Language gene induces synapse formation

Language is an extremely crucial part of the human culture. It allows us to communicate our feelings, pass on stories, and relay important information to other people. From the moment we are born, we rely on language – both body language and spoken words – to build relationships and develop the skills and knowledge that we need to survive.

The left hemisphere of the brain has long been associated with speech and language comprehension, and trauma to certain areas such as Broca’s or Wernicke’s areas can permanently affect an individual’s language processing and speaking ability. What is responsible for determining what these brain structures do, though? Scientists have tur

ned to the genetic code for an answer.

One gene, called FOXP2, was dubbed “the language gene” in the mid 1990s when it was discovered that a mutation within it disturbed normal brain and lung development and ran in a family with a history of speech and language deficits. Mice with only one functional copy of FOXP2, in fact, express speech deficits as well—they do not vocalize as much as their normal counterparts. Mice without the FOXP2 gene rarely survive for longer than 21 days.

The Institut de Neurobiologie de la Méditerranée in France later showed that FOXP2 in humans controls the activity of another gene, called SRPX2, which has since been linked to epilepsy and several human speech disorders. Mutations in either of these genes impair the formation of electrical connections called synapses in the brain. This affects the brain’s ability to transmit and store information.

Hopkins researchers, led by Howard Hughes Medical Investigator Richard Huganir, have now discovered that the SRPX2 gene is not in fact unique to the human genome. After finding that increasing the gene’s concentration above normal levels in mouse brain cells prompts the development of new synapses, the team injected an SRPX2-blocking compound into fetal mice. The pups lacking the gene did not emit distress cries when separated from their mothers, indicating that they did not develop the neural pathways needed to make these cries. In essence, their “language learning” ability had been affected by the lack of the SRPX2 gene.

The team also injected fetal mice with a human mutation of SRPX2. These pups did not emit the normal distress cries either.

Since the genetic code – the four bases that make up the molecule of DNA – is universal, it is actually not a surprise that the FOXP2 and SRPX2 genes exist in both the human and the mouse genome, especially since they are both mammals. The fact that they and their mutations affect language ability similarly in both animals is of interest to scientists seeking to better understand how genes can affect language development.