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. 6d ago

    EPISODE 66: Fix the Brain, Save the Worm!

    Welcome to the next episode of The Worm Podcast! 🧠 Can repairing damaged DNA in a worm's neurons protect the rest of its body? Every cell must cope with DNA damage. When repair systems fail, the consequences can include impaired development, loss of tissue function and accelerated ageing. But researchers have now uncovered an unexpected way that one tissue can help another survive. 🧬 Switching DNA repair back on The team studied Caenorhabditis elegans lacking XPA-1, a protein essential for nucleotide excision repair (NER), which removes certain types of DNA damage caused by ultraviolet light. These worms were especially vulnerable to UV exposure. The researchers then restored XPA-1 in selected tissues, including the intestine, muscles and neurons, to see which could improve the animal's resilience. 🔬 The surprising power of neurons Restoring DNA repair in neurons alone substantially improved the worms' resistance to UV-induced damage, even though other tissues still lacked the repair pathway. It helped protect development, movement and adult survival. In many tests, the benefit approached that of restoring repair throughout the organism, although intestinal function was not fully rescued. So how could healthier neurons protect distant tissues? 📡 Acetylcholine carries the message The researchers investigated how neurons communicate with the body. Their experiments pointed to acetylcholine, a neurotransmitter involved in transmitting signals between nerve cells and other tissues. When acetylcholine signalling was disrupted, the protective effect of neuronal DNA repair was lost. This suggests that maintaining neuronal communication is a key part of the whole-organism response to DNA damage. ⚡ Mitochondria connect the dots The study also examined mitochondria, the structures that support cellular energy production. DNA-repair-deficient worms showed reduced mitochondrial activity after UV exposure. Restoring repair in neurons helped preserve mitochondrial membrane potential and respiration across the animal. Disrupting mitochondrial function removed the protection, linking neuronal DNA repair, acetylcholine signalling and energy metabolism. 🧠 Why this matters The findings reveal how genome maintenance in one tissue can influence the health of others. They also offer a possible explanation for why defects in DNA repair can have effects far beyond the cells where damage first occurs. These results come from experiments in C. elegans. Whether similar protective pathways could be harnessed in humans remains an open question. 🪱 The take-home message DNA repair in the nervous system can help the whole worm withstand DNA damage. By maintaining acetylcholine signalling and mitochondrial activity, repaired neurons support tissues that remain unable to repair the same lesions themselves. A small nervous system can have a remarkably large influence on the rest of the body. 📄 Paper discussed Lopes da Silva et al. (2026). Neuronal DNA repair mediates systemic mitochondrial maintenance through acetylcholine signaling. Nucleic Acids Research. DOI: https://doi.org/10.1093/nar/gkag976 If you enjoyed this episode, follow and share The Worm Podcast ⭐ This podcast is generated with artificial intelligence and curated by Veeren. To suggest research for a future episode, please get in touch. www.veerenchauhan.comveeren.chauhan@nottingham.ac.uk

  2. Oct 28

    EPISODE 65: The Incredible Shrinking Worm Cell

    Welcome to the next episode of The Worm Podcast! How does a cell keep dividing accurately when it gets smaller and smaller? During early development, the Caenorhabditis elegans embryo divides repeatedly, generating progressively smaller cells. Each division requires the mitotic spindle to organise and separate chromosomes, even as the space available for this machinery shrinks. 🔬 An embryo under the microscope Researchers investigated divisions from the 2-cell to the 64-cell stage, combining lattice light-sheet microscopy and automated image analysis to track spindles and chromosomes as the embryo developed. As cells became smaller, spindle length decreased. Across these stages, final spindle length fell by approximately 55%. Yet chromosome segregation behaved differently: its speed and extent remained comparatively stable despite the smaller spindles. 🧬 Two processes, different mechanisms The mitotic spindle contains microtubules that help organise chromosomes and drive their separation during cell division. Using femtosecond laser ablation and electron tomography, the team examined the forces involved. Spindle elongation is influenced by microtubules and motor proteins acting at the cell cortex. As cell dimensions decrease, these interactions change, allowing spindle length to scale with cell size. Chromosome segregation is supported by microtubules between the separating chromosomes. These mid-spindle structures help maintain reliable separation even as the overall spindle gets smaller. ⚡ Testing the size rule The researchers also examined embryos with altered cell sizes and used mathematical models to investigate spindle dynamics. The results supported the idea that physical cell dimensions help determine spindle length, while the machinery driving chromosome segregation can remain robust across changing conditions. 🧠 Why it matters Embryonic cells need to distribute their chromosomes accurately at every division. This work helps explain how the machinery of mitosis adapts as an embryo develops, and why different components of the division process respond differently to changes in cell size. 🪱 The take-home message The worm embryo becomes a collection of progressively smaller cells. Its mitotic spindle shrinks in response, but chromosome segregation remains remarkably consistent. Understanding these separate mechanisms gives researchers a clearer picture of how development remains orderly under changing physical constraints. 📄 Paper discussed Cell size reduction distinctly scales spindle elongation and chromosome segregation in C. elegans (2026), Nature Communications.
https://doi.org/10.1038/s41467-026-76360-3 If you enjoyed this episode, follow and share The Worm Podcast ⭐ This podcast is generated with artificial intelligence and curated by Veeren. To suggest a paper for a future episode, get in touch. www.veerenchauhan.com
veeren.chauhan@nottingham.ac.uk

