The transcriptional cofactor HPK-1 (homeodomain-interacting protein kinase) functions as a key regulator of multiple proteostatic stress responses, each originating from discrete neuronal subtypes within the Caenorhabditis elegans nervous system to preserve neuronal health and maintain organismal proteostasis during normal aging.

First systemic lysosomal proteomes in association with longevity and tissue specificity in C. elegans uncover lysosomal heterogeneity across multiple scales and provide valuable resources for understanding how lysosomes modulate signal transduction, organelle communication, tissue physiology, and organism longevity.

Separate genetic pathways mediate longevity, pathogen resistance, and cell-nonautonomous regulation of xenobiotic detoxification in chemosensory defective Caenorhabditis elegans mutants.

Two SET-domain containing proteins regulate H3K4me3 by their binding to H3K4me3 through their PHD domain and directly regulate expression of a subset of genes.

Extensive molecular profiling shows how loss of highly similar, paralogous ribosomal proteins lead to distinct phenotypic outputs, through translational control of specific mRNAs.

Endo-siRNAs slow down the rate of aging and enable the maintenance of a responsive heat shock response in aging germline-less Caenorhabditis elegans.

To promote longevity under heat stress shares yeast aging factors with progeny through a down-regulation of the diffusion barrier in the membranes between the mitotic cells.

Light controls can fine tune microbiome–host interaction to qualitatively regulate host longevity with temporal and spatial precision.

Translational evidence indicates APOE2 benefits longevity independent of its protective effects on Alzheimer’s disease, which preserved activity and the metabolism of apoE protein and associated-lipids would be key to understanding.

Epigenetic drift of H3K27me3 is one of the molecular mechanisms that contribute to aging, and stimulation of glycolysis promotes metabolic health and longevity.