The distinct fur color of two of Australia’s rarest marsupials may be due to ‘split’ pigmentation genes, according to a study from La Trobe University. The mysterious marsupial mole, which inhabits the Australian deserts, and the black form of the endangered eastern quoll are examples of a genetic phenomenon more common among marsupials than previously thought.
In many species, color variations such as melanism (dark fur) or xanthism (yellowish fur) are considered chromatic abnormalities detrimental to survival. However, the investigation published in the journal Biology Letters shows that, in several marsupials, these variations are not only common, but may be universal within each species.
In the eastern quolls with black fur, scientists identified the absence of a DNA segment that deactivates the ASIP (Agouti Signalling Protein) gene, responsible for producing the yellowish or reddish pigmentation called pheomelanin. Interestingly, a nearly identical fault was detected in the Tasmanian devil, a related species, also with dark fur. By comparing the genetic sequences, the researchers concluded that both lost the ASIP gene independently — a clear example of convergent evolution.
The team also analyzed the recently published genome of the marsupial mole, a mammal known for “swimming” through desert sands. This species shows pale yellow fur, the result of the absence of eumelanin (the dark pigment). In this case, the mutation occurs in the MC1R (Melanocortin 1 Receptor) gene, which normally regulates the deposition of eumelanin, but is interrupted by a genetic change that prevents it from functioning.
According to the lead author, Charles Feigin, the ASIP and MC1R genes act as a “molecular switch” between the production of the two main mammalian pigments — eumelanin and pheomelanin. “When one side of this switch fails, the balance disappears and only one type of pigment is produced,” he explained.
“Although the evolutionary consequences of these color variations in marsupials are not yet fully understood, the so-called ‘split genes’ seem to play an essential role in their origin,” Feigin concludes.
