by Stephen F
As we begin to map out the human past and present genome, we have discovered many new and exciting discoveries. One particular discovery that has hit scientists is the reactivation of a ‘dead’ gene. A truncated IRGM gene, one of two, that was thought to be derelict, has been found to be able to produce proteins once again. This gene, known as Immune-Related GT Pases, is a gene that allows the immune system to help resist an array of heavier germs and diseases, such as tuberculosis and salmonella, which invade cells.
Interestingly, it is found that other mammals have a vast abundance of these genes active within their systems. Mice have 21 versions of this gene. As this gene’s new attention expanded, it is now thought that its mutation could be a cause of Crohn’s disease.
This opens the door to many new theories on our evolutionary processes. As the gene has passed down through the generations through millions of years, scientists have focused on tracing its path back through our closest primate ancestors. It is thought that after the gene was shut down, a ‘series of structural events’ reactivated the gene, possibly due to more resistant and stronger viruses and bacteria. This is a remarkable theory in that it suggests that our genome is very malleable over time, and adapts to our environments. With the resistance of viruses and bacteria to our drugs, our immune systems also have ways of becoming stronger and more adaptive over time.
Critical Thinking Questions:
Why do we only possess two of these genes as other mammals possess over 10?
Is there any correlation to our use of drugs to alter, assist, or destroy our own immune systems and our natural ability to cure infection?
Is this possibly evidence that we can, through powers of thought and mind, as well as our own biological processes, have more potential than previously thought?
Source:
Public Library of Science (2009, March 11). Dead Gene Comes Back To Life In Humans. ScienceDaily. Retrieved March 12, 2009, from http://www.sciencedaily.com /releases/2009/03/090305204321.htm
