WOrM Podcast: Whole Organism Analytics Podcast

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

WOrM Podcast: Whole Organism Analytics Podcast is a science podcast hosted by WOrM | Whole Organism Analytics, with 55 episodes on record and a Required Pod Score of 80. PitchCentric scores this show on Booking Probability, Listen Score, and live audience signals refreshed every 24 hours.

WOrM | Whole Organism Analytics hosts WOrM Podcast: Whole Organism Analytics Podcast, a science show with 55 episodes published.

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  Episode #55

  EPISODE 55: The Worm’s Stress Network

  Aug 18, 202624 minS1

  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

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  Episode #54

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

  Aug 11, 202620 minS1

  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

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  Episode #51

  EPISODE 51: The Worm Behind the Wild

  Jul 21, 202617 minS1

  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

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  Episode #50

  EPISODE 50: Fed by Mum, Built by Ribosomes

  Jul 14, 202620 minS1

  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

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  Episode #49

  EPISODE 49: Glowing up the Worm Proteome

  Jul 8, 202622 minS1

  <p>Welcome to the next episode of the WOrM Podcast 🪱</p><p>Today we’re looking at a paper that doesn’t answer a biological question.</p><p>Instead, it builds the tools to answer thousands of biological questions in the future.</p><p>The ambition?</p><p>To fluorescently tag every protein encoded by the C. elegans genome.  </p><p>⸻</p><p>🧬 The big idea</p><p>We already have remarkable gene expression atlases based on RNA.</p><p>But RNA isn’t the whole story.</p><p>Proteins are the molecules that actually perform the work inside cells, and protein abu...

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