WOrM Podcast: Whole Organism Analytics Podcast

WOrM | Whole Organism Analytics
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Join Dr Veeren Chauhan (University of Nottingham) as he explores whole-organism analytics, revealing how life adapts, interacts, and evolves. From nematodes to next-generation analytical tools, expect deep dives into cutting-edge research, expert insights and the discoveries shaping biology, medicine, and ecology. This podcast is generated with artificial intelligence and curated by Veeren. If you’d like your publication featured on the show, please get in touch. 📩 More info: 🔗 www.veerenchauhan.com 📧 veeren.chauhan@nottingham.ac.uk

  1. 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

    14 min

  2. Apr 29

    EPISODE 47: When Bacteria Fight Back: Bioplastic Kills the Worm

    Welcome to the next episode of the WOrM Podcast 🪱 Today we’re talking about something unexpected. A bioplastic — something we usually think of as sustainable, useful, even beneficial — can kill a worm. ⸻ 🧬 The central idea Some bacteria produce a polymer called polyhydroxybutyrate (PHB). It’s a carbon storage material. A bioplastic. But when C. elegans eats bacteria packed with PHB — it dies.  ⸻ 🔬 What’s actually going on? This is not classic toxicity. It’s not a signalling pathway. It’s physical and systemic failure. PHB accumulates inside the bacteria, and when ingested: • the pharynx becomes deformed • the intestine distends • the gut barrier breaks down • the defecation programme fails  The worm can’t process what it’s eating. It gets blocked. ⸻ ⚡ Metabolism drives the effect The key twist is this: PHB is only produced under certain metabolic conditions — when bacteria have excess carbon (like lactate or pyruvate).  So the same bacteria can be: • harmless • or lethal depending on what they’re fed. This is not just host–pathogen. It’s host–microbe–metabolism. ⸻ 🧠 Cause and effect, proven cleanly They show this properly: • knock out PHB production → worms survive • engineer E. coli to make PHB → worms die So PHB is not correlated. It is sufficient to kill.  ⸻ 🧠 The mechanism is mechanical Inside the worm: • PHB granules accumulate • the gut becomes physically obstructed • calcium waves that drive defecation become irregular or stop • the system collapses This is behaviour and physiology breaking down from the inside. ⸻ 🧠 A partial rescue — and a clue Mutations in nuc-1 rescue about half the animals.  This gene normally helps digest bacterial DNA. Without it: • worms process PHB-containing food differently • less blockage occurs • survival improves So digestion itself is part of the failure mode. ⸻ 🌍 The bigger picture This matters because: • many bacteria in natural worm environments can produce PHB • PHB production depends on nutrient context • host survival depends on bacterial metabolism, not just species So ecology is not static. It’s state-dependent chemistry interacting with biology. ⸻ 🧠 The take-home message This is not about a toxin. It’s about material inside bacteria becoming lethal through ingestion. And more broadly: what microbes make — and when they make it — can reshape host physiology completely. ⸻ 📄 Paper discussed Giese, G. E.; Richards, D. M.; Florman, J. T.; Starbard, A. N.; Xu, A. A.; Durning, D. J.; Alkema, M. J.; Walhout, A. J. M. (2026) Bacteria producing the bioplastic polyhydroxybutyrate kill the nematode Caenorhabditis elegans PLOS Biology https://doi.org/10.1371/journal.pbio.3003748 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

