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Why don't dogs talk?

Humans have developed a unique ability to communicate through speech and language. Research focusing on the development of human language and its genetic basis focuses specifically on the developmental gene FOXP2. Evo-devo research has shown that a human-specific FOXP2 variant is key for the human ability to talk. It is likely that the human variant of the rather common FOXP2 protein was already present in Neanderthals.

Many dog lovers do not like the question in the title of this article; their four-legged friend can of course talk and “he also understands every word I say”. However, the question does not relate to the broad range of different ways dogs can communicate by way of certain movements of their bodies and body parts (eyes, ears, tail, etc.) as well as barking and growling, nor does it relate to dogs’ extraordinary ability to perceive what their owners mean or intend to do. This article deals with speech as the human ability “to signify, by their (i.e. the words’) connection and order to one another, what they (i. e. humans) conceive or think of each matter” (Thomas Hobbes 1658; Leviathan). The human ability to communicate through oral language is indeed unique. Although animals are able to attach meaning to sounds or sound groups – for example when looking for food, alerting enemies or when interacting – it can be safely assumed that speech has contributed considerably to the evolutionary success of humans.

Researchers have investigated many animals, including our closest living relatives – the chimpanzees – for their ability to actively use language elements. Studies have shown that these animals can do little more than scream, grunt, groan and shriek. This is quite in contrast to their differentiated ability to understand the meaning of sounds. Scientists from a broad range of disciplines – including anthropologists, linguists, behavioural researchers, geneticists and evolutionary researchers – have focused on the question of why this is so. Modern evo-devo research, in combination with molecular genetics, comparative genomics and palaeogenomics research, has made progress in finding an answer to this question. Although many questions remain still open, researchers generally agree that the “dream dog’s” statement in Erich Kästner’s poem “Ein Hund hält Reden” (A dog gives speeches) is incorrect: “We (animals) can speak, but we do not”. Asked why they do not speak, the dog says: “Isn’t it obvious? Humans do not deserve the pleasure of socialising with us.”

FOX proteins

Prof. Dr. rer. nat. Gudrun Rappold, Director of the Department of Molecular Human Genetics © University Hospital Heidelberg

In their efforts to elucidate the development of speech, molecular biologists in London came across a valuable lead through the discovery of a severe speech disorder of autosomal dominant inheritance in a London family. The defect was the result of a point mutation in the FOXP2 gene on chromosome 7.

For quite some time, the researchers believed that they had found a “grammar gene” as the affected members of the family were unable to produce grammatically correct sentences. However, the family were unable to speak correctly at all, not simply ungrammatically.

FOXP2 is a member of a large gene family whose gene products act as transcription factors that, like the Hox genes, play a key role in embryogenesis and morphogenesis. The FOX genes were discovered in a Drosophila mutant with a fork-shaped head (forkhead); all FOX genes have a 80 to 100 amino acid long DNA-binding domain which, in analogy to the homeobox (Hox), is referred to as forkhead box or FOX.

FOXP1 expression (red) in the neurons of the mouse striatum. The axons of the neurons are dyed green using the TUJ1 marker. © Heidelberg University Hospital

Professor Gudrun Rappold is the Director of the Department of Molecular Human Genetics at the Institute of Human Genetics at the University Hospital of Heidelberg. Rappold and her team are investigating the molecular causes of hereditary growth disorders and their neuronal aberrations in humans. Their research is specifically focused on mutations in the SHOX (“short stature homeobox gene”) gene and homologous genes that cause small stature and severe growth defects of internal organs as well as on the FOXP1 gene of which little is yet known.

The researchers from Heidelberg found deletions in the FOXP1 gene in three unrelated, intellectually handicapped patients with severe speech disorders, which suggested that the transcription factor FOXP1 plays a key role in human brain development. Rappold and her team identified the corresponding mouse gene in the basal ganglia of the striatum, a subcortical part of the forebrain with important roles in movement pathways and cognitive processes.

Mice do not talk

A lot more is known about the FOXP2 gene than about the FOXP1 gene due to the gene’s role in the development of human speech and language. The FOXP2 gene, found in a broad range of animals, including humans, has been sequenced. Sequence comparisons have shown that the gene has remained highly conserved over evolution. The corresponding mouse and chimpanzee proteins differ only in one amino acid although the lineages of rodents and primates diverged more than 80 million years ago. It can therefore be safely assumed that the gene was exposed to strong selective pressure with the result that mutations were eliminated. This assumption has been substantiated with the finding that knockout mice lacking a functional FOXP2 gene are not viable. However, humans picked up two differences around 6 to 7 million years ago when the human lineage split from that of chimpanzees. These differences could be highly significant in the development of human speech.

