In a study conducted by researchers in Wellcome Sanger Institute, it has been revealed that humans outlive animals because the former’s genetic code mutates slowly.
The study conducted among 16 species including human, mouse, lion, giraffe, tiger, and the long-lived, highly cancer-resistant naked mole-rat tried to shed a light on genetic changes in ageing and cancer.
The study found that despite huge variation in lifespan and size, different animal species end their natural life with similar numbers of genetic changes.
That is to say that the study confirmed that the slower the rate at which mutations occur leads to a longer life, and therefore, mammals from tigers to humans have a long life than a giraffe.
A mutation is a change in the DNA sequence that, according to the National Human Genome Research Institute, can result from DNA copying mistakes made during cell division, exposure to ionising radiation, exposure to chemicals called mutagens, or infection by viruses. These mutations are at the root of cancer.
While it is known how mutations lead to cancer, their role in the process of aging has not been detailed.
The study, published in the journal ‘Nature’, states that somatic mutation rates are evolutionarily constrained and may be a contributing factor in ageing.
Genetic changes, known as somatic mutations, occur in all cells throughout the life of an organism. This is a natural process, with cells acquiring around 20 to 50 mutations per year in humans. Most of these mutations will be harmless, but some of them can start a cell on the path to cancer or impair the normal functioning of the cell.
“To find a similar pattern of genetic changes in animals as different from one another as a mouse and a tiger was surprising. But the most exciting aspect of the study has to be finding that lifespan is inversely proportional to the somatic mutation rate,” Dr Alex Cagan of Wellcome Sanger Institute said in a statement.
Researchers generated whole-genome sequences from 208 intestinal crypts taken from 48 individuals, to measure mutation rates in single intestinal stem cells. Analysis of the genome revealed that somatic mutations accumulated linearly over time and that they were caused by similar mechanisms across all species, including humans, despite their very different diets and life histories.
They noticed that the rate of somatic mutation decreased as the lifespan of each species increased. They, however, found no significant association between somatic mutation rate and body mass, indicating that other factors must be involved in larger animals’ ability to reduce their cancer risk relative to their size.
“Ageing is a complex process, the result of multiple forms of molecular damage in our cells and tissues. Somatic mutations have been speculated to contribute to ageing since the 1950s, but studying them had remained difficult. With the recent advances in DNA sequencing technologies, we can finally investigate the roles that somatic mutations play in ageing and in multiple diseases. That this diverse range of mammals end their lives with a similar number of mutations in their cells is an exciting and intriguing discovery,” Dr Inigo Martincorena, a co-author of the study said.
