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Background  During fetal brain development in mammals, newborn neurons undergo cell migration to reach their appropriate positions and form functional circuits. We previously reported that the atypical RhoA GTPase Rnd2 promotes the radial migration of mouse cerebral cortical neurons (Nature 455(7209):114–8, 2008; Neuron 69(6):1069–84, 2011), but its downstream signalling pathway is not well understood.    Results  We have identified BTB-domain containing adaptor for Cul3-mediated RhoA degradation 2 (Bacurd2) as a novel interacting partner to Rnd2, which promotes radial migration within the developing cerebral cortex. We find that Bacurd2 binds Rnd2 at its C-terminus, and this interaction is critical to its cell migration function. We show that forced expression or knockdown of  Bacurd2  impairs neuronal migration within the embryonic cortex and alters the morphology of immature neurons. Our  in vivo  cellular analysis reveals that  Bacurd2  influences the multipolar-to-bipolar transition of radially migrating neurons in a cell autonomous fashion. When we addressed the potential signalling relationship between Bacurd2 and Rnd2 using a Bacurd2-Rnd2 chimeric construct, our results suggest that Bacurd2 and Rnd2 could interact to promote radial migration within the embryonic cortex.    Conclusions  Our studies demonstrate that  Bacurd2  is a novel player in neuronal development and influences radial migration within the embryonic cerebral cortex.    Electronic supplementary material  The online version of this article (doi:10.1186/s13064-015-0032-z) contains supplementary material, which is available to authorized users.

Bacurd2 is a novel interacting partner to Rnd2 which controls radial migration within the developing mammalian cerebral cortex