By concealing some key genes that DNA in foot DNA, the life cycle of the animal is extended by about 500%.
That's a big leap in life: A normal way for about three to four weeks. But when there are no two goats – DAF-2 and RSKS-1 – the creatures can survive for several months.
Scientists had linked these genes to longevity long ago, noting that the genes of other worms and creatures have increased when these genes are extinguished. However, the precise role of genes in the aging process remained confidential.
Now, researchers have connected the dots between these two genes and mitochondria, the tiny power houses that perform fuel cells throughout the body. Mitochondria starts malfunction because organisms age, but silence DAF-2 and RSKS-1 seem to delay this damage and extend the life cycle – at least in worms, according to a study published in 2019. magazine Press Cell.
Only the time the anti-aging medicine could work in mammals, including humans, will be seen.
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The link between DAF-2 and aging was recognized by scientists in the early 1990s, when a research team discovered that there were pigeons there. live twice as long as usual when they carry mutated version of the gene. The result was a new era in an adult study, which is being driven genes and their by-products.
"It was like a sweater in the field… as people started believing that one gene can contribute to a lifetime," said co-author Pankaj Kapahi, professor at the Buck Institute for Research on Aging in Novato, California, with Science Live .
Over time, research groups revealed more longevity genes, including RSKS-1, but molding evidence showed that these special parts of genetic code do not work alone. Instead, they coordinate with a team of other genes and build the proteins they help, which induce a disagreement of cellular activities called "signaling trails." Consider sign paths as layers of mayors – when one stops, it falls into another and decides a complex chain reaction.
DAF-2 and RSKS-1 sit with an important signaling path, respectively: the insulin signaling path, which helps control blood sugar levels and metabolism, and the TOR path, which changes the way cells build up proteins and so how they grow and increase. But did not know how these paths intersect in an aging organism, Kapahi said.
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To find where this anti-aging effect comes from, Kapahi and his colleagues were talking about the cells of convertible worms, both of which were extinguished. Using a technique called "polymeric profiling," the team could track the proteins that were taking the cells at any time. During protein construction, cells can use different mechanisms to increase or dial specific protein production. The team found that, in mutant worms, cells took far fewer copies of protein called "cytochrome c" than ordinary worms.
This is where mitochondria comes into the picture:
A cytochrome c is present in the inside membrane of mitochondria and helps to transform negatively charged electrons through its structure. This electron transfer from protein to protein allows mitochondria to generate fuel – but in mutant worms, there appears to be a gap when cytotomy should occur. Fuel cannot normally be done as efficiently as it would, dial the energy production of mitochondria and focuses on repairing damaged tissues.
As energy stores fall, a fuel detector enzyme called AMPK starts in high gear, helping to make energy metabolism more efficient. Ultimately, the complex chain of events creates these long-term jars whose cells remain healthy and mostly free from damage in the age.
"Proteins are damaged by age, and you see less damage to these paths," said Kapahi. In addition, research suggests that certain tissues, such as those in the muscles and in the brain, may grow healthier even if these paths remain, it added.
From worms to people
Overall, mutagenic worms focused on both protein and energy production in order to repair aging cells. Specifically, the lack of c cytometry in animal reproductive cells was critical to this process, the authors noted. The worms may add reproductive processes in a low-energy manner, they said.
Organisms respond the same when they are pressed into the hunger mode – without adequate nutrition, cellular signs tell the body to take 'free time' from preparation to produce an extract, said Kapahi. This idea is also supported by the 1990s study of old round worms; In this study, mutant worms lived twice as normal as worms, but they also produced about 20% less offspring.
Far from being a passive process, it seems that there is an unhappy break of biological ways that are working together to combat metabolism, build protein and their potential. reproduction. While people have similar paths, scientists do not yet know if aging works in the same way in both organisms, Kapahi said. If there is anything there may be more complex aging in people.
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"Conservation is not clean and there are important differences between these worms and mammals," said Dr. Joseph Avruch, professor of medicine at Harvard Medical School and chief of the diabetes unit in Massachusetts General Hospital, in an email.
While the extension of signage in the insulin and TOR trails appears to contribute to the lifespan of worms, it is unclear whether people would have the same response.
"If the gene network recognized here … performs the same in mammals, then pharmacological interventions can be done," Avruch said. In other words, the anti-aging experiments carried out in worms must be replicated in mammals before anyone knows whether they could work in humans.
"The paths associated with the aging process could be" very specific to the worm, "Kapahi said." But we won't know if these questions aren't taking us. "
First published Live Science.