Kai von Fintel at semantics etc. blogs a Scientific American note to the effect that "Birds Share 'Language' Gene with Humans", along with links to a UCLA press release and two J. Neuroscience articles.
This research has to do with two genes called FoxP1 and FoxP2. The Sciam note is careful to put scare quotes around "language" in "'language' gene", but I suspect that's because they're not sure whether it's right to call birdsong language, and not because they've become convinced that it's misleading to talk about particular genes being "for" higher-level cognitive, behavioral or even structural features.
It's not surprising that birds and humans share particular genes -- after all, we share many genes with yeast. What's interesting is the claim that these particular genes seem to share a functional relationship with vocal learning and/or vocal performance in both zebra finches and humans. However, as I understand the papers involved, the connections so far are exciting and suggestive but far from conclusive. The two new papers suggest somewhat different ideas about the degree of specificity of the associated functions -- "vocal plasticity" or "sensorimotor integration and the control of skilled, coordinated movement" -- and both ideas are speculative. And, of course, treating individual genes as "for" higher-level functions and macroscopic structures is at best a convenient way of talking.
The main evidence from humans is that "[a] point mutation in FOXP2 co-segregates with a disorder in a family ("KE") in which half of the members have severe articulation difficulties accompanied by linguistic and grammatical impairment. This gene is disrupted by translocation in an unrelated individual who has a similar disorder" (quoting from abstract of 2002 Nature article by Enard et al.). Imaging studies (here and here) have shown that the affected family members have abnormalities in various speech-related areas of the brain: "reduced grey matter density bilaterally in the caudate nucleus, the cerebellum, and the left and right inferior frontal gyrus... In addition, increased grey matter density was found bilaterally in the planum temporale."
Michael Ullman and others think that human speech and language involve cooperation and competition between two distinct brain circuits whose functions overlap, one a (temporal/parietal-lobe) semantic memory system for storing and retrieving the properties of morphemes, words and fixed expressions, and the other a (frontal-lobe and basal ganglia) procedural memory system for putting bits of language together in new ways (see abstract here). The FoxP2 mutation reduces grey matter in several parts of Ullman's frontal/basal ganglia circuit: the caudate nucleus (part of the basal ganglia), the cerebellum (also involved in motor control) and the inferior frontal gyrus (related to Broca's area). The same mutation is also associated with increased grey matter (because of developmental compensation?) in the planum temporale, functionally dedicated to sound processing, and part of the temporal/parietal circuit(s) involved in speech and language.
On the basis of comparing human FoxP2 with the same genes in chimpanzee, gorilla, orang-utan, rhesus macaque and mouse, Enard et al. conclude that "although the FOXP2 protein is extremely conserved among mammals, it acquired two amino-acid changes on the human lineage, at least one of which may have functional consequences". They also compared "a segment of 14,063 base pairs (bp) covering introns 4, 5 and 6 of the FOXP2 gene in seven individuals from Africa, four from Europe, one from South America, five from mainland Asia and three from Australia and Papua New Guinea", and found what they characterize as "an extreme skew in the frequency spectrum of allelic variants at FOXP2 towards rare and high-frequency alleles", suggesting that FoxP2 "has been the target of selection during recent human evolution", and that the hominid innovations in this gene occured "during the last 200,000 years of human history, that is, concomitant with or subsequent to the emergence of anatomically modern humans". A word of caution: according to their model, the most likely time since the innovation is 0 years; they indulge in a certain amount of hand-waving to re-interpret this as "during the last 200,000 years".
The new "birdsong" stuff looks at expression of FoxP1 and FoxP2 in various parts of the brains of various creatures, including not only songbirds but also humans and crocodiles. For those of you who don't have subscriptions, here are the abstracts:
"FoxP2 Expression in Avian Vocal Learners and Non-Learners", by Sebastian Haesler, Kazuhiro Wada, A. Nshdejan, Edward E. Morrisey, Thierry Lints, Eric D. Jarvis, and Constance Scharff, from The Journal of Neuroscience, March 31, 2004, 24(13):3164-3175. For those of you
Most vertebrates communicate acoustically, but few, among them humans, dolphins and whales, bats, and three orders of birds, learn this trait. FOXP2 is the first gene linked to human speech and has been the target of positive selection during recent primate evolution. To test whether the expression pattern of FOXP2 is consistent with a role in learned vocal communication, we cloned zebra finch FoxP2 and its close relative FoxP1 and compared mRNA and protein distribution in developing and adult brains of a variety of avian vocal learners and non-learners, and a crocodile. We found that the protein sequence of zebra finch FoxP2 is 98% identical with mouse and human FOXP2. In the avian and crocodilian forebrain, FoxP2 was expressed predominantly in the striatum, a basal ganglia brain region affected in patients with FOXP2 mutations. Strikingly, in zebra finches, the striatal nucleus Area X, necessary for vocal learning, expressed more FoxP2 than the surrounding tissue at post-hatch days 35 and 50, when vocal learning occurs. In adult canaries, FoxP2 expression in Area X differed seasonally; more FoxP2 expression was associated with times when song becomes unstable. In adult chickadees, strawberry finches, song sparrows, and Bengalese finches, Area X expressed FoxP2 to different degrees. Non-telencephalic regions in both vocal learning and non-learning birds, and in crocodiles, were less variable in expression and comparable with regions that express FOXP2 in human and rodent brains. We conclude that differential expression of FoxP2 in avian vocal learners might be associated with vocal plasticity.
"Parallel FoxP1 and FoxP2 Expression in Songbird and Human Brain Predicts Functional Interaction", by Ikuko Teramitsu, Lili C. Kudo, Sarah E. London, Daniel H. Geschwind,and Stephanie A. White.
Humans and songbirds are two of the rare animal groups that modify their innate vocalizations. The identification of FOXP2 as the monogenetic locus of a human speech disorder exhibited by members of the family referred to as KE enables the first examination of whether molecular mechanisms for vocal learning are shared between humans and songbirds. Here, in situ hybridization analyses for FoxP1 and FoxP2 in a songbird reveal a corticostriatal expression pattern congruent with the abnormalities in brain structures of affected KE family members. The overlap in FoxP1 and FoxP2 expression observed in the songbird suggests that combinatorial regulation by these molecules during neural development and within vocal control structures may occur. In support of this idea, we find that FOXP1 and FOXP2 expression patterns in human fetal brain are strikingly similar to those in the songbird, including localization to subcortical structures that function in sensorimotor integration and the control of skilled, coordinated movement. The specific colocalization of FoxP1 and FoxP2 found in several structures in the bird and human brain predicts that mutations in FOXP1 could also be related to speech disorders.
In the unlikely event that you're still with me, you might want to take a look at these neat pictures of the emergence of acoustic structure during birdsong learning.Posted by Mark Liberman at April 7, 2004 06:49 AM