Further to “Another pseudogene shows function”:
Variations in non-coding sections of the genome might be important contributors to type 2 diabetes risk, according to a new study.
DNA sequences that don’t encode proteins were once dismissed as “junk DNA”, but scientists are increasingly discovering that some regions are important for controlling which genes are switched on.
The new study, published in Nature Genetics, is one of the first to show how such regions, called regulatory elements, can influence people’s risk of disease.
“The cells that produce insulin appear to be programmed to behave differently in people with type 2 diabetes,” said co-author Mark McCarthy, a Wellcome Trust Senior Investigator at the University of Oxford. “This study provides some important clues to the mechanisms which are disturbed in the earliest stages of the development of type 2 diabetes, and may point the way to novel ways of treating and preventing the disease.”
Is someone keeping track of all this for an Atlas of Junk DNA?
Memory bank: “The amount of DNA in organisms,” neo-Darwinist Richard Dawkins wrote in 1976, “is more than is strictly necessary for building them: A large fraction of the DNA is never translated into protein. From the point of view of the individual organism this seems paradoxical. If the ‘purpose’ of DNA is to supervise the building of bodies, it is surprising to find a large quantity of DNA which does no such thing. Biologists are racking their brains trying to think what useful task this apparently surplus DNA is doing. But from the point of view of the selfish genes themselves, there is no paradox. The true ‘purpose’ of DNA is to survive, no more and no less. The simplest way to explain the surplus DNA is to suppose that it is a parasite, or at best a harmless but useless passenger, hitching a ride in the survival machines created by the other DNA.” (The Selfish Gene, p. 47)