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Dev Cell. 2008 Feb;14(2):216-26. doi: 10.1016/j.devcel.2007.11.020.

The PAR-6 polarity protein regulates dendritic spine morphogenesis through p190 RhoGAP and the Rho GTPase.

Author information

1
Department of Microbiology and Center for Cell Signaling, University of Virginia School of Medicine, Charlottesville, VA 22908, USA. hz5a@virginia.edu

Abstract

The majority of excitatory synaptic transmission in the brain occurs at dendritic spines, which are actin-rich protrusions on the dendrites. The asymmetric nature of these structures suggests that proteins regulating cell polarity might be involved in their formation. Indeed, the polarity protein PAR-3 is required for normal spine morphogenesis. However, this function is independent of association with atypical protein kinase C (aPKC) and PAR-6. Here we show that PAR-6 together with aPKC plays a distinct but essential role in spine morphogenesis. Knockdown of PAR-6 inhibits spine morphogenesis, whereas overexpression of PAR-6 increases spine density, and these effects are mediated by aPKC. Using a FRET biosensor, we further show that p190 RhoGAP and RhoA act downstream of the PAR-6/aPKC complex. These results define a role for PAR-6 and aPKC in dendritic spine biogenesis and maintenance, and reveal an unexpected link between the PAR-6/aPKC complex and RhoA activity.

PMID:
18267090
PMCID:
PMC2768076
DOI:
10.1016/j.devcel.2007.11.020
[Indexed for MEDLINE]
Free PMC Article

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