A Demonstration of Evolutionary Optimization for Resilience Rather than Life Span
We see the current survivors of the relentless evolutionary process of winnowing and change all around us, and near all are examples of the point that greater life span is all too rarely a winning trait. Look at how easy it is for our early biotechnology to engineer longer lives in near all animal species. Small genetic tweaks suffice in most cases. Why were those genetic alterations not selected for long ago, given that longer-lived individuals can produce more progeny than their shorter-lived rivals? The study here provides one example of the many reasons for the current state of life span in most species: the present outcome for any given species is a balance between resistance to stress and ability to live longer, in this case mediated by the way in which the immune system acts in response to circumstances.
A shorter life may be the price an organism pays for coping with the natural assaults of daily living, according to researchers. The scientists used fruit flies to examine the relationship between lifespan and signaling proteins that defend the body against environmental stressors, such as bacterial infections and cold temperatures. Since flies and mammals share some of the same molecular pathways, the work may demonstrate how the environment affects longevity in humans.
The research identified Methuselah-like receptor-10 (Mthl10), a protein that moderates how flies respond to inflammation. The finding provides evidence for one theory of aging, which suggests longevity depends on a delicate balance between proinflammatory proteins, thought to promote aging, and anti-inflammatory proteins, believed to prolong life. These inflammatory factors are influenced by what an organism experiences in its every day environment.
Mthl10 appears on the surface of insect cells and acts as the binding partner to a signaling molecule known as growth-blocking peptide (GBP). Once Mthl10 and GBP connect, they initiate the production of proinflammatory proteins, which, in turn, shortens the fly's life. However, removing the Mthl10 gene makes the flies unable to produce Mthl10 protein and prevents the binding of GBP to cells. As a result, the flies experienced low levels of inflammation and longer lifespans. "Fruit flies without Mthl10 live up to 25 percent longer. But, they exhibit higher death rates when exposed to environmental stressors."
When the project started in 2013, scientists did not know what cell-surface protein was working with GBP to promote inflammation. So they began testing 1700 compounds that could individually suppress the production of every known cell-surface protein in the fruit fly. They looked for the protein that prevented GBP from binding and activating inflammation. They found several candidates, but all were eliminated during further testing, except Mthl10. The study proposes that the human counterpart to GBP is a protein called defensin BD2, but the nature of its binding partner is currently unknown.