RT Journal Article SR Electronic T1 Microtubule Plus-End Tracking Proteins SLAIN1/2 and ch-TOG Promote Axonal Development JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 14722 OP 14728a DO 10.1523/JNEUROSCI.1240-12.2012 VO 32 IS 42 A1 van der Vaart, Babet A1 Franker, Mariella A. M. A1 Kuijpers, Marijn A1 Hua, Shasha A1 Bouchet, Benjamin P. A1 Jiang, Kai A1 Grigoriev, Ilya A1 Hoogenraad, Casper C. A1 Akhmanova, Anna YR 2012 UL http://www.jneurosci.org/content/32/42/14722.abstract AB Development, polarization, structural integrity, and plasticity of neuronal cells critically depend on the microtubule network and its dynamic properties. SLAIN1 and SLAIN2 are microtubule plus-end tracking proteins that have been recently identified as regulators of microtubule dynamics. SLAINs are targeted to microtubule tips through an interaction with the core components of microtubule plus-end tracking protein network, End Binding family members. SLAINs promote persistent microtubule growth by recruiting the microtubule polymerase ch-TOG to microtubule plus-ends. Here, we show that SLAIN1/2 and ch-TOG-proteins are highly enriched in brain and are expressed throughout mouse brain development. Disruption of the SLAIN-ch-TOG complex in cultured primary rat hippocampal neurons by RNA interference-mediated knockdown and a dominant-negative approach perturbs microtubule growth by increasing catastrophe frequency and inhibits axon extension during neuronal development. Our study shows that proper control of microtubule dynamics is important for axon elongation in developing neurons.