    22 min

  3. Apr 22

    EPISODE 46: Turning in Time: Neural Sequences in the Worm Brain

    Welcome to the next episode of the WOrM Podcast 🪱 Today we’re looking at something deceptively simple: a turn. But not just that a worm turns — how the brain decides to do it. ⸻ 🧬 The central idea Turning in C. elegans is not a reflex. It’s a sequence. A structured, repeatable pattern of neural activity that links: • sensation • decision • and movement into a single behavioural output. ⸻ 🔬 What’s really happening? Using whole-brain calcium imaging, this study captures activity across the nervous system during olfactory navigation. What emerges is clear: • turns act as error-correction events • they occur when the worm deviates from its path • and they are executed through ordered neural sequences Each turn is not random. It is built. ⸻ ⚡ A sequence, not a signal During a turn: • specific neurons activate • in a stereotyped order • across time Some neurons respond to sensory cues. Others anticipate the direction of the upcoming turn. This is not reaction. It is prediction unfolding in time. ⸻ 🧠 The role of modulation A key player here is tyramine. It helps coordinate these neural sequences — linking circuit structure to dynamic control of behaviour. So the system is not just wired. It is tuned. ⸻ 🧠 The take-home message Behaviour is not the output of single neurons. It is the product of time-ordered neural activity. In this case: sensory input → neural sequence → predicted action And the shift is important: To understand behaviour, we need to think in time, not just space. ⸻ 📄 Paper discussed Kramer, T. S.; Wan, F. K.; Pugliese, S. M.; Atanas, A. A.; Pradhan, S.; Hiser, A. W.; Godinez, L. M.; Luo, J.; Bueno, E.; Felt, T.; Flavell, S. W. (2026) Neural sequences underlying directed turning in Caenorhabditis elegans Nature https://doi.org/10.1038/s41593-026-02257-5 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 featured on the show, please get in touch. 📩 More info: 🔗 www.veerenchauhan.com 📧 veeren.chauhan@nottingham.ac.uk

    20 min

  4. Apr 15

    EPISODE 45: Worms Shape Their World: The Hidden Power of the Microbiome

    Welcome to the next episode of the WOrM Podcast 🪱 Today we flip the usual perspective. We often think about how the environment shapes the worm. But what if the worm is shaping the environment? ⸻ 🧬 The central idea C. elegans doesn’t just respond to microbes — it actively reshapes microbial communities. Across a naturalistic “boom-to-bust” lifecycle, worm populations: • expand rapidly • consume and interact with bacteria • then collapse into dauer And through that process, they leave a lasting imprint on their surroundings.  ⸻ 🌱 What happens to the environment? Even without worms, microbial communities change over time. But with worms present, something different happens: • microbial communities follow distinct trajectories • initially different environments begin to converge • specific bacterial families are consistently depleted or enriched In other words, worms don’t just graze — they engineer microbial ecosystems. ⸻ 🦠 The microbiome connection The key link is the worm’s own gut microbiome. Bacterial families that: • thrive inside the worm • are selected during feeding are the same ones that become enriched in the environment. While others — like Pseudomonadaceae — are depleted over time.  So the worm is not just consuming bacteria. It is: • selecting • amplifying • and redistributing microbial populations ⸻ ⚡ A bidirectional system This is the important shift. We move from: environment → worm to: environment ↔ worm A feedback loop where: • microbes shape the worm • worms reshape microbes • and the ecosystem evolves as a result ⸻ 🧠 The take-home message C. elegans is not just a model organism. It’s an ecosystem engineer. And this matters, because nematodes are one of the most abundant life forms on Earth. So small-scale interactions — feeding, microbiome assembly, population cycles — may scale up to influence: • nutrient cycling • microbial diversity • and ecosystem function ⸻ 📄 Paper discussed Bodkhe, R.; Sankaran, K.; Shapira, M. (2026) Caenorhabditis elegans populations shape their microbial environment npj Biofilms and Microbiomes DOI: 10.1038/s41522-026-00975-z  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

