Drosophilafragile X mental retardation protein developmentally regulates activity-dependent axon pruning

Fragile X Syndrome Pruning
DOI: 10.1242/dev.015867 Publication Date: 2008-03-06T01:46:32Z
ABSTRACT
Fragile X Syndrome (FraX) is a broad-spectrum neurological disorder with symptoms ranging from hyperexcitability to mental retardation and autism. Loss of the fragile 1 (fmr1) gene product, mRNA-binding translational regulator FMRP, causes structural over-elaboration dendritic axonal processes, as well functional alterations in synaptic plasticity at maturity. It unclear, however, whether FraX primarily disease development, or both: distinction that vital for engineering intervention strategies. To address this crucial issue, we have used Drosophila model investigate developmental function FMRP (dFMRP). dFMRP expression regulation chickadee/profilin coincides transient window late brain development. During time, positively regulated by sensory input activity, required limit axon growth efficient activity-dependent pruning branches Mushroom Body learning/memory center. These results demonstrate has primary role neural circuit refinement during
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