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

BMC Biology

Research Article

Francisco J. Calero-Cuenca¹  José Manuel Espinosa-Vázquez¹  Sol Sotillos¹  María T. Díaz-Meco²  Jorge Moscat²  Miguel Reina-Campos² 

[1] CABD, CSIC/JA/UPO, Campus Universidad Pablo de Olavide, Ctra. De Utrera Km. 1, 41013, Seville, Spain;Sanford-Burnham Medical Research Institute, 92037, La Jolla, CA, USA;

关键词: aPKC;    Cell polarity;    Cell trafficking;    Nuclear fallout;   

DOI  :  10.1186/s12915-016-0253-6

 received in 2016-03-16, accepted in 2016-03-31,  发布年份 2016

来源: Springer

【 摘 要 】

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.

【 授权许可】

CC BY   
© Calero-Cuenca et al. 2016