A UCLA-led study reveals a new role for a gene that's associated with autism spectrum disorder, intellectual disability and language impairment.
The gene, Foxp1, has previously been studied for its function in the neurons of the developing brain. But the new study reveals that it's also important in a group of brain stem cells -- the precursors to mature neurons.
This discovery really broadens the scope of where we think Foxp1 is important. And this gives us an expanded way of thinking about how its mutation affects patients." Bennett Novitch, member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA and the senior author of the paper
Mutations in Foxp1 were first identified in patients with autism and language impairments more than a decade ago. During embryonic development, the protein plays a broad role in controlling the activity of many other genes related to blood, lung, heart, brain and spinal cord development. To study how Foxp1 mutations might cause autism, researchers have typically analyzed its role in the brain's neurons.
"Almost all of the attention has been placed on the expression of Foxp1 in neurons that are already formed," said Novitch, a UCLA professor of neurobiology who holds the Ethel Scheibel Chair in Neuroscience.
In the new study published in Cell Reports , he and his colleagues monitored levels of Foxp1 in the brains of developing mouse embryos. They found that, in normally developing animals, the gene was active far earlier than previous studies have indicated -- during the period when neural stem cells known as apical radial glia were just beginning to expand in numbers and generate a subset of brain cells found deep within the developing brain.
When mice lacked Foxp1, however, there were fewer apical radial glia at early stages of brain development, as well as fewer of the deep brain cells they normally produce. When levels of Foxp1 were above normal, the researchers observed more apical radial glia and an excess of those deep brain cells that appear early in development. In addition, continued high levels of Foxp1 at later stages of embryonic development led to unusual patterns of apical radial glia production of deep-layer neurons even after the mice were born. Related Stories
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