AI Article Synopsis
- Cdc42 is crucial for establishing cell polarity by recruiting Par-6-aPKC, a process observed across various organisms from worms to mammals.
- In Drosophila neuroblasts, Cdc42 colocalizes with Par-6-aPKC at the apical cortex, and its absence disrupts neuroblast polarity, indicated by mislocalized Par-6-aPKC.
- Cdc42 not only helps position Par-6-aPKC but also enhances aPKC activity, suggesting a feedback mechanism that is vital for proper neuroblast asymmetric cell division.
Article Abstract
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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1988841 | PMC |
| http://dx.doi.org/10.1242/jcs.014902 | DOI Listing |
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