Stathmin is required for stability of the Drosophila neuromuscular junction.

Synaptic connections can be stably maintained for prolonged periods, yet can be rapidly disassembled during the developmental refinement of neural circuitry and following cytological insults that lead to neurodegeneration. To date, the molecular mechanisms that determine whether a synapse will persist versus being remodeled or eliminated remain poorly understood. Mutations in Drosophila stathmin were isolated in two independent genetic screens that sought mutations leading to impaired synapse stability at the Drosophila neuromuscular junction (NMJ).

A retrograde neuronal survival response: target-derived neurotrophins regulate MEF2D and bcl-w.

Survival and maturation of dorsal root ganglia sensory neurons during development depend on target-derived neurotrophins. These target-derived signals must be transmitted across long distances to alter gene expression. Here, we address the possibility that long-range retrograde signals initiated by target-derived neurotrophins activate a specialized transcriptional program.

Dynein motors transport activated Trks to promote survival of target-dependent neurons.

Mutations that alter dynein function are associated with neurodegenerative diseases, but it is not known why defects in dynein-dependent transport impair neuronal survival. Here we show that dynein function in axons is selectively required for the survival of neurons that depend on target-derived neurotrophins. Stimulation of axon terminals with neurotrophins causes internalization of neurotrophin receptors (Trks).

Location, location, location: a spatial view of neurotrophin signal transduction.

Neurotrophins were originally identified as target-derived factors that regulate the survival and differentiation of innervating neurons. However, neurotrophins can also be released by presynaptic cells to stimulate postsynaptic neurons. Recent studies indicate that differences exist between the signaling pathways activated by neurotrophin stimulation of nerve terminals (retrograde signaling) and neurotrophin stimulation of cell bodies.