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Edited by Li-Huei Tsai, Massachusetts Institute of Technology, Cambridge, MA and accepted by the Editorial Board October 5, 2009 (received for review December 17, 2008)
Abstract
Cyclin-dependent kinase 5 (Cdk5) and its activator p35 are critical for radial migration and lamination of cortical neurons. However, how this kinase is regulated by extracellular and intracellular signals during cortical morphogenesis remains unclear. Here, we show that PKCδ, a member of novel PKC expressing in cortical neurons, could stabilize p35 by direct phosphorylation. PKCδ attenuated the degradation of p35 but not its mutant derivative, which could not be phosphorylated by PKCδ. Down-regulation of PKCδ by in utero electroporation of specific small interference RNA (siRNA) severely impaired the radial migration of cortical neurons. This migration defect was similar to that caused by down-regulation of p35 and could be prevented by cotransfection with the wild-type but not the mutant p35. Furthermore, PKCδ could be activated by the promigratory factor brain-derived neurotrophic factor (BDNF) and was required for the activation of Cdk5 by BDNF. Both PKCδ and p35 were required for the promigratory effect of BDNF on cultured newborn neurons. Thus, PKCδ may promote cortical radial migration through maintaining the proper level of p35 in newborn neurons.
Footnotes
- 1To whom correspondence should be addressed. E-mail: yuanxb{at}ion.ac.cn
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Author contributions: C.-t.Z. and X.-b.Y. designed research; C.-t.Z., K.L., J.-t.L., W.Z., and X.-j.L. performed research; A.-q.G. and N.L. contributed new reagents/analytic tools; C.-t.Z. analyzed data; and C.-t.Z. and X.-b.Y. wrote the paper.
The authors declare no conflict of interest.
This article is a PNAS Direct Submission. L.-H.T. is a guest editor invited by the Editorial Board.
PKCδ regulates cortical radial migration by stabilizing the Cdk5 activator p35
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