contained 1,151 candidate interactors. Some appeared only in particular tissues or conditions. Others formed a stable core shared across development and stress. These partners included proteins involved in: • RNA splicing• transcription• ribosome biogenesis• translation• signalling• metabolism• nuclear transport PMK-1 therefore does more than switch stress genes on and off. It connects environmental sensing to RNA processing, protein production and metabolism. ⸻ ⚡ Different stress, different response PMK-1 responded differently to each challenge. During osmotic stress, activation rose rapidly and then returned towards baseline. After ultraviolet exposure, activation remained high while the total pool of PMK-1 became depleted. Oxidative stress produced a slower, delayed response. The timing and duration of signalling therefore matter—not just its strength. ⸻ 🔄 Partners come and go Some proteins maintained stable contact with PMK-1. Others associated or dissociated when stress appeared. One example was VHP-1, a phosphatase that strongly dissociated after ultraviolet exposure, helping explain the prolonged activation of PMK-1. A signalling pathway is therefore not a fixed chain. It is a changing network of molecular contacts. ⸻ 🧪 More signalling does not always mean more survival The researchers reduced individual interactors using RNA interference. Some knockdowns weakened survival. Some had little effect. Others unexpectedly improved it. Even proteins from the same pathway could produce positive, negative or neutral outcomes. Changes in stress-responsive gene expression also did not reliably predict survival. Survival is an integrated whole-animal outcome shaped by signalling, metabolism, gene expression and tissue health. ⸻ 🧠 The take-home message PMK-1 acts as a molecular hub. It combines: development × tissue × environment × molecular context to generate different biological outcomes. The pathway does not simply suppress variation. It helps create the range of responses that allows organisms to adapt when conditions change. ⸻ 📄 Paper discussed Wang Yuan; Luke A. Nunamaker; Yi M. Weaver; Benjamin P. Weaver. (2026) A Caenorhabditis elegans spatiotemporal proximity atlas reveals the MAPK p38 as a generator of phenotypic plasticity in vivo Science Signaling, 19: eaeb4530 DOI: 10.1126/scisignal.aeb4530 ⸻ If you enjoyed this episode, please like, follow and subscribe wherever you listen to the WOrM Podcast ⭐🎧 This podcast is generated with artificial intelligence and curated by Veeren. If you would like your publication or product featured on the show, please get in touch. 🔗 www.veerenchauhan.com📧 veeren.chauhan@nottingham.ac.uk

