Jumping pieces of DNA may be responsible for aging

Many of the countries in the world are currently faced with an aging population. In Canada, 16% of the population is over the age of 65, while in Japan that proportion is 26.4%. Aging populations usually happen when the life expectancy of its occupants increases or when reproductive rate decreases. Both of these instances are likely contributing the aging population of developed countries. There are a number of problems that come with an aging population: 1) Economic: Older people have more money accumulated than younger people but spend less. 2) Health Care: Older people need more health care and their health care costs more. Older people suffer from more chronic diseases and are more likely to become ill. While we all have a grasp on what it means to age, we still don’t fully understand what causes it and if there is anyway to reverse the aging process or any way of slowing it down. Many theories on aging focus on the idea that throughout a lifespan a person’s cells and DNA accumulate damage to the point where the whole system fails and shuts down. The other theory is that our cells have a programmed life span in which they will work optimally, once we get beyond that life span, we begin to age and then die. While we still do not know which theory is correct, a research group at Brown University seems to have uncovered evidence that little pieces of jumping DNA may be important in the aging process.

First, a quick biology lesson. Residing in your DNA are small pieces of genetic code called transposons. These transposons have the ability to copy themselves, jump around your DNA, and then insert themselves into a new area. Think of them like this: you have a book in your hands and you cut out one sentence from the page you are currently reading. You make a copy of this sentence, put the original back in its place and then randomly open up the book to a new page. On this new page, you glue that copied sentence in place, and in the process give that sentence or paragraph a whole new meaning. This is how transposons work. Transposons are thought to have played a very important role in the evolution of the genes that currently make us human. When transposons move to a new part of the DNA, they change the way the gene at that spot reads and therefore makes a new protein with possibly a new function. This is similar to the way a random sentence’s meaning can be changed by gluing a different sentence in its place. Transposons are normally very tightly controlled, you don’t want them jumping around all the time because if they get placed in the wrong spot you end up with proteins that don’t work and diseases like Cancer, hemophilia, and Duchenes muscular dystrophy. To control the movement of these transposons, the region of DNA where they are found is usually very tightly packed together so they cannot escape.

Now, onto the research. The scientists, working with fruit flies, made the transposons in these fruit flies fluoresce green when they were on the move so that they can track where they ended up. What they found was that in young fruit flies there were almost no transposons moving around inside the DNA and cells. However, when these fruit flies got older there was a sudden explosion of activity in the movement of these transposons all over the cells. Why? Well the scientists hypothesized that it had to do with a problem in the tight packaging that normally keeps these transposons in place. When the researchers reinforced the packaging using drugs, the movement of the transposons was stopped and the lifespan of the fruit flies was increased. Additionally, when the fruit flies were given a calorie restricted diet, something that is shown to extend life span, this also stopped the movement of the transposons. Finally, using an anti-HIV drug that stops transposons from moving, the researchers were able to increase the life span of the fruit flies.

It is still to early to blame transposons for our aging but there is some evidence now that when these normally repressed pieces of DNA start jumping around aging may begin. The questions that still remain include: if we turn on transposons, can we cause premature aging in fruit flies and could this explain premature aging in some people? Also, is this even something we can target? Calorie restriction is easy to do but would we want to take drugs to prevent transposon movement as a way of preventing aging? We don’t know yet. It should also be noted that there are likely to be more than one mechanism in the cell that causes aging and its not as simple as targeting transposons as our fountain of youth.

Image Credit: Trocaire – Flickr

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