Faulty versions of the Foxp2 gene disrupt neurons’ ability to form synapses in brain regions involved in speech, a new study shows. Mutations of a gene called Foxp2 have been linked to a type of speech disorder called apraxia that makes it difficult to produce sequences of sound. A new study from
Mutations in the Foxp2 gene disrupt neuron function, causing an overproduction of a protein, dynactin1. This imbalance affects motor proteins, impairing molecule transportation within cells and hindering formation of synapses and dendrites. These changes lead to the speech disorder apraxia, according to a study by MIT and National Yang Ming Chiao Tung University.
In a study of mice, the researchers found that mutations in Foxp2 disrupt the formation of dendrites and neuronal synapses in the brain’s striatum, which plays important roles in the control of movement. Mice with these mutations also showed impairments in their ability to produce the high-frequency sounds that they use to communicate with other mice.
Fu-Chin Liu PhD ’91, a professor at National Yang Ming Chiao Tung University in Taiwan, is the senior author of the study, which was published on May 4 in the journal. Liu and Graybiel also worked together on a 2016 study of the potential link between Foxp2 andpaper are Hsiao-Ying Kuo and Shih-Yun Chen of National Yang Ming Chiao Tung University.Children with Foxp2-associated apraxia tend to begin speaking later than other children, and their speech is often difficult to understand.
In that study, the researchers showed that mice engineered to express the human version of Foxp2, which differs from the mouse version by only twobase pairs, were much better at learning mazes and performing other tasks that require turning repeated actions into behavioral routines. Mice with human-like Foxp2 also had longer dendrites — the slender extensions that help neurons form synapses — in the striatum, which is involved in habit formation as well as motor control.
One of these molecular motors is the dynein protein complex, a large cluster of proteins that is responsible for shuttling molecules along microtubule scaffolds within cells. Those motors are needed to shuttle molecules that are necessary for dendrite growth and synapse formation on dendrites. With those molecules stranded in the cell body, neurons are unable to form synapses to generate the proper electrophysiological signals they need to make speech production possible.
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