Nuclear fallout provides a new link between aPKC and polarized cell trafficking. Academic Article uri icon

Overview

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.

publication date

  • April 18, 2016

Research

keywords

  • Drosophila Proteins
  • Nuclear Proteins
  • Protein Kinase C

Identity

PubMed Central ID

  • PMC4836198

Scopus Document Identifier

  • 84963623604

Digital Object Identifier (DOI)

  • 10.1186/s12915-016-0253-6

PubMed ID

  • 27089924

Additional Document Info

volume

  • 14