Fragile X syndrome, the most common inherited form of autism, is caused by mutations that effectively turn off the FMR1 gene. People with the syndrome, as well as experimental mice lacking the FMR1 gene, show no abnormal changes in brain structure, but their cortical neurons have more dendritic spines — the sites of signaling connections, or synapses, between nerve cells. Dr. Huber and her colleagues recently found that FMRP, the protein encoded by FMR1, regulates the number and function of synapses in the hippocampus, an area of the brain involved in memory and spatial navigation. Other autism-linked genes are known to regulate synapse development and function, but whether and how they interact with FMRP has yet to be investigated. Huber's team will look for any changes in the function and structure of synapses in the hippocampi of mice lacking FMRP or other pathway genes. The scientists will also attempt to understand how the entire process is governed by signals from both the synapses and the main body of the nerve cell. The identification of other genes that interact with FMRP will begin to provide a framework for understanding the contribution of autism-linked genes to synapse development.