Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

CLIP-170 and IQGAP1 cooperatively regulate dendrite morphology.

Authors: Swiech, L  Blazejczyk, M  Urbanska, M  Pietruszka, P  Dortland, BR  Malik, AR  Wulf, PS  Hoogenraad, CC  Jaworski, J 
Citation: Swiech L, etal., J Neurosci. 2011 Mar 23;31(12):4555-68. doi: 10.1523/JNEUROSCI.6582-10.2011.
Pubmed: (View Article at PubMed) PMID:21430156
DOI: Full-text: DOI:10.1523/JNEUROSCI.6582-10.2011

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.


Gene Ontology Annotations
Objects Annotated

Additional Information

RGD Object Information
RGD ID: 11049556
Created: 2016-04-08
Species: All species
Last Modified: 2016-04-08
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.