The "Junk DNA" misnomer was put forward as a "theory" (though
totally wrong, and suspect after its first utterance) by Susumu
Ohno (1972), an otherwise serious scientist; see "So much 'Junk'
DNA in our genome" (full text in my junkdna.com domain). He
mistakenly argued that the non-genic sequences are in the
genome "for the importance of doing nothing" (p. 367).
It was only later that this catastrophic misnomer became widely
accepted at face value - as an excuse for the establishment to
(BTW negligently) ignore 98.7% of (human) DNA - while millions
if not hundreds of millions were (and still are) dying of "Junk DNA
diseases".
"The Principle of Recursive Genome Function" (2008), by
retiring both the "Junk DNA" and "Central Dogma" obsolete
axioms became the first full genome (hologenome) theory based
on sound genome informatics, sweeping away science-nonsense
that retarded genomics for over half a Century (starting from
Crick's notion in 1956, that he dared to call "Central Dogma",
that information "never" recurses from either RNA or from
PROTEINS to DNA).
Upon conclusion of ENCODE (2007) Francis Collins was the one
to issue a public call "the scientific community will have to re-
think long-held beliefs". Some lucky few did not have to re-think
as they never believed the two false axioms in the first place -
but now we have (really, not the first...) experimental evidence as
a de facto basis to discard wrong assumptions that were totally
absurd from the viewpoint of genome informatics. 1.3% of human
DNA (in fact, much less since "genes" may contain a big majority
of non-coding introns) is simply not enough information to
govern growth of as complex organisms as humans.
FractoGene (2002) clinched it in one year after it was
established that the expected 140-300,000 "genes" were
nowhere to be found by The Human Genome Project. Today,
"recursive genome function" prevails with close to 200,000 hits in
Google... "Fractal defects" such as reported, with the recursion
derailed and/or not supported with enough auxiliary information
by sufficient number of recursion not only "have been expected",
but theoretically predicted. - Pellionisz_at_JunkDNA.com
Scientists have found that junk DNA can come back to life and can cause disease.
As it turns out, a region of the genome — that is hundreds of thousands of years old, mind you — can bring on trouble.
Soon after the zombie gene wakes up, people can no longer smile and their upper body muscles begin to waste away. 
Those victims suffer from facioscapulohumeral muscular dystrophy (FSHD), one of the more common forms of the genetic disease.
1 in 20,000 people suffer from FSHD — what makes it different than diseases like diabetes is that inheriting the gene means the person will one day get the genetic disease.
While scientists knew genetics was to blame, they didn’t exactly know why and how it caused disease. Now they know, zombies are to blame.
The researchers published their results in Science.
There’s a certain rhythm to this madness. To cause disease, the gene needs to be repeated a number of times and has to have the right sequence. The trouble gene is found on chromosome 4 (which is a region scientists eyed for several decades).
If the zombie gene is repeated more than 10 times, the person will not develop FSHD. Researchers believe the surplus copies change the structure of the chromosome so the zombie gene can’t attack. Otherwise, the gene (DUX4) is allowed to be made and becomes toxic to the muscle cells.
This finding fundamentally changes how geneticists think about simple genetic diseases. It’s clear that even though FSHD was thought to be a simple disease because having the gene meant the person would definitely get the disease, it’s actually much more complex than that.
In the future, researchers could knock out this dead gene and develop new treatments.
Scientists believe they will discover that other diseases will have similar causes.
Geneticist Dr. Francis Collins told The New York Times, “the first law of the genome is that anything that can go wrong, will.”
Photo: ynse/ flickr