  3. Oct 21

    EPISODE 64: Too Hot, Too Cold, Just Worm

    Welcome to The Worm Podcast! 🌡️ How does a tiny worm know when its surroundings are too hot or too cold? Researchers have discovered that glial cells, usually associated with supporting neurons, can themselves detect temperature and help control how Caenorhabditis elegans responds. 🔥 Glia can detect warmth AMsh glial cells respond to heating through GCY-28, a guanylyl cyclase involved in heat detection. Removing GCY-28 strongly reduces their response to warming, while restoring its expression in these cells brings the response back. ❄️ And they can detect cold The same glia also use GLR-3, a receptor associated with cold sensing. Researchers showed that isolated AMsh glial cells could respond directly to both warming and cooling, demonstrating that their temperature sensitivity does not depend entirely on neighbouring neurons. 🧠 A hub-and-spoke circuit After detecting temperature, AMsh glia release GABA and influence surrounding sensory neurons in different ways. They enhance warm-sensitive AFD signalling through the excitatory GABA receptor EXP-1, while reducing prolonged cold signalling through an inhibitory receptor, LGC-38, associated with the ASH pathway. This arrangement allows one type of glial cell to influence different parts of the sensory network according to the thermal stimulus. 🔬 From cellular signals to behaviour Manipulating AMsh glial signalling changed the worms’ responses to heat and cold, including avoidance behaviour, temperature preference and thermotaxis. The findings suggest that glia participate directly in sensory processing and behavioural regulation, working alongside neurons to interpret environmental conditions. 🧠 The take-home message Worms rely on more than sensory neurons to detect temperature. Their AMsh glia can sense both heating and cooling and adjust the activity of nearby neural circuits. This expands our understanding of the role of glial cells in whole-animal behaviour. 📄 Paper discussed Zhu et al. (2026). A Glial Hub-and-Spoke Circuitry in C. elegans orchestrates bidirectional thermosensation. Nature Communications, 17:1899. DOI: https://doi.org/10.1038/s41467-026-68766-w If you enjoyed this episode, follow and share The Worm Podcast ⭐ This podcast is generated with artificial intelligence and curated by Veeren. To suggest research for a future episode, get in touch. www.veerenchauhan.com
veeren.chauhan@nottingham.ac.uk

  4. Oct 14

    EPISODE 63: The Worm That Beat the Trap

    Welcome to the next episode of The Worm Podcast 🍄 Today we have predators, escape, genetics — and worms that literally rupture in water. The predator is Arthrobotrys oligospora, a carnivorous fungus that builds adhesive networks capable of trapping nematodes. But researchers asked a fascinating question: can a worm evolve its way out of the trap? 🍄 Escaping a fungal predator The team screened around 200,000 C. elegans genomes looking for mutants capable of crossing fungal traps without being captured. Five particularly resistant strains emerged. Wild-type worms were caught almost immediately. The resistant mutants achieved escape rates of around 40%. And remarkably, all five pointed towards the same gene: nhr-66. 🧬 The secret is in the skin NHR-66 is a nuclear hormone receptor expressed in tissues responsible for producing the worm cuticle. When nhr-66 was disrupted, expression of more than 1,200 genes fell dramatically. Among the strongest effects were the cuticular collagens. Around 40% of the worm’s collagen gene family was downregulated. The fungal trap therefore appears to exploit something incredibly fundamental to the worm — the proteins forming its outer surface. Restore those collagens and the worms become easier for the fungus to catch again. The same resistant worms could also escape traps produced by several other Arthrobotrys species. So why hasn't evolution simply produced worms without NHR-66? 💧 Then came the water There is a catch. Put the resistant nhr-66 worms into deionised water and their weakened cuticle becomes a serious liability. Around 60% ruptured within just 10 minutes. Escape the fungus — but become vulnerable to osmotic stress. And when mutant and wild-type worms were placed together in soil, wild-type animals ultimately outcompeted the fungal-resistant mutants. 🧠 Evolution loves a trade-off This is what makes the study particularly interesting. Losing NHR-66 can provide a major advantage when facing a fungal predator. But that advantage comes at the expense of the structural integrity needed to survive other environmental challenges. It is a classic evolutionary compromise: avoid being eaten × maintain a strong body The best defence against one threat may create vulnerability to another. 🧠 The take-home message A worm's cuticle is much more than armour. It is part of a molecular interaction between predator and prey. NHR-66 controls the collagen-rich surface that helps fungal traps grab the worm — but those same collagens help stop the worm from bursting when its environment changes. Sometimes escaping your predator comes at a surprisingly high price. 📄 Paper discussed Han-Wen Chang, Hung-Che Lin, Ching-Ting Yang, Rebecca J. Tay, Dao-Ming Chang, Yi-Chung Tung and Yen-Ping Hsueh (2025) Cuticular collagens mediate cross-kingdom predator–prey interactions between trapping fungi and nematodes PLOS Biology, 23(7): e3003178 DOI: https://doi.org/10.1371/journal.pbio.3003178 If you enjoyed this episode, please follow, like, comment and share The Worm Podcast with someone who might enjoy it ⭐ It really helps us grow the community. If you would like your research discussed in a future episode of The Worm Podcast, please contact Dr Veeren Chauhan. 🔗 www.veerenchauhan.com📧 veeren.chauhan@nottingham.ac.uk

