Colloquium paper: the cognitive niche: coevolution of intelligence, sociality, and language.

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Abstract

Although Darwin insisted that human intelligence could be fully explained by the theory of evolution, the codiscoverer of natural selection, Alfred Russel Wallace, claimed that abstract intelligence was of no use to ancestral humans and could only be explained by intelligent design. Wallace's apparent paradox can be dissolved with two hypotheses about human cognition. One is that intelligence is an adaptation to a knowledge-using, socially interdependent lifestyle, the "cognitive niche." This embraces the ability to overcome the evolutionary fixed defenses of plants and animals by applications of reasoning, including weapons, traps, coordinated driving of game, and detoxification of plants. Such reasoning exploits intuitive theories about different aspects of the world, such as objects, forces, paths, places, states, substances, and other people's beliefs and desires. The theory explains many zoologically unusual traits in Homo sapiens, including our complex toolkit, wide range of habitats and diets, extended childhoods and long lives, hypersociality, complex mating, division into cultures, and language (which multiplies the benefit of knowledge because know-how is useful not only for its practical benefits but as a trade good with others, enhancing the evolution of cooperation). The second hypothesis is that humans possess an ability of metaphorical abstraction, which allows them to coopt faculties that originally evolved for physical problem-solving and social coordination, apply them to abstract subject matter, and combine them productively. These abilities can help explain the emergence of abstract cognition without supernatural or exotic evolutionary forces and are in principle testable by analyses of statistical signs of selection in the human genome.

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A forkhead-domain gene is mutated in a severe speech and language disorder.

Cecilia S L Lai, Simon E. Fisher, Jane Hurst … (2001)

Individuals affected with developmental disorders of speech and language have substantial difficulty acquiring expressive and/or receptive language in the absence of any profound sensory or neurological impairment and despite adequate intelligence and opportunity. Although studies of twins consistently indicate that a significant genetic component is involved, most families segregating speech and language deficits show complex patterns of inheritance, and a gene that predisposes individuals to such disorders has not been identified. We have studied a unique three-generation pedigree, KE, in which a severe speech and language disorder is transmitted as an autosomal-dominant monogenic trait. Our previous work mapped the locus responsible, SPCH1, to a 5.6-cM interval of region 7q31 on chromosome 7 (ref. 5). We also identified an unrelated individual, CS, in whom speech and language impairment is associated with a chromosomal translocation involving the SPCH1 interval. Here we show that the gene FOXP2, which encodes a putative transcription factor containing a polyglutamine tract and a forkhead DNA-binding domain, is directly disrupted by the translocation breakpoint in CS. In addition, we identify a point mutation in affected members of the KE family that alters an invariant amino-acid residue in the forkhead domain. Our findings suggest that FOXP2 is involved in the developmental process that culminates in speech and language.

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Molecular evolution of FOXP2, a gene involved in speech and language.

Wolfgang Enard, Molly Przeworski, Simon E Fisher … (2002)

Language is a uniquely human trait likely to have been a prerequisite for the development of human culture. The ability to develop articulate speech relies on capabilities, such as fine control of the larynx and mouth, that are absent in chimpanzees and other great apes. FOXP2 is the first gene relevant to the human ability to develop language. A point mutation in FOXP2 co-segregates with a disorder in a family 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. Thus, two functional copies of FOXP2 seem to be required for acquisition of normal spoken language. We sequenced the complementary DNAs that encode the FOXP2 protein in the chimpanzee, gorilla, orang-utan, rhesus macaque and mouse, and compared them with the human cDNA. We also investigated intraspecific variation of the human FOXP2 gene. Here we show that human FOXP2 contains changes in amino-acid coding and a pattern of nucleotide polymorphism, which strongly suggest that this gene has been the target of selection during recent human evolution.

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Inferring nonneutral evolution from human-chimp-mouse orthologous gene trios.

Andrew G Clark, Stephen Glanowski, Rasmus Nielsen … (2003)

Even though human and chimpanzee gene sequences are nearly 99% identical, sequence comparisons can nevertheless be highly informative in identifying biologically important changes that have occurred since our ancestral lineages diverged. We analyzed alignments of 7645 chimpanzee gene sequences to their human and mouse orthologs. These three-species sequence alignments allowed us to identify genes undergoing natural selection along the human and chimp lineage by fitting models that include parameters specifying rates of synonymous and nonsynonymous nucleotide substitution. This evolutionary approach revealed an informative set of genes with significantly different patterns of substitution on the human lineage compared with the chimpanzee and mouse lineages. Partitions of genes into inferred biological classes identified accelerated evolution in several functional classes, including olfaction and nuclear transport. In addition to suggesting adaptive physiological differences between chimps and humans, human-accelerated genes are significantly more likely to underlie major known Mendelian disorders.