ArticleBMC biology2016
Nuclear fallout provides a new link between aPKC and polarized cell trafficking.
Article in BMC biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Distinct Rab11-associated membrane trafficking pathways bidirectionally control neuronal extracellular vesicle cargo traffic.bioRxiv : the preprint server for biology · 2026Article
- Kinesin-1 patterns Par-1 and Rho signaling at the cortex of syncytial embryos of Drosophila.The Journal of cell biology · 2024Article
- Article
- PAR3-PAR6-atypical PKC polarity complex proteins in neuronal polarization.Cellular and molecular life sciences : CMLS · 2018Review
- Nuf and Rip11 requirement for polarity determinant recycling during Drosophila development.Small GTPases · 2018Article
- aPKC: the Kinase that Phosphorylates Cell Polarity.F1000Research · 2018Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundCell polarity, essential for cell physiology and tissue coherence, emerges as a consequence of asymmetric localization of protein complexes and directional trafficking of cellular components. Although molecules required in both processes are well known their relationship is still poorly understood.
resultsHere we show a molecular link between Nuclear Fallout (Nuf), an adaptor of Rab11-GTPase to the microtubule motor proteins during Recycling Endosome (RE) trafficking, and aPKC, a pivotal kinase in the regulation of cell polarity. We demonstrate that aPKC phosphorylates Nuf modifying its subcellular distribution. Accordingly, in aPKC mutants Nuf and Rab11 accumulate apically indicating altered RE delivery. We show that aPKC localization in the apico-lateral cortex is dynamic. When we block exocytosis, by means of exocyst-sec mutants, aPKC accumulates inside the cells. Moreover, apical aPKC concentration is reduced in nuf mutants, suggesting aPKC levels are maintained by recycling.
conclusionsWe demonstrate that active aPKC interacts with Nuf, phosphorylating it and, as a result, modifying its subcellular distribution. We propose a regulatory loop by which Nuf promotes aPKC apical recycling until sufficient levels of active aPKC are reached. Thus, we provide a novel link between cell polarity regulation and traffic control in epithelia.
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