    19 min

  5. Apr 8

    EPISODE 44: Fat Talks: How Worms Decide Not to Eat

    Welcome to the next episode of the WOrM Podcast 🪱 Today we’re talking about something fundamental — feeding behaviour — but through a lens you might not expect. Not calories. Not food availability. But fat composition. ⸻ 🧬 The central idea In C. elegans, feeding isn’t just about energy — it’s about lipid balance. Specifically, the ratio of: • saturated fatty acids (SFAs) • and monounsaturated fatty acids (MUFAs) And this balance determines whether worms: • stay on food • leave food • or actively ignore it ⸻ 🔬 What’s really being sensed? This isn’t happening at the surface. It’s happening at the endoplasmic reticulum (ER) — where lipid composition alters membrane properties and activates the stress sensor IRE-1. That signal is then translated into behaviour through: • neuronal serotonin • AMPK signalling • and a neuropeptide system ⸻ ⚡ A new behavioural state: “food apathy” One of the most interesting outcomes in this study is a state the authors call food apathy. Worms: • leave concentrated food • roam even when food is present • and reduce overall intake This is not starvation. It’s not avoidance of toxins. It’s a metabolically driven behavioural shift. ⸻ 🧠 The big connection: GLP-1-like signalling Here’s where it gets very interesting. The pathway that drives this behaviour — PDF-1 / PDFR-1 — shows structural and functional similarity to: • GLP-1 • GIP • glucagon-related signalling In other words, the same systems now targeted by weight-loss drugs may have deep evolutionary roots in simple organisms like worms. Even more striking — a peptide derived from this worm pathway shows: • reduced food intake • improved insulin sensitivity in mice. ⸻ 🧠 The take-home message Feeding behaviour is not just about hunger. It’s about how metabolism is sensed and interpreted. In this case: lipids → ER stress → neuronal signalling → behaviour And the implication is big: Some of the most important metabolic signalling systems in humans may have started as basic lipid-sensing circuits in simple organisms. ⸻ 📄 Paper discussed Zhu, F.; Castillo-Quan, J. I.; Ogawa, T.; Wu, Z.; Ding, L.; Sura, M.; Watanabe, Y.; Lentsch, H.; Fernández-Cárdenas, L. P.; Dag, U.; Beck-Sickinger, A.; Wang, M. C.; Kahn, C. R.; Blackwell, T. K. (2026) Fatty acid regulation of feeding in Caenorhabditis elegans reveals the potential ancestral origin of a GLP-1-like multiagonist signaling system Proceedings of the National Academy of Sciences (PNAS) DOI: 10.1073/pnas.2530979123  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 featured on the show, please get in touch. 📩 More info: 🔗 www.veerenchauhan.com 📧 veeren.chauhan@nottingham.ac.uk

    20 min

  6. Apr 1

    EPISODE 43: Drunk Worms: Dopamine, Serotonin, and Behaviour

    Welcome to the next episode of the WOrM Podcast 🪱 Today we’re looking at something surprisingly familiar in worm biology: alcohol. But not just exposure — we’re talking about behaviour, tolerance, withdrawal, and how core neurotransmitter systems shape all of it. ⸻ 🧬 The central question What actually happens when a worm is exposed to ethanol? Not just in terms of movement — but across: • behaviour • lifespan • neuronal signalling • and gene expression This study takes a multi-layered approach to understand how alcohol reshapes the worm. ⸻ 🔬 What they did Worms were exposed to ethanol for 24 hours, followed by a withdrawal phase, and then tested in a behavioural assay — the classic diacetyl race. This creates a simple but powerful 3-step model: exposure withdrawal re-exposure A framework that starts to look a lot like tolerance biology. ⸻ 🧠 What they found The response to ethanol isn’t uniform — it depends on the nervous system. • Wild-type worms show reduced lifespan at higher ethanol doses • Dopamine (dop-3) and serotonin (tph-1) mutants respond differently • Behaviour during chemotaxis is altered — not just slower, but less coordinated • Re-exposure can rescue or worsen behaviour, depending on genotype This is not just toxicity. It’s state-dependent behaviour. ⸻ ⚡ Neurons are doing the work At the cellular level, ethanol increases vesicle exocytosis in both dopaminergic and serotonergic neurons. So the system is not shutting down — it’s being actively rewired. And importantly, intact dopamine and serotonin signalling are required for normal responses to ethanol. ⸻ 🧪 The molecular layer Ethanol exposure also shifts gene expression: • Stress response genes like gst-4 and sod-3 are altered • Metabolic genes like adh-1 are downregulated • The response differs depending on dopamine and serotonin function So behaviour, neurons, and metabolism are all coupled. ⸻ 🧠 The take-home message Ethanol in C. elegans is not just a stressor. It’s a probe. A way to reveal how: • neurotransmitters • behaviour • and metabolism interact at the whole-organism level. And the key point? You don’t get the phenotype without the network. ⸻ 📄 Paper discussed Rubio-Tomás, T.; Hunn, C. A.; Hajdú, G.; Sőti, C.; Tavernarakis, N.; Barta, C. (2026) Specific genes of the dopaminergic (dop-3) and serotonergic (tph-1) pathways contribute to the effects of ethanol consumption in Caenorhabditis elegans PLOS One, 21(3): e0344966 DOI: 10.1371/journal.pone.0344966  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 featured on the show, please get in touch. 📩 More info: 🔗 www.veerenchauhan.com 📧 veeren.chauhan@nottingham.ac.uk

