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Researchers Solve the Mystery of Non-Coding DNA

Posted January 29, 2018

For nearly a decade now, scientists have been perplexed by the presence of long, winding strings of DNA which serve no apparent purpose in their animal hosts because they don’t code for proteins and therefore have no real effect on the organism.

Sequences of “ultraconserved” non-coding DNA have been found to be nearly identical in all species of vertebrates, including humans.

Now, a new paper published in the journal Cell on 18 January confirms the hypothesis that all DNA, coding or not, is vital to life – a group of US researchers have found that non-coding DNA guides brain development by fine-tuning the expression of protein-coding genes.

“People told us we should have waited to publish until we knew what they did. Now I’m like, dude, it took 14 years to figure this out,” said study co-author Gill Bejerano of Stanford University.

Back in 2004, Bejerano and his colleagues were surprised to find that mice, rats, chickens and humans share as many as 481 stretches of “dormant” DNA that’s almost completely identical across species.

Given that genes which code for proteins tend to have relatively few mutations, as even minor changes to corresponding proteins could lead to the animal dying, researchers speculated that non-coding DNA must be serving an equally important function.

While causing no immediately apparent issues, the excision of non-coding DNA leads to abnormal brain development. Image credit: Miki Yoshihito via, CC BY 2.0.

However, in 2007 it was discovered that knocking out a number of “dark matter” DNA units led to no adverse effects in mice, thereby causing trouble to the widely held hypothesis.

Revisiting the study, Diane Dickel of the Lawrence Berkeley National Laboratory in California, and colleagues used the CRISPR-Cas9 technology to delete certain strands of non-coding DNA from the genome of mice and found that while the animals looked fine, their brains were far from.

Knocking out certain genes caused abnormally low levels of brain cells that have been implicated in the progression of Alzheimer’s disease, while the lack of other genes caused problems in regions of the forebrain involved in memory formation.

Needless to say, variations in these genes would not be conserved via natural selection because animals with them would be less likely to survive and pass them on.

Although the precise function of many other ultraconserved sequences remains unknown, Bejerano feels confident it’s only a matter of time before we find out.


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