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. Author manuscript; available in PMC: 2013 May 1.
Published in final edited form as: Trends Neurosci. 2012 Feb 2;35(5):305–314. doi: 10.1016/j.tins.2012.01.002

Figure 2. A hypothetical model of a nucleolar mechanism that supports neurite growth in response to extracellular signals.

Figure 2

a, Without growth-promoting signals, basal activity of Pol1 maintains neuronal homeostasis by replacing ribosomes that were damaged by oxidation. b, Upon growth-promoting signals (e.g. BDNF), Pol1 is stimulated to produce more ribosome subunits. In BDNF-treated rat forebrain neurons, Pol1-driven transcription is activated by the TrkB-ERK1/2 signaling pathway [41]. The newly made ribosome subunits (marked in red and green) may be preferentially transferred to the growing portions of neurites supporting their growth. Such growth support may include local protein synthesis as indicated by the contribution of the newly generated ribosomes to the translating polysomes (arrowheads).