Professor Svante Pääbo’s group of researchers at the Max Planck Institute of Evolutionary Anthropology in Leipzig analysed the sequences and created mice in which the two “human” substitutions were introduced into the mouse FOXP2 transcription factor. “Despite friendly coaxing from the researchers, these mice did not speak,” explained Pääbo with his characteristic humour. However, he did not come up with an answer to the question as to whether Kästner’s dog was able to speak, but did not want to. Pääbo invited the linguist Professor Julia Fischer from the German Primate Centre in Göttingen to come to Leipzig in order to analyse the sounds made by the mice. She came to the conclusion that the mice could not speak. However, she found significant differences in the isolation-induced vocalisations emitted by baby mice, sounds which are inaudible for humans.

“But this is nothing dramatic and we do not yet know what is actually happening,” said Julia Fischer when reporting on new insights into the evolution of language at the 2008 “Bertha Benz Lecture”, an annual event organised by the Daimler and Benz Foundation to promote women’s contributions to science and society. Mice with human FOXP2 genes develop relatively normally and are healthy; FOXP2 gene-deficient mice die.

In subsequent investigations, the researchers found that in addition to the modifications of the ultrasound vocalisations, humanised FOXP2 genes result in reduced exploratory behaviour and lower than normal dopamine concentrations in the mouse brains. The researchers found that this was the result of altered basal ganglia structures in the striatum; as mentioned above, the basal ganglia of mice are also the site of FOXP1 expression. Human beings with a speech defect resulting from a non-functional FOXP2 allele also display changes in the striatum. The FOXP2 gene remains a hot candidate for a gene associated with human language although the picture becomes increasingly complicated the more time researchers spend investigating the gene and its potential impact.

The babbling of human infants and chicks

Zebra finches – an animal model that gives clues to the development of human language © Wilhelma, Stuttgart

The ability of birds – in particular parrots and songbirds - to articulate and imitate sounds and tones is superior to that of mammals, with the exception of humans, and perhaps dolphins. Zebra finches (Taeniopygia guttata) have long been used as a model species questioning the search for an answer to the question of how birds learn to sing. In recent years, the FOX2P gene of zebra finches has been studied in great detail. Of particular interest is the fact that songbirds learn to sing in much the same way as human infants – both start out babbling. It is assumed that babbling is necessary in order to establish auditory feedback, which is key for fine tuning what is being said,” Julia Fischer explained. By babbling, bird chicks and human infants learn to mimic their parents and eventually master the structural language of humans or the complex species-specific song of birds. The FOXP2 transcription factor of zebra finches differs in seven amino acids from that of humans. This is not surprising considering the fact that the lineages of birds and humans diverged around 300 million years ago, rather than 80 million years ago when the lineages of humans and mice diverged.

The finding that the FOXP2 gene sequences of bats (which are mammals and hence closer related to humans than birds) have a greater variability came as quite a surprise. Bats are able to orient themselves by echolocation – detecting the echoes of their ultrasonic cries. Their sensomotoric abilities are highly developed and it seems that the bat FOXP2 gene has developed separately from that of other mammals which have not developed the skill of echolocation.

Neanderthals

The general public is more interested in the question as to when humans learned to speak after they split from their “speechless” primate ancestors than in bats. Is it Homo sapiens who invented human language or were the Neanderthals or even Homo erectus already able to speak? Since no human species representatives other than Homo sapiens have survived, comparative evo-devo research has, for a long time, been unable to come up with an answer to this question.

Prof. Svante Pääbo holding a Neanderthal skull. © Max Planck Society

Svante Pääbo has become known to the public as the inventor of a method used to analyse DNA from fossil material. He has thus become the actual founder of a new field of research – palaeogenetics. Pääbo also coordinated the most ambitious scientific project ever, the sequencing of the total Neanderthal genome using bone fragments of Neanderthals that died out around 40,000 years ago. It took the consortium of more than 50 scientists five years to complete the project. When the scientists published the initial version of the Neanderthal genome sequence in 2010, one of the first questions they asked was, “Did Neanderthals have the same FOXP2 gene as H. sapiens?”.

The preliminary answer was, yes they did. This might suggest that Neanderthals were able to speak. But this does not need to be the final answer. The technical challenges associated with the sequencing of tiny amounts of ancient DNA are enormous, and the results are prone to errors. The role of FOXP2 in the development of human language is far from being clarified. Along with the news of the sequencing of the Neanderthal genome, a photo of Svante Pääbe holding a Neanderthal skull just like Hamlet was holding Yorick’s skull went around the world. For me it seems as if Pääbo is holding a monologue: “FOXP, or not FOXP - that is the question." 

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