One popular scientific hypothesis proposes that mitochondrial DNA plays a major role in aging. What is mitochondrial DNA and why would it play an important role in aging?
Not all of our DNA is found in our nucleus. Some is actually found in small organelles within cells called mitochondria. Scientists think these mitochondria have their own pool of DNA because they were once small free-living creatures. Sometime in our distant past, our ancestors absorbed them and now mitochondria make our energy.
It turns out that mitochondrial DNA (mtDNA) gets mutations much faster than the DNA in the nucleus. One reason for this is thought to be the presence of ROS or "reactive oxygen species" (also known as "free radical") in the mitochondria. When mitochondria make energy for us, they create ROS that can damage nearby mtDNA. In fact, this might be the reason why eating less leads to longer lives in animals -- less food, fewer ROS.
The idea is that as mtDNA becomes more and more damaged, the mitochondria cannot produce energy as well and become dysfunctional. This could lead to aging and ultimately, death. Is there any way to test this idea directly?
The most direct way to test this hypothesis would be to increase the rate of DNA mutations and see if it results in an increased rate of aging. This is exactly the experiment done by a group of researchers in Sweden. The researchers mutated a gene in mice so that the mtDNA would get more mutations faster. (The way they did this was to modify the enzyme that copies mtDNA, DNA polymerase-g, so that it made more mistakes as it copied mtDNA. The end result of this is that over time, more mutations accumulate.)
As expected, the mutant mice had more mutations in their mtDNA. So did they age faster than normal mice? Yes. At about 25 weeks of age the mutant mice started to display signs of aging that are normally seen in much older mice. The mutant mice lived for less than a year instead of for 2 to 3 years.
So, obviously mutations in mtDNA are part of the aging process. Are they everything? Probably not but they are clearly an important part of the puzzle.
Not all of our DNA is found in our nucleus. Some is actually found in small organelles within cells called mitochondria. Scientists think these mitochondria have their own pool of DNA because they were once small free-living creatures. Sometime in our distant past, our ancestors absorbed them and now mitochondria make our energy.
It turns out that mitochondrial DNA (mtDNA) gets mutations much faster than the DNA in the nucleus. One reason for this is thought to be the presence of ROS or "reactive oxygen species" (also known as "free radical") in the mitochondria. When mitochondria make energy for us, they create ROS that can damage nearby mtDNA. In fact, this might be the reason why eating less leads to longer lives in animals -- less food, fewer ROS.
The idea is that as mtDNA becomes more and more damaged, the mitochondria cannot produce energy as well and become dysfunctional. This could lead to aging and ultimately, death. Is there any way to test this idea directly?
The most direct way to test this hypothesis would be to increase the rate of DNA mutations and see if it results in an increased rate of aging. This is exactly the experiment done by a group of researchers in Sweden. The researchers mutated a gene in mice so that the mtDNA would get more mutations faster. (The way they did this was to modify the enzyme that copies mtDNA, DNA polymerase-g, so that it made more mistakes as it copied mtDNA. The end result of this is that over time, more mutations accumulate.)
As expected, the mutant mice had more mutations in their mtDNA. So did they age faster than normal mice? Yes. At about 25 weeks of age the mutant mice started to display signs of aging that are normally seen in much older mice. The mutant mice lived for less than a year instead of for 2 to 3 years.
So, obviously mutations in mtDNA are part of the aging process. Are they everything? Probably not but they are clearly an important part of the puzzle.
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