Neuronal processes (axons, dendrites) are highly autonomous from the soma. This allows for synaptic plasticity (i.e., growth or shut down of receptors), alterations in spine morphology, and specific types of navigation towards extracellular guidance cues. Holt and Bullock implicate three major examples of this capability in neurons:
1) Synapse Plasticity. mRNA localization can affect the neuron’s ability to respond to activations with structural changes. For example, consider transcription of the activity-regulated cytoskeletal associated (Arc) gene. In activated hippocampal neurons, Arc mRNA is sent to dendrites that contain recently activated synapses with NMDA receptors and is locally translated into protein, where it probably modulates spine morphogenesis (i.e., causes shape changes in dendrites). It has a critical role in long term but not short term memory, as suggested by selective knock-out mice studies, where researchers replaced the 3′ untranslated region of the gene with a nonlocalizing transcript sequence. There are other examples in which mRNA localization can be necessary for synaptogenesis, the most important form of synapse plasticity. For example, localizing the neuropeptide-encoding sensorin mRNA into synapses is probably necessary for synapse formation in mechanosensory neurons in Aplysia and Helix pomatia.
2) Directionally Responsive Axon Protrusion. In neurodevelopment, changes in growth and directional steering of axons is dependent upon extracellular cues. For example, in growth cones beta-actin mRNA is concentrated near regions of attractive stimulus gradients, indicative of how the cell can transduce extracellular gradients into intracellular asymmetry. Inhibiting local beta-actin mRNA translation blocks attractive cues, but not repulsive ones, turning towards the favored extracellular stimuli. Presumably there are similar mechanisms that target other aspects of axon guiding during neurodevelopment to weave the intricate neuronal networks that underly everything we think, do, and say.
3) Spatially Dependent Gene Expression. mRNA’s translated in particular regions of the neuron may be modified at some amino acid residues selectively depending upon which part of the cell they are in. When the protein travels back to the nucleus following translation, its pattern of phosphorylation can then signal which part of the cell the mRNA was translated in, which can change patterns of gene expression following the same transcription factor entering the nucleus. For example, mRNA encoding the transcription factor cAMP response element–binding protein (CREB), which promotes the survival of certain neurons, can be translated locally in axons in response to neurotrophic nerve growth factor. CREB is localized to the distal axons of neurons (as indicated by Boyden chamber axon isolation and fluorescent in situ hybridization), its mRNA is selectively translated in response to local innervations of nerve growth factor, and the phosphorylation patterns of CREB at sites other than serine-133 will affect its transcriptional effects. Thus the cell can tell whether the pCREB in the nucleus came from distal axons or from the soma, and alter gene expression accordingly.
Casadio A, et al. 2003 Distribution of sensorin immunoreactivity in the central nervous system of Helix pomatia: Functional aspects. 10.1002/jnr.1084.
Li L, et al. 2005 The neuroplasticity-associated arc gene is a direct transcriptional target of early growth response (egr) transcription factors. doi:10.1128/MCB.25.23.
Leung KL, et al. 2006 Asymmetrical bold beta-actin mRNA translation in growth cones mediates attractive turning to netrin-1. doi:10.1038/nn1775.
Cow LJ, et al. 2008 Intra-axonal translation and retrograde trafficking of CREB promotes neuronal survival. doi:10.1038/ncb1677.
Holt CE, Bullock SL. 2009 Subcellular mRNA localization in animal cells and why it matters. doi:10.1126/science.1176488