How Bacterial B12 Extended Lifespan in Worms With rict-1 Knocked Out
How Bacterial B12 Extended Lifespan in Worms With rict-1 Knocked Out
On 14 September 2026, Nature Communications published a study on the roundworm Caenorhabditis elegans. The authors traced the signal that triggers mitochondrial turnover in this organism: bacterial vitamin B12 acting together with loss of the gene rict-1.
The roundworm obtains vitamin B12 from the bacteria it eats. In animals with rict-1 knocked out (a gene that shapes how the cell responds to nutritional cues), a diet of the B12-rich bacterial strain HT115 extended lifespan and increased osmotic stress resistance, meaning the ability to survive a sudden spike in ambient salinity and recover. Supplementing ordinary OP50 food with B12 produced the same effect. This worked, however, only when three conditions were met simultaneously: loss of rict-1, a B12-rich food source, and a sufficient supply of methionine, an amino acid the worm obtains and metabolizes together with its bacterial diet.
A 2009 study had already linked rict-1 to diet and lifespan in the worm, and in 2022 the same laboratory identified a separate B12-dependent route to longevity in flr-4 mutants. The new paper determines which specific pathway connects B12 to the previously observed rict-1 effect.
The authors tested this chain step by step. First, they knocked out enzymes that require B12 for their activity: one participates in methionine metabolism, the other in the metabolism of propionate, an intermediate of cellular metabolism. In rict-1 mutants, levels of succinate, another participant in energy metabolism, rose. When its formation was blocked, stress resistance dropped and lifespan shortened; adding the same compound back as succinic acid restored both. Succinate thus emerged as a testable link in this chain.
Downstream, succinate triggered fission of mitochondria (the cell's energy-producing organelles) into smaller fragments. The protein DRP-1 is responsible for this step: suppressing it in the mutants reduced both stress resistance and lifespan. Following fission, mitophagy increased, that is, the intracellular dismantling and recycling of mitochondria. A fluorescent reporter confirmed this increase, and when the genes pink-1 and pdr-1, which are required for mitophagy, were knocked out, three readouts dropped together: mitophagy itself, stress resistance, and the lifespan advantage of rict-1 mutants.
Under normal conditions, rict-1 restrains the worm's sensitivity to fluctuations in dietary metabolites. When the gene is knocked out, a surge of bacterial B12 directly triggers mitochondrial fission and turnover, and the worm's lifespan depends on that process.