Short-lived killifish reveals connection between gene expression and longevity

A study that appeared in the February 24 edition of Cell Systems indicates that differences in patterns of gene expression during youth may also predict longevity. Researchers of the shortest-lived vertebrate—the African turquoise killifish—found that when genes involved in a cell’s energy production are less active at a young age, the animals tend to live longer. This is an interesting finding because it somewhat contradicts the believe keeping mitochondria and energy production strong helps to stay healthy. This warrants some study into the below mentioned “mitochondrial complex I” proteins and if the author of the blog finds interesting material about this it will be posted.

Once the researchers determined that there was a clear difference between gene expression in long-lived and short-lived individuals, the researchers decided to give diluted doses of rotenone, a natural poison that inhibits the proteins that collectively form mitochondrial complex I and are responsible for the first step of cellular respiration, to some of the fish.

After analyzing samples from these fish, the researchers found that those exposed to rotenone lived longer than those that were not exposed to the poison.

It’s not yet clear if these findings will apply to humans, but the function of mitochondria decreases with age in both humans and killifish alike, Alessandro Cellerino, lead author and researcher at the Leibniz Institute on Aging in Jena, Germany, and the Scuola Normale Superiore in Pisa, Italy, said in a statement.

“Up to the present, it was thought that improving mitochondrial function would improve health in aged people; however, our results indicate a more complex scenario where the partial inhibition of mitochondrial function paradoxically has beneficial effects,” Cellerino said.

This latest research suggests that the effects of aging on mitochondria may involve a compensatory response rather than one that causes problems. “This obviously has implications on the development of strategies to improve health in older people and prevent aging-associated diseases,” he said.

Cellerino also noted that there are FDA-approved drugs that inhibit mitochondrial complex I, such as metformin, a drug that is prescribed to treat type 2 diabetes and has been shown to extend the lifespan of mice. “Based on our data, we strongly suspect that the effect of metformin was due to inhibition of complex I and not to its anti-diabetic action,” he said.

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