  5. Oct 7

    EPISODE 62: The Worm in a Single Shot

    Welcome to the next episode of The Worm Podcast! What if we could capture an entire 3D view of a living worm in one exposure? And what if advanced microscopy could be made accessible using inexpensive, open-source hardware? This week, we explore two studies that are changing how researchers image Caenorhabditis elegans and other living specimens. ⚡ 3D microscopy in a single shot Conventional volumetric fluorescence microscopy often requires images taken at successive depths. Light-field microscopy instead uses a microlens array to capture different perspectives simultaneously, allowing computational reconstruction of a three-dimensional image from one exposure. The researchers reconstructed whole-worm fluorescence volumes containing 121 axial slices over 109 µm, across three fluorescence channels with a combined exposure time of just 112 milliseconds. 🧬 How a dye enters the worm matters The team studied FM1-43, FM4-64 and Nile Red, comparing probes delivered through labelled bacteria with those supplied directly in liquid. The distribution of fluorescence changed depending on the delivery method. This is a reminder that the route of administration can affect what an image reveals, and how its biological meaning should be interpreted. 🌌 Meet COSMIC The second study introduces COSMIC, the Compact Open-Source Multimodal Illumination Cluster. Using LEDs, 3D-printed parts and open-source electronics, it brings several microscopy methods together for approximately £100 in materials. Its modes include bright-field, dark-field and fluorescence imaging, differential phase contrast and quantitative phase imaging. 🔍 Seeing biology without fluorescent labels Quantitative phase imaging measures optical phase changes in transparent samples, providing information about cellular structure without fluorescent staining. The researchers demonstrated COSMIC with living cell systems and whole worms. Its modular design makes advanced illumination methods more accessible to laboratories and educators. 🧠 The take-home message Light-field microscopy makes rapid 3D fluorescence imaging possible, while COSMIC makes multimodal and quantitative imaging more affordable. Both illustrate how optical engineering and computation can expand the ways we investigate living organisms. 📄 Papers discussed Single-shot light-field microscopy captures delivery-dependent dye and autofluorescence patterns in Caenorhabditis elegans (2026), bioRxiv.
https://doi.org/10.64898/2026.09.07.749827 Multimodal illumination for quantitative transmitted-light microscopy (2026), Journal of Microscopy.
https://doi.org/10.1111/jmi.70156 If you enjoyed this episode, follow and share The Worm Podcast ⭐ This podcast is generated with artificial intelligence and curated by Veeren. To suggest a paper for a future episode, get in touch. www.veerenchauhan.com
veeren.chauhan@nottingham.ac.uk

