RNA-binding protein TLS transports Nd1-L mRNA, which encodes an actin-stabilizing protein, to the neuronal dendrites. TLS-null mouse (TLS-KO) hippocampal neurons display abnormal spine morphology, and thus could be attributed to actin destabilization by the improper supply of Nd1-L mRNA to the dendrites. In this study, we showed that the exogenous expression of TLS in TLS-KO neurons did not rescue the abnormal spine phenotypes. The degree of colocalization between exogenous TLS and Nd1-L mRNA was significantly decreased in both the neuronal dendrites and the spines of TLS-KO neurons. Our results indicate that formation of TLS–Nd1-L mRNA complex clusters, presumable mRNA pools for the local protein synthesis in the spines, was impaired in TLS-deficient neurons.
aWaseda-Olympus Bioscience Research Institute, Biopolis, Singapore
bInstitute of Anatomy, University of Berne, Berne, Switzerland
cDepartment of Anatomy and Cell Biology, Kochi University, Nankoku, Kochi
dOsaka Bioscience Institute, Osaka, Japan
Correspondence to Ritsuko Fujii, PhD, Waseda-Olympus Bioscience Research Institute, 11 Biopolis Way, Helios #05-01/02, Singapore 138667
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Received 13 September 2008 accepted 3 October 2008