TY - JOUR TI - The adhesion-GPCR BAI1 shapes dendritic arbors via Bcr-mediated RhoA activation causing late growth arrest AU - Duman, Joseph G AU - Mulherkar, Shalaka AU - Tu, Yen-Kuei AU - Erikson, Kelly C AU - Tzeng, Christopher P AU - Mavratsas, Vasilis C AU - Ho, Tammy Szu-Yu AU - Tolias, Kimberley F A2 - Bronner, Marianne E A2 - West, Anne E VL - 8 PY - 2019 DA - 2019/08/28 SP - e47566 C1 - eLife 2019;8:e47566 DO - 10.7554/eLife.47566 UR - https://doi.org/10.7554/eLife.47566 AB - Dendritic arbor architecture profoundly impacts neuronal connectivity and function, and aberrant dendritic morphology characterizes neuropsychiatric disorders. Here, we identify the adhesion-GPCR BAI1 as an important regulator of dendritic arborization. BAI1 loss from mouse or rat hippocampal neurons causes dendritic hypertrophy, whereas BAI1 overexpression precipitates dendrite retraction. These defects specifically manifest as dendrites transition from growth to stability. BAI1-mediated growth arrest is independent of its Rac1-dependent synaptogenic function. Instead, BAI1 couples to the small GTPase RhoA, driving late RhoA activation in dendrites coincident with growth arrest. BAI1 loss lowers RhoA activation and uncouples it from dendrite dynamics, causing overgrowth. None of BAI1’s known downstream effectors mediates BAI1-dependent growth arrest. Rather, BAI1 associates with the Rho-GTPase regulatory protein Bcr late in development and stimulates its cryptic RhoA-GEF activity, which functions together with its Rac1-GAP activity to terminate arborization. Our results reveal a late-acting signaling pathway mediating a key transition in dendrite development. KW - branching KW - retraction KW - hippocampal cultures KW - Raichu KW - Long-Evans rats KW - RhoA-FLARE JF - eLife SN - 2050-084X PB - eLife Sciences Publications, Ltd ER -