In 1953 Watson and Crick were the first to discover the 3 dimensional helix shape that we now know is DNA. They determined the role of DNA is to transfer heritable features from one generation to the next. (Campbell, et al. 2009) However within DNA there is a section they called Junk DNA. This is an area of non-coding nucleic acids called introns. (Campbell, et al. 2009)
Initially Watson and Crick thought the Junk DNA had no real use and dismissed it as non-coding proteins. However scientists now believe that the non-coding DNA that makes up 95-98% of the human genome has a much more important role than originally thought.
In recent years more and more research is being performed investigating the real role of the junk DNA and these findings are conflicting with original assumptions. In 2010 scientist set out to explore the relationship between a non-coding stretch of chromosome (9p21) and heart disease. They said that individuals with a nucleotide mutation along this stretch of DNA are at greater risk of suffering from the disease. The non-coding stretch of DNA was deleted in a group of mice. The results showed the mice that had the DNA deleted actually died earlier or developed tumours when compared with mice that had the stretch of DNA intact. They concluded that the genes that may have been deleted on the stretch of DNA may control or ultimately inhibit cell proliferation in heart and other tissues. Meaning that without these genes, cells in arteries divide faster which build up causing restriction of blood flow to the heart which causes heart disease. (Visel et al, 2010)
Another idea of the possible functions Junk DNA performs comes from research done on the genomes of fruit flies. The genome of the fruit fly is approximately 80% junk DNA and it seems that the rate in which the flies DNA mutates is far less than what was expected. This means that because of no mutations the evolution of the fly has effectively come to a halt. Furthermore, they go on to say humans and mice have similar genomes, each consisting of around 30,000 genes. However the species are hugely different. They think that it’s not the genes that separate the species but in fact the junk DNA. Humans have one of the largest proportions of junk DNA out of all species. This may explain the complexity of our species. (Andolfatto, P. 2005)
From recent research it seems to be emerging the idea that junk DNA plays a more important role in human existence than first thought. Whether or not experiments on animals can be applied to humans is yet to be seen. The nature of this type of work has many ethical issues and may take years until experiments on humans are possible. Could it be that one day junk DNA will be considered no longer trash and instead treasure? Only time will tell.
Andolfatto, Peter (2005) Adaptive evolution of non-coding DNA in Drosophila. Nature. Issue 437, Page 1149-1152
Axel Visel, Yiwen Zhu, Dalit May, Veena Afzal, Elaine Gong, Catia Attanasio, Matthew J. Blow, Jonathan C. Cohen, Edward M. Rubin & Len A. Pennacchio (2010) Targeted deletion of the 9p21 non-coding coronary artery disease risk interval in mice. Nature. Issue 464, Page 409-412
Campbell, N. A., J. B. Reece and N. Meyers (2009). Biology. French Forest, NSW, Pearsons Education Australia.
Carol Guze,(2005) The Human Genome Project. Image available online at http://carolguze.com/text/442-1-humangenome.shtml
National Human Genome Institute. Image accessed on March 19th 2012. Available online at. www.genome.gov