QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online 28 August 2007
doi: 10.1242/jcs.014902

This Article Figures Only Full Text Full Text (PDF) All Versions of this Article: jcs.014902v1 120/18/3200    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Atwood, S. X. Articles by Prehoda, K. E. Search for Related Content PubMed PubMed Citation Articles by Atwood, S. X. Articles by Prehoda, K. E.

Cdc42 acts downstream of Bazooka to regulate neuroblast polarity through Par-6–aPKC

¹ Institute of Molecular Biology and Department of Chemistry, University of Oregon, Eugene, OR 97403, USA
² Institute of Molecular Biology, Institute of Neuroscience, Howard Hughes Medical Institute, University of Oregon, Eugene, OR 97403, USA

^* Author for correspondence (e-mail: prehoda{at}molbio.uoregon.edu)

Accepted 12 July 2007

Cdc42 recruits Par-6–aPKC to establish cell polarity from worms to mammals. Although Cdc42 is reported to have no function in Drosophila neuroblasts, a model for cell polarity and asymmetric cell division, we show that Cdc42 colocalizes with Par-6–aPKC at the apical cortex in a Bazooka-dependent manner, and is required for Par-6–aPKC localization. Loss of Cdc42 disrupts neuroblast polarity: cdc42 mutant neuroblasts have cytoplasmic Par-6–aPKC, and this phenotype is mimicked by neuroblast-specific expression of a dominant-negative Cdc42 protein or a Par-6 protein that lacks Cdc42-binding ability. Conversely, expression of constitutively active Cdc42 leads to ectopic Par-6–aPKC localization and corresponding cell polarity defects. Bazooka remains apically enriched in cdc42 mutants. Robust Cdc42 localization requires Par-6, indicating the presence of feedback in this pathway. In addition to regulating Par-6–aPKC localization, Cdc42 increases aPKC activity by relieving Par-6 inhibition. We conclude that Cdc42 regulates aPKC localization and activity downstream of Bazooka, thereby directing neuroblast cell polarity and asymmetric cell division.

Key words: Asymmetric cell division, Cell polarity, Kinase regulation, Par complex

This article has been cited by other articles:

				S. X. Atwood, C. Chabu, R. R. Penkert, C. Q. Doe, and K. E. Prehoda Cdc42 acts downstream of Bazooka to regulate neuroblast polarity through Par-6-aPKC Development, October 1, 2007; 134(19): e1 - e1. [Full Text]