Serotonin deficiency from constitutive SKN-1 activation drives pathogen apathy.

Unlabelled: When an organism encounters a pathogen, the host innate immune system activates to defend against pathogen colonization and toxic xenobiotics produced. employ multiple defense systems to ensure survival when exposed to including activation of the cytoprotective transcription factor SKN-1/NRF2. Although wildtype quickly learn to avoid pathogens, here we describe a peculiar apathy-like behavior towards PA14 in animals with constitutive activation of SKN-1, whereby animals choose not to leave and continue to feed on the pathogen even when a non-pathogenic and healthspan-promoting food option is available.

A dicer-related helicase opposes the age-related pathology from SKN-1 activation in ASI neurons.

Coordination of cellular responses to stress is essential for health across the lifespan. The transcription factor SKN-1 is an essential homeostat that mediates survival in stress-inducing environments and cellular dysfunction, but constitutive activation of SKN-1 drives premature aging thus revealing the importance of turning off cytoprotective pathways. Here, we identify how SKN-1 activation in two ciliated ASI neurons in results in an increase in organismal transcriptional capacity that drives pleiotropic outcomes in peripheral tissues.

A dicer-related helicase opposes the age-related pathology from SKN-1 activation in ASI neurons.

Unlabelled: Coordination of cellular responses to stress are essential for health across the lifespan. The transcription factor SKN-1 is an essential homeostat that mediates survival in stress-inducing environments and cellular dysfunction, but constitutive activation of SKN-1 drives premature aging thus revealing the importance of turning off cytoprotective pathways. Here we identify how SKN-1 activation in two ciliated ASI neurons in results in an increase in organismal transcriptional capacity that drives pleiotropic outcomes in peripheral tissues.

Different methods of killing bacteria diets differentially influence physiology.

Across species, diet plays a critical role in most, if not all life history traits. is an important and facile organism for research across modalities, but the use of live bacteria as sources of nutrition can exert pleiotropic outcomes that stem from the action of host-pathogen defenses. Recently, a powerful new approach to readily generate dead and metabolically inactive was developed that enabled reproducible measures of health across the lifespan.

Ether lipid biosynthesis promotes lifespan extension and enables diverse pro-longevity paradigms in .

Biguanides, including the world's most prescribed drug for type 2 diabetes, metformin, not only lower blood sugar, but also promote longevity in preclinical models. Epidemiologic studies in humans parallel these findings, indicating favorable effects of metformin on longevity and on reducing the incidence and morbidity associated with aging-related diseases. Despite this promise, the full spectrum of molecular effectors responsible for these health benefits remains elusive.

Riboflavin depletion promotes longevity and metabolic hormesis in Caenorhabditis elegans.

Riboflavin is an essential cofactor in many enzymatic processes and in the production of flavin adenine dinucleotide (FAD). Here, we report that the partial depletion of riboflavin through knockdown of the C. elegans riboflavin transporter 1 (rft-1) promotes metabolic health by reducing intracellular flavin concentrations.

Rapid Lipid Quantification in by Oil Red O and Nile Red Staining.

The ability to stain lipid stores allows for the facile assessment of metabolic status in individuals of a population following genetic and environmental manipulation or pharmacological treatment. In the animal model , lipids are stored in and mobilized from intracellular lipid droplets in the intestinal and hypodermal tissues. The abundance, size, and distribution of these lipids can be readily assessed by two staining methods for neutral lipids: Oil Red O (ORO) and Nile Red (NR).

Genetic variation in is associated with muscle health over the lifespan and across species.

The influence of genetic variation on the aging process, including the incidence and severity of age-related diseases, is complex. Here, we define the evolutionarily conserved mitochondrial enzyme ALH-6/ALDH4A1 as a predictive biomarker for age-related changes in muscle health by combining genetics and a gene-wide association scanning (GeneWAS) from older human participants of the US Health and Retirement Study (HRS). In a screen for mutations that activate oxidative stress responses, specifically in the muscle of , we identified 96 independent genetic mutants harboring loss-of-function alleles of , exclusively.

Bacterial diets differentially alter lifespan and healthspan trajectories in C. elegans.

Diet is one of the more variable aspects in life due to the variety of options that organisms are exposed to in their natural habitats. In the laboratory, C. elegans are raised on bacterial monocultures, traditionally the E.