  6. Sep 30

    EPISODE 61: Wormspy: Watching the Worm Brain Move

    Welcome to the next episode of The Worm Podcast 🔬 Today we are looking at a new imaging system called Wormspy. The problem it tackles is a familiar one in neuroscience: how do you record what neurons are doing without stopping the animal from behaving normally? Many high-resolution imaging systems restrain the worm, compress it, or use complex microscope setups that can alter behaviour. Wormspy takes a different approach. It is a low-cost, open-source epifluorescence microscope designed to track freely moving C. elegans while recording fluorescence and behaviour at the same time. 🤖 How Wormspy works The system uses two cameras and a motorised XYZ platform. One channel records fluorescence, while the other tracks the worm and its behaviour. Instead of moving the animal, Wormspy moves the microscope around a fixed behavioural arena to keep the worm centred and in focus. The software supports manual tracking, threshold-based automatic tracking and DeepLabCut integration, with automatic focus correction during recording. 🧠 Watching neurons during real behaviour The authors demonstrated Wormspy across several different experiments. They recorded body-wall muscle calcium activity during locomotion and reproduced the known deeper body bends of gar-3 mutants. They then imaged the ASH sensory neuron as worms encountered an aversive glycerol barrier. ASH activity rose as the worms entered the barrier and peaked around the start of the reversal response. 🍽️ Neurons at the edge of food The system was also used to image the food-sensing AWC neuron while worms moved around a bacterial lawn. As the worm’s nose left the food patch, AWC activity increased. That is exactly the sort of experiment that becomes difficult when the animal is restrained. Wormspy lets researchers connect neuronal activity directly to where the worm is and what it is doing. 🔬 Imaging inside a neuron Perhaps the most impressive demonstration was in the RIA interneuron. Wormspy could resolve calcium events in separate regions of the RIA axon while the worm moved freely. Those local calcium signals tracked dorsal and ventral head movements. Interestingly, the timing differed slightly from previous measurements in restrained animals, suggesting that the imaging setup itself can influence the behaviour being measured. 🛠️ Why this matters Wormspy is: open-source × modular × relatively low-cost × behaviour-friendly It can also be adapted for different fluorophores, optogenetic stimulation and other small organisms. The aim is not simply to make microscopy cheaper. It is to make high-resolution neural imaging more accessible while preserving the natural behaviour that researchers actually want to understand. 🧠 The take-home message If you want to understand the relationship between a neuron and a behaviour, ideally you should watch both at the same time. Wormspy makes that possible without forcing the worm to stay still. Sometimes the best way to understand the worm brain is simply to let the worm move. 📄 Paper discussed Sebastian N. Wittekindt, Hannah Owens, Aurélie Guisnet, Lennard Wittekindt and Michael Hendricks (2026) An epifluorescence microscope design for naturalistic behavior and cellular activity in freely moving Caenorhabditis elegans Nature Communications, 17:4411 DOI: https://doi.org/10.1038/s41467-026-72709-w 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

  7. Sep 23

    EPISODE 60: Why Worms Switch Their Immune System Off

    Welcome to The Worm Podcast! 🧠 Why would a worm deliberately suppress its own immune system? This episode explores a study showing how an endogenous small-RNA pathway restrains antibacterial innate immunity in Caenorhabditis elegans. The central players are TCER-1, a factor involved in transcription and RNA processing, and WAGO-associated 22G-RNAs. 🧬 A molecular brake on immunity Small interfering RNAs help regulate gene expression and are well known for their roles in genome defence. This study identifies a TCER-1–siRNA regulatory pathway that also keeps antibacterial responses under control. When tcer-1 was disrupted, worms became more resistant to infection by Pseudomonas aeruginosa PA14. Mutations affecting the WAGO 22G-RNA pathway produced similar effects. 🔬 Selective control of immune genes The researchers found that this pathway regulates a restricted group of immune-relevant genes rather than silencing the entire transcriptome. One important target is scrm-4, which encodes a phospholipid scramblase. SCRM-4 contributes to immune activation, and the TCER-1–22G-RNA system helps repress its expression. ⚖️ Why restrain host defence? Immune responses consume resources and must be regulated. A continuously activated defence programme can be costly, even when it protects against infection. This work shows how small RNAs can tune the strength of antibacterial immunity, providing another layer of control over the worm’s response to its environment. 🧠 The take-home message In C. elegans, the TCER-1–siRNA axis helps suppress antibacterial innate immunity. Removing that restraint can improve resistance to bacterial infection, revealing an unexpected immune-regulatory role for endogenous small RNAs. 📄 Paper discussed Naim et al. (2026). A TCER-1-siRNA regulatory axis suppresses antibacterial innate immunity in C. elegans. PLOS Pathogens, 22(7):e1013972. DOI: https://doi.org/10.1371/journal.ppat.1013972 If you enjoyed this episode, follow and share The Worm Podcast ⭐ This podcast is generated with artificial intelligence and curated by Veeren. To suggest research for a future episode, get in touch. www.veerenchauhan.com
veeren.chauhan@nottingham.ac.uk

  8. Sep 16

    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

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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
    66
  • Rating
    Clean
  • Copyright
    © Dr Veeren Chauhan
  • Show Website
    The Worm Podcast