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Microtubule plus-end tracking proteins SLAIN1/2 and ch-TOG promote axonal development

Authors :
Vaart, B. (Babet) van der
Franker, M.A.M. (Mariella)
Kuijpers, M. (Marijn)
Hua, W. (Wei)
Bouchet, B.P. (Benjamin Pierre)
Jiang, K. (Kai)
Grigoriev, I. (Ilya)
Hoogenraad, C.C. (Casper)
Akhmanova, A.S. (Anna)
Vaart, B. (Babet) van der
Franker, M.A.M. (Mariella)
Kuijpers, M. (Marijn)
Hua, W. (Wei)
Bouchet, B.P. (Benjamin Pierre)
Jiang, K. (Kai)
Grigoriev, I. (Ilya)
Hoogenraad, C.C. (Casper)
Akhmanova, A.S. (Anna)
Publication Year :
2012

Abstract

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 hippo campal 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.

Details

Database :
OAIster
Notes :
The Journal of Neuroscience vol. 32 no. 42, pp. 14722-14728, English
Publication Type :
Electronic Resource
Accession number :
edsoai.ocn929970399
Document Type :
Electronic Resource
Full Text :
https://doi.org/10.1523.JNEUROSCI.1240-12.2012