New research from the laboratory of Whitehead Institute member Yukiko Yamashita confirms that junk DNA plays a key role in speciation.
More than 10% of our genome is made up of repetitive, meaningless sections of genetic material that do not code for any proteins.
In a series of papers over the years, Whitehead Institute member Yukiko Yamashita and his colleagues have proven that so-called junk DNA is not as useless as it seems at first glance. In fact, it plays an important role in the cell: this DNA works with cellular proteins to keep all of the cell’s individual chromosomes together in one nucleus.
During their work, the authors studied how this part of DNA affects the fertility and survival of species, then scientists got the first hint that these repetitive sequences may play a role in speciation.
To test this, the researchers removed a protein called Prod, which binds to a specific junk DNA sequence in the Drosophila melanogaster fruit fly, causing their chromosomes to scatter outside the nucleus into tiny balls of cellular material and kill the insects.
If this piece of “junk” DNA was necessary for the survival of one species, but was absent in the other, it could mean that the two species of flies over time have developed different sequences for the same role. And since junk DNA played a role in keeping all chromosomes together, researchers wondered if these evolutionary differences could be one of the reasons different species are reproductively incompatible.
To understand how differences in satellite DNA can lead to reproductive incompatibility, the researchers decided to focus on two branches of the fruit fly family tree: the classic laboratory model of Drosophila melanogaster and its closest relative, Drosophila simulans. These two species diverged from each other about 2-3 million years ago.
Researchers can breed a female Drosophila melanogaster with a male Drosophila simulans, but as a result, the offspring are either sterile or die.
The authors bred flies and then studied the tissues of the offspring to understand why this is so. When the authors looked at the hybrid tissues, they found that their phenotype was exactly the same as if someone had violated the “junk” DNA of a pure species. The chromosomes were scattered around rather than encapsulated in a single nucleus.
As a result, the authors concluded that “junk” DNA mutates regularly and literally sets the crossing strategy for different species.