The Worm Podcast

Dr Veeren Chauhan
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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. 1d ago

    EPISODE 59: Food or Sex? The Worm Has to Choose

    Welcome to the next episode of The Worm Podcast 🧠 Today we are talking about a problem every animal faces: where should I spend my energy? For C. elegans, the answer depends partly on sex. Hermaphrodites need to balance food, reproduction and survival. Males have an extra problem: they also need to find a mate. This new study identifies SKN-1B, a neuronal version of the conserved Nrf transcription factor, as part of the switch that helps control those competing priorities. 🍽️ Food or mate? SKN-1B is expressed in sensory neurons involved in food sensing and metabolism. In hermaphrodites, SKN-1B promotes food-seeking behaviour. But males behave differently. Male skn-1b mutants left food faster when no mate was present, suggesting increased mate-searching behaviour. Give them a hermaphrodite, or even just hermaphrodite pheromones, and they stayed. So the worms were not simply more active. They were changing what they prioritised. 🧬 The effect lasts into older age The difference became even more interesting as the worms aged. Wild-type male exploration declined with age. But skn-1b mutant males maintained exploratory behaviour and were more likely to retain mating ability at day 5 of adulthood. The authors therefore suggest that SKN-1B normally acts to suppress male mate-searching behaviour, including later in life. 🧠 A sex-specific molecular switch The transcriptomic effects were striking. Loss of skn-1b changed only hundreds of genes in hermaphrodites, but thousands in males. The paper also found sex-specific effects on mitochondrial organisation and function. So the same neuronal transcription factor can produce very different whole-animal outcomes depending on whether the worm is male or hermaphrodite. 🔬 The signalling pathway The authors traced part of the behavioural effect through a neuroendocrine pathway involving: • DAF-7 TGF-β signalling• insulin signalling• ODR-10, an olfactory receptor involved in food sensing In skn-1b mutant males, DAF-7 increased while odr-10 expression fell. Reducing ODR-10 in wild-type males also increased exploration and food-leaving behaviour. That links SKN-1B directly to the neural machinery balancing feeding and mating. 🧠 The take-home message This is not simply a story about male worms being more interested in mating than food. It is about how the nervous system decides where energy should go. SKN-1B acts as a sex-specific behavioural and metabolic switch, helping balance: food × energy × reproduction × ageing And in males, removing that switch seems to keep mate-searching behaviour going for longer. 📄 Paper discussed Noviann McLean, Minaxi S. Gami, Nathan Dennis, Yasir Malik, Justin De Araujo, James Evans, Lydia Bennett, Marina Ezcurra and Jennifer M. A. Tullet (2026) Neuronal Nrf/SKN-1B controls a sexually dimorphic neuroendocrine pathway for C. elegans exploratory behaviour PLOS Genetics, 22(8): e1012239 DOI: https://doi.org/10.1371/journal.pgen.1012239 If you enjoyed this episode, please like, follow and subscribe 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. Sep 9

