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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.

Genetic analysis in Drosophila melanogaster has identified molecules important for the function of insect circadian clocks, and this has resulted in the elaboration of explicit biochemical models of the clock mechanism. Comparable molecular genetic analysis coupled with neuroanatomical approaches has also delineated cellular elements of the circadian pacemaker controlling insect activity rhythms. However, not much is known about the transfer of temporal information from clock cells in the insect brain to downstream neural elements or other target cells that are regulated by the clock (i.e. clock output pathways). In this review, we focus on the insect literature, with special reference to the fruitfly D. melanogaster and the hawkmoth Manduca sexta, to discuss the candidate molecules, biochemical mechanisms and cell types implicated in the clock control of behavior.