FIG. 8.

JNK binding to BMPRII is required for BMP-induced dendritogenesis and microtubule stabilization. (A and B) Deletion of JNK binding regions, JBR-AB, of BMPRII blocks BMP-dependent dendrite formation. Primary cortical neurons were infected with adenoviruses encoding GFP empty vector, BMPRII full length (FL), or BMPRII ΔJBR-AB and treated with BMP7 for 48 h after 4 DIV. The number of dendrites per neuron in GFP-expressing neuronal cells (A) that costained with the dendrite-specific Map2 (a+b) antibody (data not shown) was quantified. The fold changes in dendrite numbers relative to the unstimulated GFP empty control are shown (B), with 30 to 40 neurons analyzed per condition. Shown are the means + the SEM of three independent experiments (P < 0.0001 [Student t test] for points infected with GFP, FL). Scale bar, 20 μm. (C) Deletion of JBR-AB on BMPRII blocks BMP7-induced microtubule stabilization in dendrites of cortical neurons. Primary cortical neurons were infected with the indicated adenoviral constructs and incubated with nocodazole (5 μM) in the presence or absence of BMP7 for 1 h. The length of stable microtubules in dendrites (Ace MT) was expressed as a percentage of total dendrite length (GFP staining) and analyzed as shown in Fig. 1B. Shown are the means ± the SEM for two independent experiments with at least 20 cells analyzed per condition (P < 0.05 [Student t test] for the category of 40% and up in points infected with GFP, BRII). (D) Model of BMP7-induced dendrite formation in neurons. BMPRII serves as a scaffold that binds cytoskeletal regulators such as JNK and LIMK1 and thus is poised in neurite tips to mediate rapid remodeling of the actin and microtubule networks in response to BMP7.