EPISODE 50: Fed by Mum, Built by Ribosomes

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

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 genes * three different fluorescent proteins * 10 pooled CRISPR experiments The 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: * germline * gonadal sheath * sperm * specific neurons * glial cells These 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

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. elegans * predatory search, predatory biting, predatory feeding — unique to a predatory context The worm doesn't attack randomly. It switches modes. ⸻ ⚡ Two chemicals. Opposite effects. The key twist is this: * Octopamine pushes the worm into aggressive, predatory states * Tyramine pulls it back into passive, docile states They 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 systems * the same molecules can serve completely different functions in closely related species * sensory neurons are a key site of neuromodulatory innovation Evolution 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 [https://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 [http://www.veerenchauhan.com]📧 veeren.chauhan@nottingham.ac.uk [veeren.chauhan@nottingham.ac.uk]

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

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