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BMC Biol. 2016 Apr 18;14:32. doi: 10.1186/s12915-016-0253-6.

Nuclear fallout provides a new link between aPKC and polarized cell trafficking.

Author information

1
CABD, CSIC/JA/UPO, Campus Universidad Pablo de Olavide, Ctra. De Utrera Km. 1, Seville, 41013, Spain.
2
Sanford-Burnham Medical Research Institute, La Jolla, CA, 92037, USA.
3
CABD, CSIC/JA/UPO, Campus Universidad Pablo de Olavide, Ctra. De Utrera Km. 1, Seville, 41013, Spain. ssotmar@upo.es.

Abstract

BACKGROUND:

Cell 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.

RESULTS:

Here 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.

CONCLUSIONS:

We 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.

KEYWORDS:

Cell polarity; Cell trafficking; Nuclear fallout; aPKC

PMID:
27089924
PMCID:
PMC4836198
DOI:
10.1186/s12915-016-0253-6
[Indexed for MEDLINE]
Free PMC Article

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