Journal
JOURNAL OF NEUROSCIENCE
Volume 31, Issue 12, Pages 4555-4568Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.6582-10.2011
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Funding
- Polish Ministry of Science and Higher Education [2P04A 015 30, PBZ-MNiI-2/1/2005]
- Polish-Norwegian Research Fund [PNRF-96-AI-1/07]
- European Union [223276]
- FP7-HealthProt grant [229676]
- Polish Cell and Molecular Biology Network
- Centre of Excellence in Molecular Bio-Medicine
- Netherlands Organization for Scientific Research (NWO-ALW/ECHO)
- Netherlands Organization for Health Research and Development (ZonMw-VIDI/TOP)
- European Science Foundation
- European Young Investigator Award
- European Molecular Biology Organization Young Investigators Programme
- Human Frontier Science Program Career Development Award (HFSP-CDA)
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Dendritic arbors are compartments of neurons dedicated to receiving synaptic inputs. Their shape is an outcome of both the intrinsic genetic program and environmental signals. The microtubules and actin cytoskeleton are both crucial for proper dendritic morphology, but how they interact is unclear. The present study demonstrates that microtubule plus-end tracking protein CLIP-170 and actin-binding protein IQGAP1 regulate dendrite morphology of rat neurons by coordinating the interaction between microtubules and the actin cytoskeleton. Moreover, we show that mTOR kinase interacts with CLIP-170 and is needed for efficient formation of a protein complex containing CLIP-170 and IQGAP1. Dynamic microtubules, CLIP-170, and IQGAP1 are required for proper dendritic arbor morphology and PI3K-mTOR-induced increase in dendritic arbor complexity. Moreover, CLIP-170 and IQGAP1 knockdown modulates dendritic arbor growth via regulation of the actin cytoskeleton. We postulate that mTOR controls dendritic arbor morphology by enhancing cross talk between dynamic microtubules and actin through CLIP-170 and IQGAP1.
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