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Department of Molecular Neurobiology, Max-Planck Institute of Neurobiology, 82152 Munich-Martinsried, Germany
* To whom correspondence should be addressed. Email: rklein{at}neuro.mpg.de.
| Abstract |
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The development of a highly branched dendritic tree is essential for the establishment of functional neuronal connections. The evolutionarily conserved immunoglobulin superfamily member, dendrite-arborization-and-synapse-maturation (Dasm)-1 is thought to play a critical role in dendrite formation of dissociated hippocampal neurons. RNAi-mediated Dasm1 knock-down was previously shown to impair dendrite, but not axonal, outgrowth and branching (23). Here we report the generation and analysis of Dasm1 null mice. We find that genetic ablation of Dasm1 does not interfere with hippocampal dendrite growth and branching in vitro and in vivo. Moreover, the absence of Dasm1 does not affect the modulation of dendritic outgrowth induced by brain-derived neurotrophic factor (BDNF). Importantly, the previously observed impairment in dendrite growth after Dasm1 knock-down is also observed when the Dasm1 knock-down is performed in cultured hippocampal neurons from Dasm1 null mice. These findings indicate that the dendrite arborization phenotype was caused by off-target effects and that Dasm1 is dispensable for hippocampal dendrite arborization.
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
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| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
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