C. elegans is a powerful model organism for ageing studies. However, the traditional protocols, which continue to be broadly used, rely on manual handling, making them labor-intensive and time-consuming. Automation of these processes would greatly benefit long-term studies of C. elegans. Significant progress has been achieved over the past decade in the techniques to study…
Here we describe an innovative microfluidic platform using the nematode Caenorhabditis elegans, as an ideal model organism for the study of aging due to its short lifespan and tractable genetics. Our platform allows full automation of the entire process of culture, treatment, imaging and analysis of C. elegans, at unprecedented levels of throughput and standardization. The…
Longevity is regulated by a network of closely linked metabolic systems. We used a combination of mouse population genetics and RNA interference in Caenorhabditis elegans to identify mitochondrial ribosomal protein S5 (Mrps5) and other mitochondrial ribosomal proteins as metabolic and longevity regulators. MRP knockdown triggers mitonuclear protein imbalance, reducing mitochondrial respiration and activating the mitochondrial unfolded protein response.…
Making muscle work better Degenerating muscle—whether from muscular dystrophies, myopathies, or other diseases—loses its mitochondria (the energy supply) and an essential cofactor nicotinamide adenine dinucleotide (NAD+), while gaining an extra load of enzymes that use up NAD+, as reported by Ryu and colleagues. The resulting loss of NAD+ is exacerbated by a drop in NAD+…
Caenorhabditis elegans (C. elegans) constitutes an important model organism for use in nutrition and aging studies. We report a novel method for studying the dynamics of Escherichia coli (E. coli) bacterial transit through the worms’ intestine. A microfluidic chip was designed for alternating C. elegans on-chip culture and immobilization, thereby enabling periodic high-resolution time-lapse imaging…
NAD(+) is an important cofactor regulating metabolic homeostasis and a rate-limiting substrate for sirtuin deacylases. We show that NAD(+) levels are reduced in aged mice and Caenorhabditis elegans and that decreasing NAD(+) levels results in a further reduction in worm lifespan. Conversely, genetic or pharmacological restoration of NAD(+) prevents age-associated metabolic decline and promotes longevity…