Bacterial enterobactin and worm behaviour, lifespan: abstract only
In an abstract, a screen of E. coli gene-deletion mutants in C. elegans linked bacterial iron genes and enterobactin to worm movement, lifespan and healthspan via host mitochondria. [1]
Automatic summary · not editorially reviewed
The key findings
The screen combined 3,985 E. coli single-gene deletion mutants with C. elegans and profiled 768 behavioural features per clone. [1]
Loss of enterobactin biosynthesis abolished the bacteria-induced changes in worm movement. [1]
Enterobactin-binding targets included mitochondrial glutaryl-CoA dehydrogenase and electron-transfer flavoproteins A and B. [1]
The source at a glance
- Study type / format
- Abstract of an experimental screening study
- Population / context
- E. coli Keio deletion mutants and the worm C. elegans
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- October 8, 2026
E. coli mutants screened in C. elegans
The authors built a screening platform to test how bacterial genes shape behaviour. They used the E. coli Keio library of 3,985 non-essential single-gene deletion mutants together with the worm C. elegans, and profiled 768 behavioural features per bacterial clone. This identified a group of bacterial genes involved in iron homeostasis that changed host behaviour.
Supporting source [1]
Enterobactin and worm movement in the abstract
Bacterial analyses showed that altered iron homeostasis increased siderophore production in a TCA-cycle-dependent way. Loss of enterobactin biosynthesis abolished the bacteria-induced changes in worm movement. Further studies indicated that bacterial enterobactin activates host neuromuscular responses and shapes lifespan and healthspan depending on the mitochondrial unfolded protein response.
Supporting source [1]
Binding targets and redox pathway in the abstract
Thermal proteome profiling identified mitochondrial glutaryl-CoA dehydrogenase and electron-transfer flavoproteins A and B as enterobactin-binding targets that control mitochondrial function. Genetic manipulation of neuronal mitochondrial and cytosolic reactive oxygen species via superoxide dismutase and catalase showed that redox state modulates enterobactin-driven changes in movement and lifespan through the neuropeptide receptor PDFR-1. The authors describe enterobactin as a non-canonical neurotransmitter.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from E. coli and C. elegans experiments and do not establish human lifespan or health benefits.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Wu Y, Moore S, Backes C, Koh A, Zečić A, Djamriani DW, Heinemann B, Angermann C, Balachandran R, Peres TV, van der Laan J, Ahmadi A, Strippel J, Wesseling A, Kaneva I, Montoya A, Brodesser S, Cochemé HM, Kath-Schorr S, Trifunovic A, Hildebrandt T, Brown AE, Cabreiro F. · europepmc.org · October 8, 2026