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The Journal of Neuroscience, February 2, 2005, 25(5):1122-1131; doi:10.1523/JNEUROSCI.3853-04.2005

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Cellular/Molecular
A Novel Phenylalanine-Based Targeting Signal Directs Telencephalin to Neuronal Dendrites

Sachiko Mitsui,¹ Michiko Saito,¹ Ken Hayashi,¹ Kensaku Mori,² and Yoshihiro Yoshihara¹

¹Laboratory for Neurobiology of Synapse, RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan, and ²Department of Physiology, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033, Japan

Neurons sort out a variety of functional molecules to appropriate subcellular destinations. Telencephalin (TLCN; intercellular adhesion molecule-5) is a cell adhesion molecule specifically localized to somatodendritic membranes in the telencephalic neurons. Here, we established a new in vivo strategy to analyze neuronal sorting mechanisms by ectopic expression of molecules of interest in the cerebellar Purkinje cells of transgenic mice. By using this system, we identified a novel dendritic targeting determinant in the cytoplasmic tail region of TLCN. A full-length TLCN ectopically expressed in the Purkinje cells was localized exclusively to dendrites but not to axons. In contrast, a deletion of cytoplasmic C-terminal 12 amino acids (residues 901-912) or a point mutation of Phe905 to Ala abrogated the dendrite-specific targeting with appearance of the truncated and point-mutated TLCN in both axons and dendrites. Furthermore, an addition of the C-terminal 17 amino acids (residues 896-912) of TLCN to an unrelated molecule (CD8) was sufficient for its specific targeting to dendrites in several types of neurons. Because the C-terminal region of TLCN does not contain any canonical dendritic targeting sequences such as the tyrosine-based motif or the dileucine motif, this study suggests a novel mechanism of protein trafficking to the dendritic compartment of neurons.

Key words: cell adhesion molecule; telencephalin; dendrite; sorting signal; transgenic mouse; Purkinje cells

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Received Sep 16, 2004; revised December 13, 2004; accepted December 16, 2004.

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