Cool Genes

A thermosensitive ion channel helps C. elegans live longer at cold temperatures.

By | July 1, 2013


LONG-LIVED WORMS: C. elegans worms, pictured here, can live longer in the cold, thanks to an ion channel called TRP. © SINCLAIR STAMMERS/SCIENCE SOURCE

The paper
R. Xiao et al., “A genetic program promotes C. elegans longevity at cold temperatures via a thermosensitive TRP channel,” Cell, 152:806-17, 2013.

The finding
Many animals live longer at cold temperatures. The dominant explanation has been that low temperatures simply slow down all chemical reactions, including the ones that lead to aging. “People assume that it’s just a passive process,” says Shawn Xu, a neurobiologist and geneticist at the University of Michigan. But he and colleagues have found that in C. elegans, the cold-sensitive ion channel TRP is involved in actively promoting longevity when the temperature drops.

The approach
For years, Xu had been studying how TRP channels, encoded by the TRPA-1 gene, influence neuronal signaling and behavior. His team found that C. elegans engineered to lack TRPA-1 had shorter life spans at low temperatures than worms without the mutation, whereas worms producing higher levels of TRPA-1 lived longer at low temperatures. Both mutants lived a normal life span at normal temperatures.

The pathway
The TRP channel activates an anti-aging pathway by letting calcium ions into the cell, Xu and his team found. The calcium signaling sets off a cascade of kinases, which activate the transcription factor DAF-16, famous for its involvement in anti-aging pathways.

Human implications
Xu and colleagues engineered worms to express human TRP channels instead of their own and found that the worms still had enhanced longevity at low temperatures. The horseradish-like condiment wasabi also activates human TRP channels, and Xu was able to promote longevity even at normal temperatures by giving the transgenic worms wasabi’s active ingredient. “It’s a very exciting finding from a basic-science point of view, and possibly from an application point of view,” says Bruno Conti, a chemical physiologist at The Scripps Research Institute in California.

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Avatar of: James V. Kohl

James V. Kohl

Posts: 476

July 31, 2013

For comparison, after 2000 generations of thermal stress, 13 of
114 E. coli clones exhibited resistance to rifampicin. Evolution of Escherichia coli rifampicin resistance in an antibiotic-free environment during thermal stress.

The explanation was based on mutations theory, but seems more likely to be due to nutrient-dependent pheromone-controlled adaptive evolution. In my model, for example, olfactory/pheromonal input is responsible for changes in the thermodynamics of intercellular signaling and intranuclear interactions that allow the epigenetic landscape to become the physical landscape of DNA via alternative splicings and more efficient organism-level thermoregulation. Thus,  C. elegans subjected to nutrient stress associated with over-feeding of particular dietary components might link the nutrient stress to mutations and cancer, but not to adaptive evolution via mutations theory.

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