The average human genome consists of many millions of defunct retroviral elements and even more copies of mobile elements called transposable elements (TEs). These are virus-like pieces of DNA that can move about in genomes. Since the initial completion of the Human Genome Project, these elements have been estimated to comprise at least half of a typical human genome, but more recent analysis puts the proportion closer to 2/3.
This fact about the human genome is well known to biologists but carefully ignored by those purveying a picture of the human genome as an exemplar of “design.” But we know a lot about the consequences of carrying these TEs around in our genomes. They can come back to life, as mobile genetic elements, and wreak havoc. In fact, mammalian cells deploy an arsenal of tools to struggle against this. When/if these systems are inactivated, lots of bad things happen, most notably the disruption of the structural integrity of the genome itself. The study of damaging effects of TEs in human cells is strong and ongoing, and now there’s a new report that implicates TEs in aging.
We already knew that TEs increase during aging, at least in cells, which suggested that aging could be either a cause or a consequence (or both) of the partial unleashing of these things. Now we have some direct evidence for this, and an explanation for what’s going.
The basic summary is that a phenomenon associated with aging, called senescence, triggers a collection of problematic responses called SASP (senescence-associated secretory phenotype, if you must know), in some cells in the body. The new work shows that this response includes the sudden and dramatic liberation of a specific human TE called LINE-1. Interfering with these LINE-1 elements can protect cells (and animals) from age-related health decline.
In other words, the mobile elements in our genomes, which are DNA parasites operating on huge scales and using specific strategies to propagate themselves and which account for as much as 2/3 of our total DNA payload, are potentially a big reason for loss of health in aging.
Can “design” explain this? Yes, if by “design” you include the machinations of DNA parasites.
News article about the new paper:
As always, I’m happy to send a PDF to anyone who asks.