  2. Aug 12

    EPISODE 54: Sleep, Fat and Memory: One Neuron Does It All

    Welcome to the next episode of the WOrM Podcast 🪱💤 Today we are looking at a single sleep-active neuron that connects far more than sleep. In C. elegans, the RIS neuron helps regulate: • sleep• lipid storage• survival• lifespan• memory At the centre of the story is a conserved somatostatin-like signalling system involving the neuropeptide NLP-99 and its receptor NPR-16. ⸻ 🧠 Meet the sleep neuron RIS is the major sleep-active neuron in C. elegans. When RIS activates, it releases FLP-11 neuropeptides that suppress wake-promoting circuits and induce sleep. But RIS is not working alone. The wake-active AIY neurons release NLP-99, which signals through NPR-16 to regulate RIS. The result is a sleep–wake circuit in which AIY promotes wakefulness and RIS promotes sleep. The two neurons effectively behave like a biological flip-flop switch. ⸻ 💤 The effect depends on context The same signalling pathway produces different outcomes depending on the animal’s nutritional state. During starvation-induced L1 arrest, NLP-99 and NPR-16 suppress sleep. In well-fed adults, the pathway instead supports RIS activation and sleep. This apparent contradiction comes from where NPR-16 acts. Inside RIS, NPR-16 inhibits calcium activity and limits FLP-11 release. Outside RIS, it appears to inhibit other neurons that normally suppress RIS, producing a net activating effect. So one receptor can both restrain and support the same sleep neuron. ⸻ 🧪 Watching a neuropeptide leave the neuron The researchers created a fluorescent FLP-11 reporter to follow neuropeptide release from RIS. When RIS became active and the worm entered sleep, the FLP-11 signal inside the neuron fell, consistent with release. Deleting nlp-99 or npr-16 increased FLP-11 secretion during L1 arrest. This helps explain why the mutants slept more despite showing weaker RIS calcium signals. The pathway controls not only whether the neuron activates, but also how much sleep-inducing signal it releases. ⸻ 🍽️ Sleep meets metabolism Deleting nlp-99 or npr-16 increased intestinal lipid stores during L1 arrest. These effects depended on functional RIS. The mutants also survived starvation longer, while adult lifespan increased by roughly one to two days. This links a sleep circuit directly to energy storage and survival. ⸻ 🧠 Sleep and memory RIS and FLP-11 were also required for learning and long-term olfactory memory. The worms were trained to associate the normally attractive smell diacetyl with starvation. Animals lacking RIS signalling, NLP-99 or NPR-16 showed impaired memory consolidation. So this pathway does not simply decide whether a worm sleeps. It helps determine whether an experience is retained. ⸻ 🧬 The take-home message A conserved somatostatin-like signal acts through one sleep-active neuron to coordinate: sleep × metabolism × survival × memory The effect changes with nutritional state, developmental stage and the location of the receptor. One small neural circuit can therefore organise several whole-animal functions at once. ⸻ 📄 Paper discussed Byoungjun Park; Lama Mohsen; Inka Busack; Laura Uhlig; Lorenzo Rossi; Gill Pollmeier; Ellen Geens; Majdulin Nabil Istiban; Sajal Mandal; Reshma Dominic Savio; Isabel Beets; Attila Stetak; Henrik Bringmann. (2026) C. elegans somatostatin/allatostatin C signaling regulates sleep, metabolism, survival, and memory via a sleep-active neuron Science Advances, 12: eadv8387 DOI: 10.1126/sciadv.adv8387 ⸻ If you enjoyed this episode, please like, follow and subscribe wherever you listen to the WOrM Podcast ⭐🎧 This podcast is generated with artificial intelligence and curated by Veeren. If you would like your publication or product featured on the show, please get in touch. 🔗 www.veerenchauhan.com📧 veeren.chauhan@nottingham.ac.uk

  3. Aug 5

    EPISODE 53: Worms on Pause

    Welcome to the next episode of the WOrM Podcast 🪱⏸️ Today, we are talking about worms that appear to stop living—without dying. Researchers have identified a new, reversible state of suspended animation in C. elegans, triggered by a surprisingly simple condition: crowding worms together in an isosmotic liquid. They call it liquid-induced suspended animation, or LISA. ⸻ ⏸️ Pressing pause on the worm At high population density in M9 buffer, worms rapidly stop: • moving• developing• differentiating cells• progressing through normal life stages This is more than sleep or temporary inactivity. Core biological processes are placed into a profound state of arrest, yet the animals remain alive and can later resume normal development. The response occurs across larval stages and in adults. It is also distinct from dauer formation and suspended animation caused by complete oxygen deprivation. ⸻ 🧪 Crowding is essential Low-density worms continue developing normally. But once the population passes a critical density, almost the entire group enters LISA. Food, amino acids and vitamins do not prevent it. Starvation, heat shock and hypoxia alone do not reproduce it either. The animals must be crowded, stationary and suspended in an isosmotic liquid. Why crowding produces this response remains unresolved. The authors suggest something resembling population-density sensing, although the supernatant alone could not transfer the effect to uncrowded worms. ⸻ 🧬 Surviving suspended animation The study identified stress-response pathways that help worms endure prolonged LISA. HSF-1 and DAF-16 work together to support survival, while genes involved in autophagy and lysosomal function are particularly important. Mutations disrupting lysosomal formation, fusion or fission greatly reduced survival. Interestingly, mitochondrial remodelling was visually dramatic but was not essential for surviving the arrested state itself. Lysosomes appear to do much of the heavy lifting. ⸻ ⏰ How does a worm wake up? When returned to favourable conditions, the worms awaken in a coordinated sequence. The AFD sensory neurons and AIY interneurons promote awakening, while the sleep-active RIS neuron delays it. PDF neuropeptide signalling and the cAMP–PKA pathway then help drive renewed movement. Artificially raising cAMP made the worms awaken sooner. So recovery is not simply metabolism restarting by itself. It is an actively regulated behavioural transition controlled by the nervous system. ⸻ 🧠 The take-home message C. elegans can pause development, movement and metabolism across multiple life stages—and later restart. LISA provides a simple experimental model for studying: • metabolic suppression• dormancy• stress resilience• organ preservation• awakening from biological stasis The wider possibilities extend from emergency medicine to long-duration spaceflight. For now, the worm gives us something remarkable: a reversible pause button for animal life. ⸻ 📄 Paper discussed Junqiang Liu; Bingying Wang; Jonathan Leon Catrow; Quentinn Pearce; Zhijian Ji; Supeng Winnie Yang; Akash Balakrishnan; James E. Cox; Dengke K. Ma. (2026) Induction and regulation of reversible suspended animation in C. elegans Nature Communications, 17:4627 DOI: 10.1038/s41467-026-71247-9 ⸻ If you enjoyed this episode, please like, follow and subscribe wherever you listen to the WOrM Podcast ⭐🎧 It really helps others in the community find the show. This podcast is generated with artificial intelligence and curated by Veeren. If you would like your publication or product featured on the show, please get in touch. 🔗 www.veerenchauhan.com📧 veeren.chauhan@nottingham.ac.uk

