C Elegans Diets

I was reading up on proline and found some curious points about the possible diets that C Elegans can have so I got an extract from ChatGPT

Great question — the bacterial food source is one of the strongest modulators of C. elegans lifespan. Researchers discovered long ago that worms don’t just eat bacteria; they metabolically interact with them, so different E. coli strains change nutrient supply, signaling, and stress exposure.

Here’s a rundown of the main bacterial diets in worm aging studies:


1. OP50 (E. coli B strain, uracil auxotroph)

  • Metabolic features: Slow-growing because it requires uracil supplementation. Produces less biomass, forms a thin lawn (makes handling worms easier). Nutrient composition differs from other strains: moderate in folate and B-vitamins, relatively lower in some amino acids compared to HT115.
  • Effect on lifespan: Considered the “standard lab diet.” Worm lifespan is relatively “baseline” on OP50. Some interventions (like added proline) shorten lifespan on OP50, likely because proline catabolism interacts with OP50-derived metabolic environment in a pro-oxidant way.

2. HT115(DE3) (E. coli K-12 derivative used for RNAi feeding)

  • Metabolic features: Engineered to be deficient in RNase III (so it maintains dsRNA for RNAi). Metabolically, it produces more folate and certain amino acids than OP50. Faster growth and thicker lawns.
  • Effect on lifespan: Worms on HT115 often live longer than on OP50, even without RNAi. Likely due to improved nutrient supply and reduced bacterial pathogenicity. Some pro-longevity effects (e.g., dietary restriction mimetics, ROS hormesis) are more pronounced on HT115.

3. HB101 (E. coli B/K-12 hybrid)

  • Metabolic features: Intermediate between OP50 and HT115. Richer in nutrients than OP50 but still relatively low pathogenicity.
  • Effect on lifespan: Typically yields longer lifespan than OP50. Worms accumulate less fat and have altered mitochondrial metabolism compared to OP50.

4. Comamonas DA1877 (a non-E. coli bacterium)

  • Metabolic features: Natural soil bacterium, metabolically very different — provides a distinct profile of amino acids and cofactors. In particular, very low in vitamin B12 compared to E. coli.
  • Effect on lifespan: Worms on Comamonas usually have a shortened lifespan, develop faster, and show altered one-carbon metabolism (methionine/SAM cycle). Adding vitamin B12 rescues some of these defects.

5. Other specialized diets

  • Dead bacteria (UV- or γ-irradiated OP50/HT115): Prevents bacterial proliferation inside the worm gut → usually extends lifespan, because pathogenicity is removed.
  • Pathogenic bacteria (e.g., Pseudomonas aeruginosa PA14, Enterococcus faecalis): Used in “pathogen resistance” assays. Worms typically die much faster.
  • Synthetic axenic diet (CeMM, defined medium): No bacteria, just defined nutrients → worms live longer but are smaller and less fertile.

Why this matters for aging experiments

  • Metabolite availability: B12, folate, and amino acids (proline, methionine, tryptophan) vary by strain → changes one-carbon metabolism, mitochondrial ETC flux, and ROS production.
  • Pathogenicity/toxicity: OP50 is mildly pathogenic; HT115 is less so. Dead bacteria eliminate infection risk, extending lifespan.
  • Energy balance: Richer diets (HB101, HT115) often promote faster growth but can paradoxically increase lifespan if they reduce stress from nutrient limitation or bacterial toxicity.
  • Interaction with interventions: The effect of drugs/nutrients (rapamycin, metformin, proline) can flip direction depending on bacterial strain because bacteria metabolize the compound first.

:white_check_mark: Summary table:

Bacterial diet Key metabolic traits Effect on lifespan Notes
OP50 Thin lawn, lower nutrients, mild pathogen Baseline lifespan Standard lab diet; proline can shorten lifespan here
HT115 More nutrients, RNAi-compatible, less pathogenic Longer than OP50 Used for RNAi feeding
HB101 Nutrient-rich hybrid Longer than OP50 Alters fat metabolism
Comamonas DA1877 Low B12, distinct amino acid profile Shorter than OP50 Alters 1-C metabolism
Dead bacteria No replication/pathogenicity Longer Removes bacterial stress
CeMM (axenic) Defined medium, no bacteria Longer but smaller worms Eliminates bacterial metabolism confounders

Would you like me to map which interventions (metformin, proline, rapamycin, glucose, etc.) change outcome depending on diet, so you can see how diet–compound interactions shape lifespan results?

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