Talking Headlines: Simon Fisher

Simon is director of the Max Planck Institute for Psycholinguistics, and Professor of Language and Genetics at the Donders Institute for Brain, Cognition and Behaviour, both in Nijmegen, the Netherlands. He is interested in tracing the functional links between genes, brains and human traits like speech, language and reading. Simon’s research aims for a multi-disciplinary viewpoint, trying to integrate data from genomics, psychology, neuroscience, developmental biology and evolutionary anthropology. He is keen on communicating science in an accessible but accurate way, on Twitter (@ProfSimonFisher) and beyond. He has given talks at international conferences across a diverse range of fields, and spoken to school, student and public audiences, including at the Rome Science Festival and New Scientist Live. Simon is an elected fellow of the Royal Society of Biology, awards include the Francis Crick Lecture and Medal, and the Eric Kandel Young Neuroscientists Prize.

Hi Simon, one of your main contributions to the field of neurogenetics is the discovery of the FOXP2 gene. Why is this gene special?

I’m not sure that “special” is the right word, but the main reason why I find FOXP2 so interesting is because of what happens when this gene is disrupted. People who carry rare mutations that damage FOXP2 have unexpected problems mastering the rapid coordinated movement sequences involved in speech. Most people with FOXP2 mutations also show impairments in diverse aspects of spoken and written language. Although affected people sometimes have reduced general cognitive performance, the disproportionate impact on verbal skills makes this disorder different from the kinds of intellectual disability that geneticists typically study. By investigating effects of FOXP2 on brain development and function, the gene offers a molecular window into some of the neurobiological pathways that help us learn to speak.

Is it true that FOXP2 is still referred to as “the gene for language”? Can you tell us why this is not a great definition.

Over the years, I’ve repeatedly emphasized in research articles, reviews, talks and interviews that FOXP2 can’t accurately be called “the gene for language” (or “the language gene”). It’s frustrating how often the phrase shows up, particularly in the media. To be clear, FOXP2 doesn’t exist specially to bestow humans with the gift of the gab. It’s a regulatory gene with a deep evolutionary history, present in similar form in many distantly related non-human animals. In zebra finches the gene apparently contributes to learning of birdsong, and in mice it has been linked to motor skills and vocal behaviours; that’s just a few findings from studying species that carry it. Plus, FOXP2 is not only important for the brain, but is active in other tissues, including the lung, heart and skeleton, for example. That FOXP2 has multiple roles in the body isn’t unusual – most regulatory genes work this way. Like other genes that aren’t on the sex chromosomes, people normally inherit two working copies of FOXP2, one from mum, the other from dad. When one FOXP2 copy carries a mutation, that’s enough to disturb brain function, derailing speech and language development, while other tissues seem to do fine with only one working copy.

Very recently FOXP2 was again at the centre of media coverage in the context of new studies looking at its potential role in human evolution. Was the reporting accurate?

That’s another complex scenario that, in oversimplistic form, has fuelled the popular “language gene” perspective. After we implicated FOXP2 in a speech/language disorder, it made sense to examine the evolutionary trajectory of the gene, and the protein it encodes, in primates and hominins. These analyses revealed that a couple of protein sequence changes occurred on our lineage, after splitting from the lineage that led to chimpanzees. Initial studies suggested that the changes arose within the past 100,000 years or so, but sequencing of archaic hominin DNA supports a more ancient origin, by showing that we share these changes with Neanderthals (who split from us >600,000 years ago). The early studies also reported recent Darwinian selection at the human FOXP2 locus, but a new paper, armed with more comprehensive datasets from next-generation sequencing of different populations, has clearly refuted that. So now, older headlines lauding FOXP2 as the magical trigger that made us human have been replaced by similarly confused statements like “it turns out the evolution of language can’t be explained by one gene after all”. The bottom line, of course, is that language is a complex trait, a sophisticated suite of cognitive abilities, and the underlying genetic architecture involves many genes, interacting with each other in intricate networks. The idea that one molecular factor could by itself explain the emergence of unique human capacities is not (and was never) biologically plausible. FOXP2 was only ever going to be one piece of a complicated puzzle.

Is it safe to say that there is no such thing as a gene for language, for maths, for IQ or other particular ability?

Geneticists often test for correlations between particular gene variants that people carry and variations in an observed trait, using the human population as a kind of natural experiment. A trait might involve inter-individual variability (for example: IQ, maths skills, reading abilities) or pathology (intellectual disability, dyscalculia, dyslexia, and so on), but similar principles apply. On seeing association between variation in a gene and a trait, some people use the “gene for X” terminology as a convenient shorthand. But that framing reinforces the popular misconception of genes as abstract entities that directly specify traits, including key aspects of human cognition and behaviour. Actually, there’s an enormous gap between DNA and the distal outcome. Many genes encode information for building proteins (enzymes, signals/receptors, transporters etc.) which interact with each other to provide the molecular machinery of our cells. Networks of proteins work together to influence how brain cells (neurons) first proliferate, move to their final locations, become specialized, and wire up to other neurons. When, where and at what level a gene is active are also crucial for the changing of strengths of neural connections during learning. But there is no one-to-one mapping between a single gene and a specific neural circuit, and the indirect paths from circuits to behaviour add another layer. That doesn’t mean that genetic studies are a waste of time, but rather that we should appreciate the tangled webs of mechanisms that connect genes and cognition, and ensure our thinking about these questions is rooted in biological realities.

Are there other concepts of genetics that are often misunderstood? How do you think we can get past routine misconceptions about this field of science?

I believe it’s possible to get people engaged with science without the need for sensationalism and while still including the grey areas. I never seem to find time to write a blog, but in the past few months I’ve been experimenting with using threads on Twitter to try and remedy some more common misconceptions of genetics. For instance, I’ve tweeted about how heritability is a statistical description of variation in a population, rather than an inherent property of a person’s biology. I’ve explained what it means to share ~98.8% of your genes with a chimpanzee, but only 50% of your genes with your sister (spoiler: “sharing” is a notoriously slippery concept in genetics). And I’ve argued that genomes are absolutely nothing like blueprints. If it’s possible to get across a nuanced picture of science, even within the limitations of Twitter then perhaps there is hope!

Well, now you have a blog post Simon! Thank you for explaining very clearly many complex concepts. I feel this post might remain current for a while, but hopefully we will stop seeing “the language gene” and “the language for X” expressions in the headlines.