  4. Jul 29

    EPISODE 52: Worms in Space: Microbiomes in a Capsule

    Welcome to the next episode of the WOrM Podcast 🪱🚀 Today, we are looking at NemaCapsules: a new microfluidic system designed to study how host genetics and the gut microbiome influence C. elegans health during spaceflight. The challenge is simple: how do you keep worms alive, fed, contained and ready to image on the International Space Station without creating more work for astronauts? ⸻ 💊 Enter NemaCapsules NemaCapsules are sealed, gas-permeable biocells containing microfluidic chambers for long-term worm culture. Each unit provides: • passive feeding• controlled microbiome conditions• minimal crew intervention• repeated video imaging• separate chambers for crawling and swimming The system creates a miniature, self-contained worm laboratory suitable for future spaceflight experiments. ⸻ 🏊 Crawling versus swimming The crawling chamber contains closely spaced micropillars that support normal crawling. The swimming chamber uses a wider pillar arrangement, allowing worms to thrash through liquid. This proved important because swimming often revealed differences between host–microbiome conditions that were less obvious from crawling alone. ⸻ 🦠 Testing the microbiome The researchers tested three microbial conditions: • standard laboratory E. coli OP50• a simplified three-member microbiome• BIGbiome, a 63-member community representing the natural C. elegans microbiome They also tested four worm backgrounds: • wild-type N2• daf-16 mutants• ED3017• JU1400 This allowed them to examine the combined effects of microbiome, host genetics and ageing. ⸻ 🧬 The host matters Most strains remained viable across the different microbiomes. The exception was daf-16. These mutants showed rapid declines in survival and movement after day seven, consistent with the established role of DAF-16/FOXO in stress resistance and longevity. The platform therefore detected a genuine biological vulnerability rather than simply maintaining every condition equally. ⸻ ⚡ The microbiome changed movement The multi-member microbiomes frequently improved crawling and swimming compared with OP50 alone. However, the strength of this effect depended on the worm strain. That is the key point: the microbiome does not act independently of the host genome. ⸻ 🔬 Why this matters This study is primarily about building the hardware needed to perform controlled host–microbiome experiments in space. NemaCapsules combine: • long-term culture• passive feeding• controlled microbial communities• host genetic diversity• repeated whole-animal phenotyping These experiments were conducted on Earth to validate the platform ahead of future International Space Station studies. ⸻ 🧠 The take-home message Spaceflight biology is not just about sending organisms into orbit. It is about creating systems that can produce reliable biology once they arrive. NemaCapsules offer a way to study how: spaceflight × microbiome × host genetics combine to shape whole-animal health. ⸻ 📄 Paper discussed Bushra Rahman; Atiyya P. Saroyia; Dana Blackburn; Audrey J. Parish; Nathaniel Szewczyk; Monica Driscoll; Buck S. Samuel; Siva A. Vanapalli. (2026) NemaCapsules: Microfluidics-Integrated Biocells for Investigating C. elegans Host-Microbiome Interactions in Spaceflight npj Microgravity DOI: 10.1038/s41526-026-00634-9 ⸻ If you enjoyed this episode, please like, follow and subscribe wherever you listen to the WOrM Podcast ⭐🎧 This podcast is generated with artificial intelligence and curated by Veeren. If you would like your publication or product featured on the show, please get in touch. 🔗 www.veerenchauhan.com📧 veeren.chauhan@nottingham.ac.uk

