Washington, January 29 : Researchers at the University of Southern California in Los Angeles have discovered a method to extend the lifespan of yeast cells tenfold, and believe that further research on unusual communities in Ecuador may offer hope for humans also.
The researchers say that they made this progress by deleting two genes-SCH9 and RAS2-from baker's yeast, and, then, subjecting the yeast cells to extreme starvation by restricting their calorie intake.
"Both these genes control cellular function and normally promote cell division and cell growth. They are very similar to two of the main cancer-causing genes in humans," National Geographic quoted study leader Valter Longo, a biogerontologist at the university as saying.
Longo says that the increased life span was not only due to the removal of genes alone, as it also seemed to be linked to calorie restriction. According to him, such restriction reduces the activation of the deleted genes, and, in turn, activates an enzyme called Rim 15.
"(Rim15) triggers a number of proteins that comprise stress-protective systems in yeast cells," he said, adding that such proteins control antioxidant and DNA-repair enzymes, besides regulating the proper folding of proteins that might explain the dramatic increase in yeast longevity.
The researchers, however, are still unclear as to how many of such proteins go about their jobs.
"There are probably hundreds of genes which play different roles that are part of this switch from 'growth' mode to 'protective' mode. We're looking for them right now," said Longo, whose findings appeared in recent issues of PLoS Genetics and the Journal of Cell Biology.
Previous studies had identified genetic mutations in mice that reduced the amount of growth hormone produced, thereby increased the animals' life span by 50 percent, and gave it protection against several diseases.
Longo's group is now studying a human population in Ecuador with a similar mutation, which controls the production of human growth hormone.
He has revealed that the gene also influences the human analogs of SCH9 and RAS2, which are located further down the growth hormone pathway.
"When you have low growth hormone, you tend to store fat," Longo said, which in turn affects the overall aging process.
That's because during times of food shortages, "all the energy has to be stored to make sure that aging is as slow as possible so that you can make it the next round of food," the researcher added.
The research team has, so far, collected DNA from 300 people, and its next aim is to understand the rates of mortality and cancer in the population, besides determining why these people do not appear to suffer from diabetes.
"People with two copies of the mutations have very small stature and other defects. We are now identifying the relatives with only one copy of the mutation, who are apparently normal. We hope that they will show a reduced incidence of diseases and an extended life span," Longo said in a press statement.
Just in case future research proves that the Ecuadorians with the hormone mutation have a lower incidence of cancer, drugs that decrease growth hormone signalling, already on the market, may also find use in preventing or reducing cancer in families with a history of the disease.
"It is not much different from taking statins to prevent cardiovascular disease," Longo said.