Indole produced during dysbiosis mediates host-microorganism chemical communication.

An imbalance of the gut microbiota, termed dysbiosis, has a substantial impact on host physiology. However, the mechanism by which host deals with gut dysbiosis to maintain fitness remains largely unknown. In , , which is its bacterial diet, proliferates in its intestinal lumen during aging.

Vitellogenin accumulation leads to reproductive senescence by impairing lysosomal function.

The maintenance of proteostasis is essential for cellular and organism healthspan. How proteostasis collapse influences reproductive span remains largely unclear. In Caenorhabditis elegans, excess accumulation of vitellogenins, the major components in yolk proteins, is crucial for the development of the embryo and occurs throughout the whole body during the aging process.

The p38 MAPK/PMK-1 Pathway Is Required for Resistance to Infection in .

is an opportunistic pathogen that causes nocardiosis primarily in patients with compromised immune systems. In this study, we used the genetically tractable organism as a model to study the innate immune responses to infection. We found that unlike other pathogenic bacteria such as and , failed to kill adult worms.

A conserved klo-1-mpk-1 pathway regulates autophagy and modulates longevity in Caenorhabditis elegans.

There are six different longevity models in Caenorhabditis elegans. Previous studies have identified several convergence points, such as hlh-30, daf-16, and klf-3, required for lifespan extension in these longevity models. However, it is not clear whether there other such convergence points.