One of the many endeavors of scientists around the world would be to find the solution to the inevitable aging of human beings. Even if there are a number of researches and studies concerning the topic, the solution has not been fully defined.
That is until researchers from the University Of Rochester have found evidence that the mystery of longevity could be unlocked by the arrangement of one's genes.
The team, spearheaded by biology professors Vera Girbunova and AndreiSeluanov, joined by Dirk Bohmann. a professor of biomedical genetics and a number of students and postdoctoral researchers have recently published their new paper that discusses the gene sirtuin 6 (SIRT6).
In the paper, the team describes SIRT6 as the gene responsible for more efficient DNA repair especially for species with a longer lifespan. The scientists explained that the paper has a goal to improve anti-aging interventions and help prevent diseases that are age-related.
The scientists pointed out that as living organisms grow older, the DNA of humans and other mammals will be prone to breaks. This could lead to gene rearrangement and mutation, an opportunity for aging and cancer to take over the gene.
The age-old hypothesis was that DNA repair plays an important role in determining an organism's life span. Whereas, behaviors like smoking and lack of sleep can accelerate double-strand breaks in the DNA.
However, the scientists pointed out that the breaks are always going to be there and are unavoidable even for a very healthy person. This is because living organisms need to breathe in oxygen, thereby allowing for oxidative damage on the DNA.
The team of researchers pointed out in the research that organisms with shorter lives, such as mice, have a small a chance to accumulate double-strand breaks in their DNA, whereas, organisms with a longer lifespan are more exposed to DNA breaks.
A nickname given to SIRT6 is the "Longevity gene" because of the gene's role in organizing proteins and recruiting enzymes in repairing broken DNA.
The scientists have observed that mice without the gene age prematurely while the mice with extra copies of the longevity gene are observed to live longer.
One hypothesis that the researchers have is that there is more efficient DNA repair for organisms with longer lifespans which means that they might have evolved more efficient DNA repair regulators. The researchers analyze DNA repair in 18 rodent species with varying lifespans to test this theory.
The team has observed that the rodents with longer lifespan have more efficient DNA repair because SIRT6 proteins which are products of their SIRT6 genes are more potent. Bohmann explains that SIRT6 is not the same in every species. The scientist later added that SIRT6 protein is a promising and dominant determinant of lifespan.
The SIRT6 in human genes is already optimized. To this, Seluanov explains that there are other species that have longer lifespans which can be looked into. The team's research would definitely aid studies pertaining to the prevention of age-related diseases in humans. Gurbonova pointed out that the research could be significant for studies on target interventions that could delay cancer among other degenerative diseases. The scientist later added that the next step in the research is to analyze if the species with a longer lifespan than humans do have a more involved SIRT6 gene.