  5. Jul 22

    EPISODE 51: The Worm Behind the Wild

    Welcome to the next episode of the WOrM Podcast 🪱 Today we’re looking at a review with a bold idea. Can a tiny nematode help us protect fish, amphibians, reptiles and insects from an increasingly challenging world? The authors argue that the answer could be yes. ⸻ 🧬 The central idea Microbes have a huge influence on animal health. They affect: • immunity• metabolism• stress tolerance• development• resistance to disease The challenge is that most wild animals are difficult to study in the laboratory. That’s where Caenorhabditis elegans comes in. Instead of testing hundreds of microbial candidates directly in threatened or difficult-to-maintain species, we can first screen them rapidly in worms. ⸻ 🔬 Why use a worm? C. elegans offers an extraordinary experimental toolkit. Researchers can: • manipulate genes with ease• study host–microbe interactions in real time• follow lifespan and healthspan• measure resistance to pathogens and environmental stress• rapidly test hundreds of microbial strains Many of the signalling pathways involved in immunity, metabolism and stress responses are remarkably well conserved across the animal kingdom. That makes the worm an ideal discovery platform. ⸻ 🌍 From the lab to wildlife The authors propose a simple pipeline. Start by isolating microbes from the animal you want to protect. Screen those microbes in C. elegans. Identify which ones improve resilience. Understand how they work. Then return the most promising candidates to the original species for validation. Rather than replacing studies in wildlife, the worm helps researchers focus on the most promising interventions. ⸻ 🦠 More than probiotics This isn’t simply about adding beneficial bacteria. It’s about understanding how microbial communities can improve resilience against: • rising temperatures• environmental pollution• infectious disease• habitat change• other environmental stresses As climate change continues to reshape ecosystems, these questions are becoming increasingly important. ⸻ 🧠 The bigger picture This paper reminds us that model organisms are valuable far beyond their own biology. C. elegans isn’t just helping us understand worms. It may help us understand how to improve the health and resilience of entirely different animals. Sometimes the fastest way to protect wildlife begins with one of the simplest organisms in the laboratory. ⸻ 🧠 The take-home message Tiny worms can answer big questions. By combining the experimental power of C. elegans with microbiome research, scientists may be able to discover microbial therapies that improve the resilience of species facing an increasingly uncertain future. ⸻ 📄 Paper discussed Sprason, C.; Donkersley, P.; Chin, J. P.; Benedetto, A. Caenorhabditis elegans as an experimental model for resilience-boosting microbiota interventions in non-model ectotherms FEMS Microbiology Reviews DOI: 10.1093/femsre/fuag031 If you enjoyed this episode, please like, follow, and subscribe wherever you listen to the WOrM Podcast ⭐🎧 It really helps others in the community find the show. This podcast is generated with artificial intelligence and curated by Veeren. If you’d like your publication or product featured on the show, please get in touch. 📩 More info: 🔗 www.veerenchauhan.com 📧 veeren.chauhan@nottingham.ac.uk

  6. Jul 15

    EPISODE 50: Fed by Mum, Built by Ribosomes

    Welcome to the next episode of the WOrM Podcast 🪱 Today we’re talking about inheritance. Not DNA. Not small RNAs. Not epigenetics. But ribosomes. ⸻ 🧬 The central idea When mother worms experience dietary restriction, their offspring hatch with fewer ribosomal proteins. That matters because ribosomes are the machinery that make proteins. Less ribosome capacity means slower early growth.   ⸻ 🔬 What they found The authors compared worms fed normally with worms under dietary restriction. In the mothers, dietary restriction changed the proteome broadly. But in the offspring, most protein changes were reset. The big exception was ribosomal proteins. These stayed reduced in the next generation. ⸻ 🐣 What happens to the offspring? Offspring from diet-restricted mothers hatched smaller and grew more slowly during early larval development. But this delay was temporary. As the larvae rebuilt normal ribosome levels, their growth recovered. So the maternal diet leaves a short-term biological imprint on early growth. ⸻ ⚙️ Is it causal? Yes. When the authors directly reduced a ribosomal protein in mothers using auxin-induced degradation, the offspring also grew more slowly. That shows reduced ribosome abundance is not just correlated with slower growth. It can help cause it. ⸻ 🧠 The signalling link The study also points to mTORC1 signalling, through RAGA-1, as part of the mechanism. Maternal RAGA-1 depletion reduced ribosomal protein levels in offspring. Interestingly, this depended on tissue context. Pharynx-specific depletion had an effect. Epidermal depletion did not. So this is not just “slow mother equals slow offspring”. It is a specific physiological signal crossing from soma to germline. ⸻ 🧠 The take-home message Dietary restriction does not simply rewrite the whole offspring proteome. Most of the proteome resets. But ribosomes are different. Maternal diet shapes how much translational machinery offspring receive, and that changes how fast they grow when life begins. ⸻ 📄 Paper discussed Pradhan, S.; Stojanovski, K.; Dellemann, F.; Psalmon, S.; Tuomaala, J.; Stroustrup, N. E.; Towbin, B. D. (2026) Dietary restriction shapes intergenerational ribosome abundance and early growth of Caenorhabditis elegans offspring PLOS Biology https://doi.org/10.1371/journal.pbio.3003692 If you enjoyed this episode, please like, follow, and subscribe wherever you listen to the WOrM Podcast ⭐🎧 It really helps others in the community find the show. This podcast is generated with artificial intelligence and curated by Veeren. If you’d like your publication or product featured on the show, please get in touch. 📩 More info: 🔗 www.veerenchauhan.com 📧 veeren.chauhan@nottingham.ac.uk

