The Worm Podcast

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

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Welcome to the next episode of The Worm Podcast 🔬

What if you could press pause on an animal’s life — and then press play again later?

That is essentially what researchers have found in C. elegans.

Simply crowding worms together in an isosmotic liquid can push them into a profound but reversible state of suspended animation. Development stops. Visible movement stops. Metabolism changes.

And when conditions improve, the worms wake up.

🧠 Meet LISA

The researchers call the phenomenon LISA — Liquid-Induced Suspended Animation.

Worms placed at high population density in static M9 buffer rapidly entered this state, while animals kept at lower density or continuously dispersed continued developing.

Remarkably, LISA could be induced across larval stages and even in adults.

It was not simply starvation, dauer, heat shock or hypoxia. Adding food did not prevent it, and several familiar stress pathways were not required for entry.

Something about being crowded together in the right liquid environment appears to tell the animal: stop.

🔬 What happens when a worm pauses?

The worms are not simply doing nothing.

RNA sequencing, metabolomics and live imaging showed extensive biological reprogramming.

Mitochondria changed shape and showed signs of reduced activity. Energy and redox metabolism shifted. Lysosomes became highly remodelled, and disrupting key autophagy–lysosomal genes reduced survival during the suspended state.

So LISA looks less like biological failure and more like an actively regulated survival programme.

🧠 How does the worm wake up?

Perhaps the most interesting part comes when the animals are returned to normal conditions.

Their nervous system helps control the restart.

AFD sensory neurons and AIY interneurons promote awakening, while the sleep-associated RIS neuron acts in the opposite direction.

PDF neuropeptide signalling and cAMP/PKA pathways then help drive behavioural recovery.

And when the researchers artificially increased cAMP — including using optogenetic stimulation — the worms woke up faster.

The return to activity is therefore not simply metabolism drifting back to normal.

The animal appears to have a regulated wake-up programme.

🔬 Why this matters

Suspended animation is interesting far beyond worms.

Understanding how a multicellular animal can safely suppress development, movement and metabolism — and then restart them — could help reveal general principles of dormancy, stress resilience and biological time.

The authors also highlight possible long-term relevance to areas such as organ preservation, trauma and deep-space travel, although controlled suspended animation has not been demonstrated in humans.

🧠 The take-home message

Crowd enough worms together in the right liquid and life appears to hit pause.

But underneath that stillness, the animal is actively reorganising its metabolism, organelles and nervous system so that it can survive — and eventually wake up again.

Sometimes doing nothing takes a lot of biology.

📄 Paper discussed

Junqiang Liu, Bingying Wang, Jonathan Leon Catrow, Quentinn Pearce, Zhijian Ji, Supeng Winnie Yang, Akash Balakrishnan, James E. Cox and Dengke K. Ma (2026)

Induction and regulation of reversible suspended animation in C. elegans

Nature Communications, 17:4627

DOI: https://doi.org/10.1038/s41467-026-71247-9

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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

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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

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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
📧 [email protected]

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

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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

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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.

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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

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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

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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.

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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.

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📧 [email protected]