    EPISODE 58: The Diet That Gave a Worm Its Copper Back

    Welcome to the next episode of The Worm Podcast 🧠 Today we are looking at copper, bacteria and a surprising dietary rescue. Copper is an essential micronutrient. Cells need it for mitochondrial energy production, antioxidant defence and many other processes. In humans, mutations in the copper transporter CTR1 can cause severe copper deficiency and developmental problems. Now researchers have created a C. elegans model of this disorder — and discovered that simply changing what the worms eat can dramatically rescue the phenotype. 🧬 Meet CHCA-1 C. elegans has its own version of CTR1 called CHCA-1. When chca-1 mutant worms were fed the commonly used laboratory bacterium HT115, they became copper deficient and showed a severe developmental delay. Their ATP levels also fell, consistent with copper deficiency disrupting mitochondrial energy production. Adding copper directly rescued the worms. So far, so straightforward. But then came the surprise. 🍽️ Change the bacteria, change the worm When exactly the same mutant worms were fed OP50 instead of HT115, they developed much more normally. Was OP50 simply providing more copper? No. The two bacterial diets contained similar amounts of copper. Something about the composition of the bacterial diet was helping the worm absorb and use copper more effectively. Even adding just 1% OP50 to HT115 produced a substantial rescue. 🧪 Finding the ingredient The researchers compared metabolites enriched in OP50-like bacteria. One stood out: glutathione disulphide — GSSG. Adding GSSG to HT115 increased copper levels inside the mutant worms and partially rescued their developmental defects. It also improved pumping, movement and brood size. Importantly, GSSG did not simply increase the copper content of the bacteria. It appeared to help the worm obtain copper despite its defective primary transporter. 🧬 A human mutation in a worm The researchers then recreated a mutation corresponding to one found in a human patient with CTR1-associated copper deficiency. The engineered worms developed the same copper-deficiency phenotype. Wild-type human CTR1 could rescue chca-1 mutant worms, whereas the patient-associated CTR1 variant could not. And once again, OP50, 1% OP50 supplementation or GSSG improved the phenotype. This makes the worm a potentially useful model for studying a rare human copper-transport disorder. 🔬 How does the diet rescue the defect? RNA sequencing showed that OP50 and GSSG shifted the mutant transcriptome back towards the wild-type state. They also increased expression of several CTR1-like copper transporters. So when the main copper-import pathway is damaged, diet appears able to activate alternative routes that partially compensate. 🧠 The take-home message This paper shows just how important the bacterial diet can be in C. elegans experiments. Two standard laboratory foods — HT115 and OP50 — produce dramatically different outcomes in the same genetic mutant. More importantly, it suggests something broader: genetics does not act alone. Diet and microbial metabolism can expose a disease phenotype, suppress it, and even activate alternative biological pathways that compensate for a genetic defect. Sometimes changing the worm’s food changes everything. 📄 Paper discussed Yang Fu, Xu Bai, Lei Chun, X. Z. Shawn Xu and Jianfeng Liu (2026) A C. elegans model of copper deficiency: Dietary interventions rescue CTR1/CHCA-1 copper transporter mutant phenotype PLOS Genetics, 22(1): e1012013 DOI: https://doi.org/10.1371/journal.pgen.1012013 If you enjoyed this episode, please like, follow and subscribe 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. Sep 2

    EPISODE 57: AI Watches Worms Eat

    Welcome to the next episode of The Worm Podcast 🤖 Today we are talking about feeding. More specifically, how do you measure a worm eating when the worm refuses to stay still? The answer might be PumpKin — a new machine-learning pipeline that automatically measures pharyngeal pumping in freely moving C. elegans. 🍽️ Watching the grinder When C. elegans feeds, its pharynx pumps rapidly and a tiny structure called the grinder moves back and forth. That movement gives us a direct measure of feeding rate. The problem? The grinder is less than 30 µm wide, can move around five times per second, and is attached to a worm that is also moving. Traditionally, researchers often count pumps manually, which is slow and can vary between people. Other automated methods may require immobilising the worm, specialised equipment or fluorescent reporters — all of which risk changing the behaviour being measured. 🤖 Enter PumpKin PumpKin takes a different approach. It uses machine learning to find the pharynx and grinder in ordinary brightfield videos while the worm moves freely. The pipeline combines: • Faster R-CNN object detection• motion compensation• optical flow• noise filtering• automated pump detection First it follows the pharyngeal bulb. Then it zooms in on the grinder. Finally, it separates genuine grinder movement from movement of the worm or the plate. 🍽️ Does it actually work? The researchers tested PumpKin across eight experimental conditions involving: • wild-type N2 worms• eat-2 feeding mutants• fed and starved animals• worms recorded on and off food PumpKin's estimates closely matched those of experienced human observers. For instantaneous pumping dynamics, its agreement with the human consensus was actually greater, on average, than the agreement between individual human annotators. 🧠 And it revealed some biology Wild-type worms on food pumped at around 4.7 pumps per second, while eat-2 mutants were much slower at around 1.4 pumps per second. Take the food away and something interesting happens. Across genotype and previous satiety state, worms settled around a common basal pumping rate of approximately 0.5 pumps per second. PumpKin also revealed that feeding is not simply a constant rate. Worms move through bursts and pauses, and those dynamics change depending on food availability and genotype. 🔬 Why this matters PumpKin is: automated × non-invasive × freely moving × label-free That means researchers can measure feeding without fixing the worm in place or genetically modifying it. And because PumpKin focuses on the movement of a very small body structure inside a moving animal, the approach could potentially be adapted to other behaviours and other organisms. 🧠 The take-home message Sometimes the interesting behaviour is not the worm moving across the plate. It is one tiny structure moving inside the worm. PumpKin gives us a way to watch that behaviour automatically — and lets AI count the pumps so we don't have to. 📄 Paper discussed Erin Shappell, Debra Buggs, Jennah Walcott and Hang Lu (2026) PumpKin: A machine-learning pipeline for automatically tracking localized kinematics in freely moving C. elegans PLOS Computational Biology, 22(7): e1014489 DOI: https://doi.org/10.1371/journal.pcbi.1014489 If you enjoyed this episode, please like, follow and subscribe 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