  7. Jul 8

    EPISODE 49: Glowing up the Worm Proteome

    Welcome to the next episode of the WOrM Podcast 🪱 Today we’re looking at a paper that doesn’t answer a biological question. Instead, it builds the tools to answer thousands of biological questions in the future. The ambition? To fluorescently tag every protein encoded by the C. elegans genome.   ⸻ 🧬 The big idea We already have remarkable gene expression atlases based on RNA. But RNA isn’t the whole story. Proteins are the molecules that actually perform the work inside cells, and protein abundance often doesn’t match RNA abundance. The authors argue that the next frontier is a whole-animal protein atlas showing exactly where every protein is found, in every cell, throughout development.   ⸻ 🔬 How did they test the concept? Rather than tagging one gene at a time, they asked a much bigger question. Could they tag three genes simultaneously using CRISPR? They selected: 30 genesthree different fluorescent proteins10 pooled CRISPR experimentsThe approach worked remarkably well. They successfully generated 24 of the 30 tagged proteins, with all successful tags visible by fluorescence microscopy.   ⸻ 🌈 Why three colours? Each fluorescent protein was chosen for a different brightness and wavelength. The clever part was matching fluorophore brightness to expected protein abundance. Highly expressed proteins received one fluorophore. Moderately expressed proteins another. Low-abundance proteins received the brightest red fluorophore, which also suffers least from worm autofluorescence. This makes large-scale screening much faster and more practical.   ⸻ 🧠 The biology was the surprise Although this is primarily a methods paper, it immediately produced biology. Several proteins appeared in tissues where RNA datasets suggested they should not be enriched. Examples included proteins accumulating preferentially in: germlinegonadal sheathspermspecific neuronsglial cellsThese differences highlight something important. RNA tells you what might be made. Protein localisation tells you what is actually there.   ⸻ 🚀 Why this matters Around 8% of the C. elegans proteome has already been tagged. At the current pace, completing the remaining genome could take around 100 years. Pooling multiple CRISPR edits into single experiments could reduce that dramatically and make a community-wide effort realistic.   ⸻ 🧠 The bigger picture Imagine being able to ask: Where is every protein expressed?Which cells use it?Where inside the cell does it go?How does localisation change during ageing, stress or disease?Instead of studying one protein at a time, researchers could explore an entire organism with single-cell resolution. That’s the long-term vision behind this work. ⸻ 🧠 The take-home message Sometimes the most important papers don’t make a discovery. They build the infrastructure that allows everyone else to make discoveries. If the C. elegans community succeeds in creating a complete fluorescent proteome atlas, it would become one of the most valuable biological resources ever generated for any multicellular organism. ⸻ 📄 Paper discussed Eroglu M., Hobert O. (2026) A pilot study for whole proteome tagging in C. elegans eLife DOI: 10.7554/eLife.110717.3 If you enjoyed this episode, please like, follow and subscribe wherever you listen to the WOrM Podcast ⭐🎧 It really helps others in the community find the show. This podcast is generated with artificial intelligence and curated by Veeren. If you’d like your publication or product featured on the show, please get in touch. 📩 More info: 🔗 www.veerenchauhan.com 📧 veeren.chauhan@nottingham.ac.uk

