Skip to main content
. Author manuscript; available in PMC: 2011 Nov 24.
Published in final edited form as: Cell. 2010 Nov 24;143(5):826–836. doi: 10.1016/j.cell.2010.10.029

Figure 7. Model of Stk25 as a scaffolding protein acting competitively with Reelin-Dab1 signaling.

Figure 7

LKB1 is known to act in complex with STRAD to regulate cellular polarity (Alessi et al., 2006). Reelin, the receptors ApoER2 and VLDLR, and Dab1 also form a signaling complex (Hiesberger et al., 1999; Trommsdorff et al., 1998). STK25 coimmunoprecipitates with STRAD and GM130 (Fig. 2S). Overexpression of LKB1, and STRAD are known to induce the formation of multiple axons (Barnes et al., 2007; Shelly et al., 2007). Independent of its kinase activity, STK25 does so also and induces Golgi condensation (Fig. 1F, 4A). Knocking down LKB1, Stk25 or GM130 causes Golgi fragmentation/dispersion and lost axon production; the opposite to Golgi condensation and multiple axon formation (Fig. 1, 3, 4, Barnes et al., 2007; Shelly et al., 2007). The overexpression phenotypes are suppressed by Reelin stimulation. Dab1−/− neurons (Reelin signaling deficient) have multiple axons and shorter dendrites (Fig. 1F, Niu et al., 2004). Reelin stimulation induces Golgi deployment and dendrite growth, phenotypes suppressed by Stk25 expression/overexpression (Fig. 2, 6).