Researchers examine the effects on the fruit fly intestine of the protein responsible for Fragile X syndrome in humans. 

Researchers uncover the central role of a protein linked to Fragile X Syndrome in mice, one of the leading causes of autism and intellectual disability.

In Fragile X syndrome—a genetic mishap that results in cognitive delays—the lack of a translation-repressing protein leads to the rampant accumulation of other proteins in the mouse brain.

The protein encoded by the gene that causes Fragile X in humans partners with another protein, dNab2, to alter gene expression in fruit fly neurons.

Defects in TOP3β may lead to neural development problems in people with fragile X syndrome and schizophrenia.