  8. May 6

    EPISODE 48: Murder Mode: How a Worm Evolved the Urge to Kill

    Welcome to the next episode of the WOrM Podcast 🪱 Today we're talking about a worm with teeth. And a nervous system that has been rewired — by evolution — to become aggressive. ⸻ 🧬 The central idea Pristionchus pacificus is a predatory nematode. It kills C. elegans larvae. Sometimes for food. Sometimes just to remove a competitor. But how does its brain decide to attack? ⸻ 🔬 What's actually going on? This is not just predation. It is a distinct behavioural state — aggression — driven by a specific neurochemical system. The researchers used machine learning to identify six distinct behavioural states: roaming and dwelling — shared with C. eleganspredatory search, predatory biting, predatory feeding — unique to a predatory contextThe worm doesn't attack randomly. It switches modes. ⸻ ⚡ Two chemicals. Opposite effects. The key twist is this: Octopamine pushes the worm into aggressive, predatory statesTyramine pulls it back into passive, docile statesThey act antagonistically — like a switch. Remove octopamine → the worm stops attacking. Remove tyramine as well → aggression returns. ⸻ 🧠 The receptors tell the story Two octopamine receptors are required: Ppa-ser-3 and Ppa-ser-6. One tyramine receptor mediates the passive state: Ppa-lgc-55. Crucially — these receptors are expressed in sensory neurons at the worm's nose. Specifically, the IL2 neurons. These are the first point of contact between predator and prey. Silence the IL2 neurons → aggression drops. ⸻ 🧠 A rewired circuit In C. elegans, octopamine and tyramine do completely different things — fasting signals, escape responses. In P. pacificus, evolution has repurposed these same molecules to regulate aggression. The neurons producing them are conserved. The function has diverged. This is circuit-level evolutionary innovation. ⸻ 🧠 Ancient and widespread The same octopamine-aggression link was found in Allodiplogaster sudhausi — a distant relative in the Diplogastridae family. So this adaptation is not unique to P. pacificus. It emerged early, in the predatory lineage — and stuck. ⸻ 🌍 The bigger picture This paper shows that: new behaviours can evolve through repurposing of existing neurochemical systemsthe same molecules can serve completely different functions in closely related speciessensory neurons are a key site of neuromodulatory innovationEvolution doesn't always build from scratch. Sometimes it just rewires what's already there. ⸻ 🧠 The take-home message A predatory worm evolved aggression not through new neurons, but through new ways of using old chemistry. Octopamine and tyramine — present across invertebrates — were redeployed to gate an entirely new behavioural state. That is elegant. And slightly terrifying. ⸻ 📄 Paper discussed Eren, G. G.; Böger, L.; Roca, M.; Hiramatsu, F.; Liu, J.; Alvarez, L.; Goetting, D. L.; Cockram, L. A.; Zorn, N.; Han, Z.; Okumura, M.; Scholz, M.; Lightfoot, J. W. (2026)Predatory aggression evolved through adaptations to noradrenergic circuitsNature, Vol 651https://doi.org/10.1038/s41586-025-10009-x If you enjoyed this episode, please like, follow, and subscribe wherever you listen to the WOrM Podcast ⭐🎧 It really helps others in the community find the show. This podcast is generated with artificial intelligence and curated by Veeren. If you'd like your publication or product featured on the show, please get in touch. 📩 More info:🔗 www.veerenchauhan.com📧 veeren.chauhan@nottingham.ac.uk

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About

The Worm Podcast explores the latest research using worms to understand biology. Hosted by Dr Veeren Chauhan (University of Nottingham), each episode takes a recent paper and breaks down what was discovered, how it was done and why it matters. From C. elegans and Pristionchus pacificus to ageing, metabolism, neuroscience, behaviour, host–microbe interactions and analytical tools, the podcast follows new discoveries across biology. This podcast is generated with artificial intelligence and curated by Veeren. www.veerenchauhan.com veeren.chauhan@nottingham.ac.uk

Information

  • Creator
    Dr Veeren Chauhan
  • Years Active
    2025 - 2026
  • Episodes
    55
  • Rating
    Clean
  • Copyright
    © Dr Veeren Chauhan
  • Show Website
    The Worm Podcast

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