Jan. 18 (UPI) -- New research shows humans and mice regulate their genes in similar ways.
Because many living organisms face similar problems and ecological pressures, they sometimes develop similar solutions. When species that aren't closely related evolve similar adaptations, it's called convergent evolution.
A new study, published this week in the journal PNAS, presents new evidence of convergent evolution among humans and mice. The pair deploy similar mechanisms for regulating noncoding RNA, segments which aren't translated into proteins.
"This study highlights the importance of noncoding RNA and transposable elements in the regulation of gene expression and in the evolution of gene expression networks in mammalian genomes," Manuel Ares, professor of molecular, cell and developmental biology at UC Santa Cruz, said in a news release.
Only about 2 percent of the human genome is translated into messenger RNA molecules, which control the production of proteins responsible for all cellular functions. Scientists previously referred to all the rest as junk DNA, but more recent studies suggest the remaining 98 percent of the genome is involved in gene regulation and evolution. However, exactly what role the majority of noncoding RNA plays remains a mystery.
Many segments of noncoding RNA molecules are copied from DNA sequences known as short interspersed nuclear elements, or SINEs. The copies are inserted throughout the genome through a process called retrotransposition. When inserted near messenger RNA, the SINEs can damage genes or create new genes -- and potentially new adaptations.
In the human genome, the most common SINEs belong to a group of sequences known as Alu elements. The mouse genome doesn't feature Alu elements. The most common SINEs in the mouse genome are called B/ID elements.
The random nature of retrotransposition ensures that as lineage and species diverge, organisms develop different SINE patterns and families. The lineages of mice and humans diverged 90 million years ago.
"Surprisingly, when the mouse and human genomes were compared, the locations of SINEs were very similar, even though the SINEs themselves and the events that placed them at those locations were very different," Ares said. "We wondered what could explain this apparent convergence of SINE insertion in two independently evolving genomes."
Scientists found SINEs in mice and humans are regulated by the same mechanism when inserted into a region of messenger RNA called 3-prime untranslated region. The regulation mechanism is called Staufen-mediated decay, or SMD
Though mice and humans have evolved different types of SINEs, they both evolved the same mechanism for regulating SINE insertions.
When scientists looked at the entire genome of each species, they found 24 genes involving species-specific SINEs that are regulated by SMD.
"Normally we think of important gene expression control systems as having evolved long ago, but for regulation by SINE-mediated SMD, this cannot be the case," Ares said.