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'Junk' DNA Has Important Role,
Researchers Find
Treatment of autoimmune disease read
e-book
Junk DNA' could be key to treating diseases
Among the many mysteries
of human biology is why
complex diseases like
diabetes, high blood
pressure and psychiatric
disorders are so
difficult to predict
and, often, to treat. An
equally perplexing
puzzle is why one
individual gets a
disease like cancer or
depression, while an
identical twin remains
perfectly healthy. Medical
researchers at the
Australian National
University have
discovered how genetic
material previously
referred to as so-called
'junk DNA' could help
treat auto-immune
diseases.
Now scientists have discovered a vital clue to unraveling these
riddles. The human genome is packed with at least four million gene
switches that reside in bits of DNA that once were dismissed as
“junk” but that turn out to play critical roles in controlling how
cells, organs and other tissues behave. The discovery, considered a
major medical and scientific breakthrough, has enormous implications
for human health because many complex diseases appear to be caused
by tiny changes in hundreds of gene switches.
The findings, which are the fruit of an immense federal project
involving 440 scientists from 32 laboratories around the world, will
have immediate applications for understanding how alterations in the
non-gene parts of DNA contribute to human diseases, which may in
turn lead to new drugs. They can also help explain how the
environment can affect disease risk. In the case of identical twins,
small changes in environmental exposure can slightly alter gene
switches, with the result that one twin gets a disease and the other
does not.
As scientists delved into the “junk” — parts of the DNA that are not
actual genes containing instructions for proteins — they discovered
a complex system that controls genes. At least 80 percent of this
DNA is active and needed. The result of the work is an annotated
road map of much of this DNA, noting what it is doing and how. It
includes the system of switches that, acting like dimmer switches
for lights, control which genes are used in a cell and when they are
used, and determine, for instance, whether a cell becomes a liver
cell or a neuron.
One in eight
Australians suffers from
auto-immune diseases
like type 1 diabetes or
lupus.
Senior medical
research fellow Carola
Vinuesa says the
discovery could change
the way patients are
treated.
"We might have
treatments that actually
hopefully might actually
cure disease rather than
just treating some
symptoms," she said.
"We might be able to
prevent diseases from
progressing."
Dr Vinuesa says the
research could lead to
more specific therapies.
"At the moment
treatments are going to
knock off the whole
immune system and that's
the current treatments
like using high doses of
steroids or the strong
drugs we use to treat
lupus which is very
non-specific," she said.
"So hopefully using
this more targeted
treatments they will be
able to treat the
diseases in a way that
they suffer less from
the side effects."
Professor Chris
Goodnow says it could be
years till treatment
stemming from the
research is available.
"This is a major
advance but in terms of
'here's something that
can go in the bottle'
that we know is safe and
effective, the shortest
you can do that from
discovery to is rarely
less than 10 years," he
said.
"It's the only way to
work well and work
safely in the
translation phase."
'Junk' DNA Has Important
Role, Researchers Find
ScienceDaily (May 21,
2009) — Scientists have called it "junk DNA."
They have long been perplexed by these extensive strands
of genetic material that dominate the genome but seem to
lack specific functions. Why would nature force the
genome to carry so much excess baggage?
The term "junk DNA" was originally coined to refer to
a region of DNA that contained no genetic information.
Scientists are beginning to find, however, that much of
this so-called junk plays important roles in the
regulation of gene activity. No one yet knows how
extensive that role may be.
Instead, scientists sometimes refer to these regions
as "selfish DNA" if they make no specific contribution
to the reproductive success of the host organism. Like a
computer virus that copies itself ad nauseum, selfish
DNA replicates and passes from parent to offspring for
the sole benefit of the DNA itself. The present study
suggests that some selfish DNA transposons can instead
confer an important role to their hosts, thereby
establishing themselves as long-term residents of the
genome.
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