Like babbling babies, songbirds learn to vocalize by mimicking their elders. Now, researchers have found that a gene responsible for clear pronunciation in humans is also critical for proper song development in zebra finches. The study, reported 4 December in PLoS Biology, suggests that bird brains can help scientists understand speech and speech disorders in humans.
Dubbed the "speech gene," FOXP2 was first identified in 2001 when scientists found a mutated version in a family with severe speech problems. The gene is believed to code for a protein that influences coordination between mouth movements and speech (ScienceNOW, 3 October 2001). Since its discovery, researchers have found that the gene plays a role in the development of language (ScienceNOW, 14 August 2002), that mice need the gene to emit characteristic ultrasonic sounds (ScienceNOW, 21 June 2005), and that it plays a role in bat echolocation (ScienceNOW, 19 September).
After researchers discovered in 2004 that FOXP2 is expressed in the same areas of the brain in humans and zebra finches, a song-learning bird, neurobiologist Constance Scharff of the Max Planck Institute for Molecular Genetics in Berlin began to investigate whether such birds could help scientists understand how humans learn language. Scharff and her colleagues used RNA interference (RNAi), a procedure that inhibits gene expression, to reduce the levels of FOXP2 in zebra finches. When the birds were 23 days old, the age at which song learning is known to begin, the researchers injected the gene-silencing RNA strands into seven male zebra finches' brains, using 10 finches as controls. The birds were kept in sound isolation chambers with adult males, who acted as tutors just as they would in the wild. Over a period of 60 days, the team recorded the songs of the RNAi-treated birds and their control counterparts and analyzed them to see how well they replicated their tutors' songs.
Birds with reduced FOXP2 were less accurate in copying the songs and their syllables were more "wobbly," meaning they varied each time they were produced, the researchers discovered. Scharff says this suggests that the birds had difficulty using the sensory information from the tutors to modify their motor outputs. The condition looks similar to that seen in patients with developmental verbal dyspraxia, a disorder that affects word production and grammar. "The general language community hasn't yet accepted the bird as a model," Scharff says. "But birds are not stupid. This study brings that home."
Because the RNAi wasn't used to dampen FOXP2 activity until 23 days after the birds hatched, the new study shows that the gene has a role beyond embryonic development, says neurogeneticist Simon Fisher of the University of Oxford in the U.K. "The gene, at least in songbirds, may have important active functions in [neural] circuits," he says. Neurogeneticist Daniel Geschwind of the University of California, Los Angeles, agrees, adding that the study opens a window into the integration of sensory and motor functions. "It's a beautiful system for looking at this learning," he says.