Longevity in C. elegans Eat mutants is largely attributable to reduced bacterial infection

Dietary restriction (DR) extends lifespan in many animal species. In C. elegans, Eat mutants with pharyngeal defects that impair feeding exhibit reduced growth rate and fertility and are typically long-lived, suggesting a DR effect. We report that Eat mutant longevity is largely or wholly a consequence of suppression of feeding activity-dependent infection of the pharynx by their E. coli food source. eat-2 mutants, widely used as a DR model, were among only 2/8 Eat mutants tested whose longevity were to any degree independent of bacterial infection. Moreover, among Eat mutants, phenotypic indicators of reduced nutrition correlated with one another, yet not with longevity. These findings document how, if infection is excluded, Eat mutants experience reduced nutrition, but in most cases not longevity, i.e. life-extending DR effects are not typical of Eat mutants. Thus, eat-2 longevity is partially due to infection resistance rather than DR, and residual, pharyngeal infection-independent longevity (contributing [~]40% of the total increase in lifespan) could reflect DR, or alternatively some other consequence of their nicotinic acetylcholine receptor defect.