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Source of extended lifespan in animals identified
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Researchers at Massachusetts General Hospital (MGH) have found that the expression of certain genes usually found in reproductive cells in normal, somatic cells is behind the extended lifespans of certain animals. This research may lead to new treatments of age-related damages to other tissue, effectively increasing the life of mortal cells.
Most cells are restricted by the Hayflick limit, the number of times division can occur before the cell enters a pre-programmed self-destruct. Those cells that aren’t governed by the Hayflick limit are considered “immortal” cells; they can divide without end. Cancer cells fall into is category, as do stem cells. But it is the germ cells, sperm and egg cells, that are most immortal of all. Because they give rise to every cell in the body, including more germ cells in the developing fetus, our germ cells can technically be traced back to the very first human ancestor.
Scientists at MGH have tapped into this immortality, isolating the distinct genes that allow germ cells to survive so much longer than their mortal counterparts. These genes help protect the cell from damage incurred on DNA by outside sources such as sunlight and reactive oxygen species—in other words, things that cause aging. But a certain animal has a unique mutation, one in which the genes for immortality appear in mortal cells. Because of this, some C. elegans roundworms* have an extended lifespan.
In fact, researchers found that the “simple mutations in genetic pathways conserved throughout evolution can double or triple the lifespan of C. elegans, and that similar mutations in the corresponding pathways also dramatically extend mammalian lifespan.” [EurekAlert]
It is hoped that this research may one day help attenuate the damage caused in tissues by the pressures of aging. In the C. elegans, the longevity mutations help bolster the immune system, and especially the expression of certain genes through RNA inference which help protect DNA against damage caused by illness and other stresses. Using this basic theory, inducing other mutations along two different pathways that deal with detoxification and stress response also caused an “increased expression of germline markers.” [EurekAlert]
To study the opposite effect, researchers eliminated the mutation. That process effectively halted the extended lifespan of the roundworms. This simple experiment shows that it is indeed expression of the “immortality” genes in non-germ cells that plays a part in extending the lifespan.
Dr. Gary Ruvkun, lead author on the study which is published in Nature states,"The idea that somatic cells can reacquire genetic pathways usually restricted to germline cells is fascinating, and since germline protection is seen across species, the activity of these genes may play a role in controlling mammalian lifespan. Understanding the mechanisms involved in this transformation could help us develop new ways to repair and even regenerate key cells and tissues." [EurekAlert]
Of course, there is a long way to go. As mentioned previously, cancer cells also fall into the immortal category. As do stem cells which can cause cancer themselves if allowed to divide without supervision. Undoubtedly, careless inducing of immortality genes in somatic (non-stem cell) cells could result in the same problems. However, learning the basic biology behind how C. elegans live for so long is the first step in finding new treatments for age-induced damage to the body.
*Yes, worms. Use of C. elegans usually incites a more fevered version of the argument against the use of mice as models. How is what happens in a worm relevant to what happens in humans? In short, it’s not. A worm physiology is wildly different from a human’s, but that hasn’t stopped scientists from using C. elegans for decades as a model of basic biology. By studying smaller animals, researchers can get a general feel for how a biological system works, then go on to investigate a more complicated model. It is not unlike an architect, who must first sketch the building on paper before making the transition to carving marble.
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