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Published 14 August 2006. doi:10.1083/jcb.200602043
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 174, Number 4, 569-580
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Article

 N-syndecan deficiency impairs neural migration in brain

Anni Hienola, Sarka Tumova, Evgeny Kulesskiy, and Heikki Rauvala

Neuroscience Center, University of Helsinki, 00014 Helsinki, Finland

Correspondence to Anni Hienola: anni.hienola{at}helsinki.fi; or Heikki Rauvala: heikki.rauvala{at}helsinki.fi

N-syndecan (syndecan-3) is a transmembrane proteoglycan that is abundantly expressed in the major axonal pathways and in the migratory routes of the developing brain. When ligated by heparin-binding (HB) growth-associated molecule (GAM; pleiotrophin), N-syndecan mediates cortactin–Src kinase-dependent neurite outgrowth. However, the functional role of N-syndecan in brain development remains unexplored. In this study, we show that N-syndecan deficiency perturbs the laminar structure of the cerebral cortex as a result of impaired radial migration. In addition, neural migration in the rostral migratory stream is impaired in the N-syndecan–null mice. We suggest that the migration defect depends on impaired HB-GAM–induced Src kinase activation and haptotactic migration. Furthermore, we show that N-syndecan interacts with EGF receptor (EGFR) at the plasma membrane and is required in EGFR-induced neuronal migration.

Abbreviations used in this paper: CASK, calcium/CaM-dependent serine protein kinase; CP, cortical plate; EGFR, EGF receptor; FRET, fluorescence resonance energy transfer; GAM, growth-associated molecule; HB, heparin binding; HB-EGF, HB EGF-like growth factor; HS, heparan sulfate; OB, olfactory bulb; PG, proteoglycan; RMS, rostral migratory stream; SVZ, sub-VZ; VZ, ventricular zone.


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