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.
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?