Abstract
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.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adenoviridae / genetics
-
Animals
-
Cells, Cultured
-
Dendritic Spines / metabolism*
-
Green Fluorescent Proteins / genetics
-
Green Fluorescent Proteins / metabolism*
-
Hippocampus / cytology
-
Hippocampus / metabolism
-
In Situ Hybridization, Fluorescence
-
Mice
-
Mice, Knockout
-
Microscopy, Confocal
-
Neurons / cytology
-
Neurons / metabolism
-
RNA, Messenger / genetics
-
RNA, Messenger / metabolism
-
RNA-Binding Protein FUS / genetics
-
RNA-Binding Protein FUS / metabolism*
-
Recombinant Fusion Proteins / genetics
-
Recombinant Fusion Proteins / metabolism
-
Ribonucleoproteins / metabolism*
-
Transfection
Substances
-
RNA, Messenger
-
RNA-Binding Protein FUS
-
Recombinant Fusion Proteins
-
Ribonucleoproteins
-
messenger ribonucleoprotein
-
Green Fluorescent Proteins