Whether they're staring at us, barking at us or licking our faces, dogs are often eager to interact with humans and are highly attuned to our behaviors. But how did man's best friend go from weary wolf to friendly Fido?
New research suggests that the answer may be genetic. The study, published in the journal Science Advances, identifies a series of gene mutations that may make your puppy more amenable to playing with people. Similar mutations are found in humans and are known to eliminate a fear of strangers.
Princeton University biologist Bridgett vonHoldt has spent much of her career studying genetic structures of canines, trying to figure out just what makes a dog a dog. About seven years ago, she led a study that examined more than 48,000 genetic mutations that separate domestic dogs from wolves. One of the gene regions that piqued her interest can be found on chromosome 6. It's similar to one in humans that is associated with a disorder called Williams syndrome.
One of the most noticeable symptoms of Williams syndrome is that people with it are often "hypersocial," vonHoldt tells Smithsonian.com, and often display no fear of strangers.
"This seemed like a pretty decent place to start to give a molecular mechanism for changes in behavior that might be important for a species to be domesticated," vonHoldt says.
About three years ago, she came into contact with Monique Udell, an Oregon State University psychologist who has focused her research on the social bonds between dogs and humans, and how that's affected the animals.
"It seemed like a really great idea to join forces," vonHoldt says.
Udell already had quite a few blood samples that she collected from a variety of dogs and captive wolves—creatures that had been tested to determine how much they paid attention to people and whether they sought contact with people, even strangers. Through sequencing DNA from these blood samples and comparing them to how the dogs performed in the behavioral tests, vonHoldt and Udell were able to show significant differences in the drive to socialize with humans between dogs and wolves, according to the study.
"Dogs spend a lot of time looking at a human and wolves spend very little time," vonHoldt says. When looking at the genetic data, they found that these differences strongly correlated with mutations on the genetic region associated with Williams syndrome. Dogs with the mutations on the genes studied that were linked to Williams syndrome were much more socially inclined toward people than the wolves (and occasional dogs) that didn't have them.
VonHoldt stresses that this study doesn't seek to explain the process through which dogs were domesticated, a hotly debated and controversial topic. Instead, it attempts to explain a biological mechanism for how dogs evolved through domestication.
"This can be built on whatever domestication origin hypothesis you have," vonHoldt says, speculating that wolves with these mutations might have been the first creatures to stray near humans for food and companionships thousands of years ago.
“It is great to see initial genetic evidence supporting the self-domestication hypothesis or ‘survival of the friendliest,’” Brian Hare, an evolutionary anthropologist at Duke University who studies how dogs think and learn, tells Science News about vonHoldt's research. “This is another piece of the puzzle suggesting that humans did not create dogs intentionally, but instead wolves that were friendliest toward humans were at an evolutionary advantage as our two species began to interact.”
This research "may be one of the first studies to ever identify the specific genetic variants that were important for turning wolves into dogs," Cornell University biologist Adam Boyko tells The New York Times. But he cautioned not to draw strong conclusions because of the latest study's small sample size (just 18 dogs and ten wolves).
Already, vonHoldt is working on the next step for this research: investigating how (and if) these genetic mutations lead to behavioral changes in dogs. In humans with Williams syndrome, she noted, the deletions of certain genes suppress the expression of other "core genes," leading to the disorder.
"What I don't know is if that's what the [mutations] are doing in the canines," vonHoldt tells Smithsonian.com.