Finches. Click to hear the two male finches, a zebra finch and a society finch, singing. It seems they need a properly functioning FoxP2 gene to learn their songs, just as humans need the gene to master articulate speech.
The FoxP2 gene is the only genetic basis of speech yet identified, although exactly what it contributes has remained a mystery. Without a normal FoxP2 gene people do not articulate their words well and also have some problems with syntax. It turns out that songbirds also require a properly functioning FoxP2 gene if they are to sing their song accurately and completely, says an article in the December PLoS Biology (available online here) by Constance Scharff and others. Thus, we at last have an experimental method of probing the role of FoxP2 in vocal development. Apparently the gene is important in helping young birds/people learn to imitate the sounds chirped/spoken around them.
An earlier posting (Cheep Cheep vs Mama) reported that zebra finches learn to sing by hearing a more experienced bird singing. : "The young bird remembers the sound and through some 'magical' motor process makes something like the same sound. The bird hears the sound it makes and compares it with the remembered sound. Cycling through this process many times the bird is able to reproduce the sound with greater and greater accuracy. At first the sounds the birds make are quite nondescript; essentially they are undifferentiated noise. But over time the birds become more and more adept at making the sounds they have heard and by the time they are mature they can make the characteristic song of the zebra finch." It appears that Foxp2 is critical to this cycling
In experiments with zebra finches whose FoxP2 gene were 'knocked down' (disabled) the birds went through this cycling process but did not have good results. The fact that they respond to the sounds of their 'tutors' and try to master the song suggests that the gene is irrelevant to the basic urge to sing and, by extension, it also suggests the gene is irrelevant to the human urge to speak. Urges are one thing; ability another. Without a functioning FoxP2 neither birds nor humans become very adept.
The experimental design leaves the reason for the failure somewhat ambiguous. The birds could have a problem with either their motor learning or their motor activity, although the authors lean heavily to the failed-motor-learning explanation. They suggest further experimentation might test this hypothesis by having finches learn the songs normally and then, once they are adults, knocking down FoxP2 and observing their behavior. If they can still sing normally, the problem would seem to be in the learning stage.
Their current hypothesis is that disabling FoxP2 interferes with the cycling process in which steady practice moves the bird from making random noises to singing the zebra finch's song. Evidence for this explanation comes from a set of experiments in which other young finch's were prevented from going through normal cycles even though they had normal FoxP2 functioning. Perturbed auditory feedback in young birds leads to syllabic repetitions in songs and, of course, deafening young birds leads to highly variable syllables. These problems are similar in kind to the ones produced by disabling FoxP2.
In normally functioning young birds, FoxP2 might be providing some kind of reinforcement when a birds own vocalizations match the soun ds ohe older, "tutor" bird. It cannot be quite that direct, however, because FoxP2 is a transcription factor. In other words, it controls the operation of other genes, either by promoting or inhibiting their activity. In this case, FoxP2 might be promoting or inhibiting the plasticity of the brain during learning. At this point in the research there is not enough evidence to prefer one explanation over the other.
Even so, the research is making discoveries that are surprisingly useful to this blog. Songbirds seem so distantly related to humans that there is no special reason to expect them to provide useful guides to speech biology. The need to learn the sounds of one's fellows, however, suggests a similar process could underlie the phonological development of both species. And now the discovery that this development shares a common dependence on FoxP2 is both startling and encouraging. The relation between birdsong and human speech had always seemed a bit too Disneyesque to be true, but now that the idea is demonstrated we can take encouragement from the thought that the biology of speech's phonological component can be explored in the laboratory.
For this blog, the research strongly argues that the gene is critical to mastering the phonological ability to make the sounds used by the speaking community where a person is reared. Infants must somehow compare their output with the sounds others make and learn to be more accurate in their pronunciation. If FoxP2 controls this process, it is fundamental to speech.
And if the existence of a speaking community truly requires Foxp2, dating the rise of that gene becomes crucial to the story of speech origins. When it was first identified as important to human speech, FoxP2 was calculated to have reached its human form only about 200,000 years ago. If that date holds, the scenario developed on this blog is going to need very heavy revision. Either speech has developed a number of subtle features with amazing speed, or else the gesture theory of speech origins has been given a strong boost.
A Third possibility is that the date is wrong. I lean in that direction because it does the least damage to the existing scenario, and because there is evidence to support a later date. Back in 2006 this blog reported a paper (See: Conference:: FOXP Gene May be Older) that pushed the date back to 1.8/1.9 million years ago, much more in tune with the work on this blog.
Supporting evidence for an older date has also come from a report in Current Biology (abstract here) that Neanderthals had the same form of FoxP2 as found today in Homo sapiens. Since the two lines split well before the originally proposed date for the gene, the date has strong empirical evidence against it.