A new study has found that humans acquired from ancient viruses play an important role in switching parts of their genetic codes on and off.
Almost half of the human genome is made up of segments called mobility elements (TEs) and can hop around the genome, which is also called “jump genes.” Some of these TEs are the remains of ancient viruses that have been handed down over millions of years, embedding themselves into our ancestors’ genomes.
For decades after TES was discovered, scientists assumed they would not serve a useful purpose. However, this new study adds to increasing evidence that this statement is inaccurate.
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Far from being an infunctional fossil, these ostensibly extensible, studies suggest that dormant elongation of our DNA may be important, especially in regulating gene expression during early development. Scientists published their findings in the journal Science Advances on July 18th.
“Our genome was sequenced long ago, but many of the functions of that portion remain unknown,” said research co-author Hiromi Nakao-Inoue, a research co-author, in a statement that he is the research coordinator at Kyoto University’s Advanced Research Institute for Human Biology. “Transvertible elements are thought to play an important role in genome evolution, and its importance is expected to become more clear as research continues to progress.”
After all, it’s not that junk
TE was considered “junk” because it appears to be unrelated to protein creation. This is a molecule that builds and runs cells. Although genes hold protein blueprints, these repetitive transposeable elements have long been dismissed as “nonfunctional” DNA.
Related: Best Maps of the Human Genome Shedding Light on “Jump Genes”, Junk DNA, etc.
However, in recent years, evidence has begun to build up that these repeating parts of our genome play a role in gene regulation. For example, their codes are often used to create non-coding RNAs, molecules that act on other genes to differentiate cells and regulate embryo growth.
CRISPR also allowed for more detailed studies of dislocatable elements. The well-known gene editing tool allows scientists to peer into how TES affects chromatin structure (a mixture of DNA and proteins from which chromosomes are made), jumping the genetic activity of the embryo after fertilization.
The scientists behind the new research focused on a specific TES family called MER11. The family belongs to a large TES that entered the primate genome about 40 million years ago.
Researchers categorized sequences within the MER11 family based on their evolutionary relationships with one another. This generated four subgroups from MER11_G1 (oldest) to MER11_G4 (youngest).
To see how these TEs affect the cells, they inserted approximately 7,000 sequences into the cells in the lab dish. Sequences collected from humans and other primates were placed within stem cells and early stage neurons, and their gene activity was measured.
Their results showed that MER11_G4, the youngest member of the MER11 family, has a strong ability to activate genes. They were equipped with a unique “transcription factor binding site,” a DNA motif that serves as a key to development and a docking pad for proteins that regulate gene expression.
Subtle variations of the MER11_G4 sequence also existed between humans, chimpanzees and macaques, altering the regulatory effects of species-to-species sequences.
“The study highlights how much we still need to learn from genome sequences,” Christina Tufarelli, a geneticist at the University of Leicester’s Cancer Research Center, told Live Science that she was not involved in the study. “There is little overlooked between and within the family, especially when transposons like viruses are repeated.”
She added that the work paves several ways for future research. “This approach can be applied to translocatable elements that help to gain deeper knowledge of other elements with potential modulatory capabilities,” she said.
Tufarelli added that future experiments could remove certain portions of TES in CRISPR to help unravel the role of regulating gene expression in both health and disease.
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