THIS ARTICLE IS MORE THAN FIVE YEARS OLD
This article is more than five years old. Autism research — and science in general — is constantly evolving, so older articles may contain information or theories that have been reevaluated since their original publication date.
People with fragile X syndrome, the most common inherited form of autism, show a wide range of symptoms, including intellectual disability, speech delay and social anxiety. But it all starts with the loss of one protein: FMRP.
Kimberly Huber, associate professor of neuroscience at the University of Texas Southwestern in Dallas, has spent much of her career studying the complex role of FMRP in a neuron.
On Saturday, Huber sat with SFARI.org at the 2011 Society for Neuroscience annual meeting in Washington, D.C. In this video, she describes how FMRP helps make proteins at the synapse, the junction between neurons, even when the genetic instructions for doing so are located far away in the nucleus.
FMRP binds to messenger RNA in the nucleus, preventing it from being translated into protein, and shuttles it down neuronal branches called dendrites. Once at the synapse, activation by the chemical messenger glutamate triggers FMRP to release its cargo. Synaptic activity, in other words, can affect protein production in large thanks to FMRP.
For more reports from the 2011 Society for Neuroscience annual meeting, please click here.
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