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  • EPISODE 46: Turning in Time: Neural Sequences in the Worm Brain
    2026/04/22

    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


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    20 分
  • EPISODE 45: Worms Shape Their World: The Hidden Power of the Microbiome
    2026/04/15

    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


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    19 分
  • EPISODE 44: Fat Talks: How Worms Decide Not to Eat
    2026/04/08

    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


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    20 分
  • EPISODE 43: Drunk Worms: Dopamine, Serotonin, and Behaviour
    2026/04/01

    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:


    1. exposure

    2. withdrawal

    3. 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


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    21 分