Study pinpoints genes involved in diet-mediated life-extension

August 14, 2012 By Julie Owens

Researchers at the University of Liverpool have developed a new method to identify genes involved in diet-mediated life-extension which allowed them to find three novel genes that extend lifespan in yeast.

The researchers in Liverpool, in collaboration with researchers at the University of Arkansas, studied , which consists of limiting certain factors in diet (like calories) without malnutrition and has been shown to increase lifespan from yeast to monkeys. Many genes had been associated with dietary restriction before, and the researchers developed a method to study how the genes interact with each other as part of networks to decipher the mechanisms involved and find possible missing links. This allowed them to identify new genes that mediate life-extension in response to dietary restriction. Three of such genes they then showed to extend in yeast via dietary restriction-related mechanisms.

Some of the new genes identified may have similar functions in humans and could be potential targets for anti-ageing interventions. Dr Joao Pedro de Magalhaes, who led the study, explains: "Some targets for retarding ageing in humans being clinically tested were initially discovered in yeast, so we definitely want to continue this work with a view of ultimately tackling the human and developing treatments for age-related diseases. Besides, our method can be used to predict genes involved in life-extension mediated by dietary restriction in mammals and even in humans. We just tested our predictions in because it was quicker and cheaper, but we are now looking to obtain funding to pursue this line of research in more complex models. I am definitely optimistic that it is possible to develop an anti-ageing pill."

The work is published in August in .

Explore further: Is the 'longevity gene' nearing the end of its life?

More information: doi:10.1371/journal.pgen.1002834

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1 / 5 (1) Aug 15, 2012
Nutrient chemical-dependent aging altered by the epigenetic effects of dietary restriction via the interactome seems to be less a function of random mutations than one that could be attributed to a pattern of design in biology. For example, in microbes the nutrient chemicals metabolize to pheromones that control reproduction. This links what organisms eat to the species specific pheromones they produce in a linear progression across adaptive evolution exemplified here in species from microbes to mice (i.e., mammals). That might be an important pattern to consider in the context of chemical ecology and adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction that appears to begin with the role of the nutrient, glucose, in yeasts. Of course, glucose is essential to the construction of our socio-cognitive niche, which makes me think -- and allows me to think -- that much more than a theory of random mutations are involved.
1 / 5 (1) Aug 15, 2012
The essential genes tend to be located in the center of the interactome rather than in the periphery, which suggests the central role for regulation of cell division by nutrient chemicals, like glucose. Glucose also regulates gonadotropin releasing hormone (GnRH) from what might be called the center of the mammalian interactome: the hypothalamic GnRH pulse.

In mammals, GnRH pulsatility links the epigenetic effects of nutrient chemicals and pheromones to the interactome and thus directly to nutrient chemical-dependent species-specific behaviors via adaptive evolution through ecological, social, neurogenic, and socio-cognitive niche construction. However, there is no denying the role of dietary fatty acids in GnRH-directed socio-cognitive niche construction.

The article makes clear that yeast cells managed to evolve into intelligent mammals. The yeast mating pheromone is so similar to mammalian GnRH--a molecule conserved across 400 million years of vertebrate evolution that...

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