You are here: Home News Martin Becker to defend thesis on understanding the regulation of the FOXP2 gene in the brain

Martin Becker to defend thesis on understanding the regulation of the FOXP2 gene in the brain

People with FOXP2 mutations develop speech and language problems. Causative mutations in the vicinity of the gene can impair the production of the FOXP2 gene product. Martin Becker has identified DNA-sequences that regulate the production of FOXP2 and determined their activity in human cells and mouse brains. The findings may facilitate the identification of mutations causing speech problems and help understand the role of FOXP2 in normal brain development.
Martin Becker to defend thesis on understanding the regulation of the FOXP2 gene in the brain

The FOXP2 gene regulates the switching on and off of many other genes. It does so in neurons that form the neuronal circuits underlying speech and language, and mutations that change the FOXP2 protein cause problems in the development of speech. Investigating the genes that are switched on or off by FOXP2 increases our understanding of the molecular mechanisms that underlie neuronal development.

Martin Becker took another angle and studied how the FOXP2 gene itself is switched on in neurons. Using the three-dimensional structure of DNA in living cells, he identified genomic regions that enhance the production of FOXP2 and characterized their activity in cultured neurons and the brains of mice.

Martin Becker identified multiple DNA elements, called enhancers, that may regulate the FOXP2 gene in the developing brain. Importantly, he saw that in a child with speech impairment a genetic rearrangement would remove enhancers from the gene, which may consequently impair the production of FOXP2 in some neurons. Becker further discovered that the activity of some enhancers is increased in the presence of the FOXP2 protein, suggesting that FOXP2 potentially increases the production of its own protein product. As this process occurs on enhancers active in the brain, it may explain why individuals with a mutated FOXP2 protein show neuronal deficits but have no problems with other organs that produce this protein. In summary, Becker’s findings reveal molecular mechanisms involved in the regulation of FOXP2 and may aid the identification of this gene’s role in typical and atypical neurodevelopment.

More information

  • Martin Becker will defend his thesis on Wednesday, October 26 at 16:30 in the Aula of the Radboud University
  • The thesis appears in the MPI Series (no 112).
About MPI

This is the MPI

The Max Planck Institute for Psycholinguistics is an institute of the German Max Planck Society. Our mission is to undertake basic research into the psychological,social and biological foundations of language. The goal is to understand how our minds and brains process language, how language interacts with other aspects of mind, and how we can learn languages of quite different types.

The institute is situated on the campus of the Radboud University. We participate in the Donders Institute for Brain, Cognition and Behaviour, and have particularly close ties to that institute's Centre for Cognitive Neuroimaging. We also participate in the Centre for Language Studies. A joint graduate school, the IMPRS in Language Sciences, links the Donders Institute, the CLS and the MPI.


Max Planck Institute
for Psycholinguistics


Street address
Wundtlaan 1
6525 XD Nijmegen
The Netherlands

Mailing address
P.O. Box 310
6500 AH Nijmegen
The Netherlands

Phone:   +31-24-3521911
Fax:        +31-24-3521213

Public Outreach Officer
Charlotte Horn

Image right