Male C. elegans die through two distinct mechanisms – mating-induced germline activation, and potent male pheromone toxicity – but the latter is unique to males of androdioecious species (made up of hermaphrodites and males).
Autophagic flux assays in the nematode Caenorhabditis elegans suggest that autophagy decreases during normal aging, whereas long-lived daf-2 and glp-1 mutants maintain autophagic capacity in distinct spatiotemporal-specific manners to extend lifespan.
Experiments reveal mechanisms through which Caenorhabditis elegans zygotes depleted of Aurora A or lacking centrosomes spontaneously establish two posterior PAR-2 domains, one at each pole, in a curvature-dependent manner.
Collective responses of animals are generally controlled by complex biological mechanisms and in Caenorhabditis eleganscollective dynamics are purely controlled by physical parameters such as oxygen penetration and bacterial diffusion.
By controlling the SUMOylation of the protein CAR-1, the aging-regulating pathways downstream of the Insulin/IGF signaling cascade and of the germ cells of the nematode Caenorhabditis elegans are integrated.