The story of how the leopard got its spots or the tiger its stripes offers just enough intrigue to be the subject of myth. But now modern science can one-up those “Just So Stories,” with genetics.
By tracking the DNA tweaks that give rise to the blotchy patches of white that adorn piebald (or pinto) horses, dogs and other animals, scientists created models to explain the spots, reports Ian Sample for The Guardian. The work could help researchers understand other conditions that cause disease in humans, Sample writes.
Past research showed that altering the so-called Kit gene could turn off melanocytes—pigment-producing structures inside cells. The prevailing thought was that this mutation could also slow down those pigment-carrying cells in the embryo’s early development. This would prevent them from spreading evenly through the body, leaving leave the bellies and head of some animals free of melanocytes, producing white patches.
Upon closer study, mathematical biologist Christian Yates and his colleagues found that cells carrying mutated Kit genes actually move faster than other cells. But as the cells spread out, they didn’t multiply very well, causing the white, unpigmented patches. The team also found out that the pigment cells moved and multiplied in a random way, which is why two piebald animals can look very different from one another.
Based on these observations, they were able to build a model to replicate the piebald patterns and examine how different rates of cell growth and movement could affect the patch size. They report their findings in a paper published last week in Nature Communications.
“There’s a randomness in the way the cells behave which means that the white patch you get is never the same, even in genetically identical individuals,” Ian Jackson, an author on the paper from Edinburgh University, tells Sample.
“We’re interested in the patterning because it’s an analogy for these more serious diseases,” Yates tells The Guardian. If applied to other conditions and diseases, the model also explains why even genetically identical twins could have the same disease but may not necessarily experience the same severity of symptoms.
The model could help research in conditions such as Hirschsprung’s disease, where nerve cells don’t grow as needed in the gut, or Waardenburg syndrome, a form of deafness, Sample reports.