    21 min

  7. Mar 11

    EPISODE 42: Sand, Soil, and Screen: The Rise of the Giant Worm

    Welcome to the next episode of the WOrM Podcast 🪱🎬 Today we’re stepping slightly outside the lab… but not too far. We’re asking a serious question with absolutely no serious consequences: If there were an Oscar for Best Giant Movie Worm, who would win? ⸻ 🪱 From soil to cinema Worms in biology are elegant, transparent, genetically tractable. Worms in film? They’re enormous. They’re apocalyptic. They swallow cities. From desert-dwelling leviathans to subterranean monsters shaking small towns apart, giant worms have carved out a strange and persistent niche in popular culture. ⸻ 🎥 Why are we obsessed with giant worms? There’s something primal about them. No eyes. No clear front or back. Emerging from below. They represent unpredictability — something ancient and unstoppable. But what’s interesting is how different films use them. Sometimes they’re villains. Sometimes ecological forces. Sometimes metaphors for nature pushing back. ⸻ 🧠 The worm perspective Here’s the twist. Real worms are foundational to ecosystems. They aerate soil, regulate microbes, recycle nutrients. They are engineers of the environment. Cinema flips that script and scales them up into existential threats. It’s fascinating how the same body plan — elongated, segmented, simple — can be interpreted as either ecological hero or planetary horror. ⸻ 🏆 So who wins? This episode walks through the contenders, looks at design, biological plausibility (yes, we go there), cultural impact, and sheer screen presence. Because if we’re going to award an Oscar for Best Giant Movie Worm… We need criteria. ⸻ 🪱 The take-home message Even in fiction, worms capture something fundamental. They tap into scale, fear, ecology, and the unknown. And maybe that’s why, whether under a microscope or under a desert planet, worms continue to fascinate us. ⸻ 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 featured on the show, please get in touch. 📩 More info: 🔗 www.veerenchauhan.com 📧 veeren.chauhan@nottingham.ac.uk

    14 min

  8. Mar 4

    EPISODE 41: Stress, Signal, Survive: Rethinking Longevity Pathways in C. elegans

    Welcome to the next episode of the WOrM Podcast 🪱 Today we return to a core question in worm biology: when stress extends lifespan, what is really doing the work? Is it damage repair? Is it signalling rewiring? Or is it something more coordinated at the whole-organism level? In this episode we explore new insights into how longevity pathways intersect with stress signalling in C. elegans, and what this means for how we interpret lifespan extension. ⸻ 🧬 The central idea Many longevity paradigms begin with a perturbation — mitochondrial disruption, metabolic alteration, environmental stress — and end with a longer-lived worm. But the key question is not whether lifespan increases. It’s why. This paper dissects the signalling architecture behind stress-induced longevity and challenges overly simple models where one pathway equals one outcome. ⸻ 🔬 What’s happening under the hood? Rather than acting in isolation, canonical longevity regulators intersect with stress-activated signalling networks. We see coordination between: • stress response transcription factors • metabolic regulators • immune signalling components • and tissue-specific effects The result is not just stress resistance — but systemic adaptation. ⸻ 🧠 Why this matters In worm biology, lifespan extension is often treated as the final readout. But lifespan is an emergent property. It reflects how well the organism integrates: • damage sensing • metabolic state • immune tone • and signalling fidelity This episode steps back and asks whether we should think less about single “longevity genes” and more about network behaviour across the whole animal. ⸻ 🪱 The worm lesson C. elegans continues to show us that longevity is rarely about silencing stress. It’s about interpreting it correctly. Stress is not always damage. Sometimes it’s information. ⸻ 📄 Paper discussed TJ O’Brien, EP Navarro, C Barroso, L Menzies, E Martinez-Perez, D Carling, AEX Brown High-throughput behavioural phenotyping of 25 C. elegans disease models including patient-specific mutations BMC Biology 23:281 ⸻ 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 featured on the show, please get in touch. 📩 More info: 🔗 www.veerenchauhan.com 📧 veeren.chauhan@nottingham.ac.uk

    11 min
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About

Join Dr Veeren Chauhan (University of Nottingham) as he explores whole-organism analytics, revealing how life adapts, interacts, and evolves. From nematodes to next-generation analytical tools, expect deep dives into cutting-edge research, expert insights and the discoveries shaping biology, medicine, and ecology. This podcast is generated with artificial intelligence and curated by Veeren. If you’d like your publication featured on the show, please get in touch. 📩 More info: 🔗 www.veerenchauhan.com 📧 veeren.chauhan@nottingham.ac.uk

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