Drosophila fragile X protein DFXR regulates neuronal morphology and function in the brain

Joannella Morales, P. Robin Hiesinger, Andrew J. Schroeder, Kazuhiko Kume, Patrik Verstreken, F. Rob Jackson, David L. Nelson, Bassem A. Hassan

Research output: Contribution to journalArticlepeer-review

202 Scopus citations


Mental retardation is a pervasive societal problem 25 times more common than blindness for example. Fragile X syndrome the most common form of inherited mental retardation is caused by mutations in the FMR1 gene. Fragile X patients display neurite morphology defects in the brain suggesting that this may be the basis of their mental retardation. Drosophila contains a single homolog of FMR1 dfxr (also called dfmr1). We analyzed the role of dfxr in neurite development in three distinct neuronal classes. We find that DFXR is required for normal neurite extension guidance and branching. dfxr mutants also display strong eclosion failure and circadian rhythm defects. Interestingly distinct neuronal cell types show different phenotypes suggesting that dfxr differentially regulates diverse targets in the brain.

Original languageEnglish (US)
Pages (from-to)961-972
Number of pages12
Issue number6
StatePublished - Jun 13 2002

ASJC Scopus subject areas

  • Neuroscience(all)


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