  4. Aug 26

    EPISODE 56: A Little Heat Makes a Stronger Worm

    Welcome to the next episode of The Worm Podcast 🔥 Can a little bit of stress actually make you stronger? In C. elegans, the answer appears to be yes. This episode explores heat hormesis — the idea that a short exposure to mild heat can prepare an animal to cope better with a much harsher challenge later. Researchers exposed young adult worms to 30 °C for six hours, allowed them to recover, and then subjected them to a stronger heat shock. The primed worms were considerably more resistant. 🔥 The worm remembers Immediately after mild heat exposure, thousands of changes appeared across gene expression and chromatin accessibility. But after 12 hours of recovery, most of those changes had returned towards normal. So had the worms forgotten? Not quite. When the worms encountered a second, stronger heat stress, previously primed animals responded differently from worms experiencing heat for the first time. The initial stress had left a molecular memory. 🧬 Looking beyond gene expression The researchers combined RNA-seq and ATAC-seq to follow both gene expression and chromatin accessibility throughout the entire process. This revealed that mild heat and severe heat do not simply trigger stronger and weaker versions of the same response. They produce distinct molecular programmes. And the previous experience of heat changes how the worm responds the next time. 🧠 New regulators of heat hormesis The study also identified several conserved regulators involved in the protective response, including: • HSF-1• FOS-1• SNPC-4• MARS-1• ELT-2• DPY-27 These connect heat hormesis to transcription, chromatin organisation, piRNA biology and protein synthesis. ⏳ And the worms lived longer Mild heat exposure also extended lifespan in wild-type worms. One particularly interesting clue came from the germline. Heat priming temporarily disrupted reproductive activity, reduced brood size and preserved the ability to induce heat-shock proteins later in adulthood. However, the same treatment did not further extend lifespan in germline-less glp-1 mutants. This suggests that temporarily shifting resources away from reproduction may contribute to the longer-term benefits of heat hormesis. 🧠 The take-home message A short period of mild stress can leave a lasting biological memory. The worm may look completely recovered, but when the next challenge arrives, its molecular response has changed. Sometimes a little stress really can make a worm stronger. 📄 Paper discussed Hsin-Yun Chang, Sarah E. McMurry, Sicheng Ma, Charles L. Heinke, Christian A. Mansour, Sophia Marie T. Schwab, Charles G. Danko and Siu Sylvia Lee (2026) Transcriptomic and chromatin accessibility profiling unveils new regulators of heat hormesis in Caenorhabditis elegans PLOS Biology, 24(2): e3003639 DOI: https://doi.org/10.1371/journal.pbio.3003639 If you enjoyed this episode, please like, follow and subscribe 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

  5. Aug 19

    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

  6. 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

  7. 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

  8. 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

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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
    59
  • Rating
    Clean
  • Copyright
    © Dr Veeren Chauhan
  • Show Website
    The Worm Podcast

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