APKC regulates apical localization of Lgl to restrict elongation of microridges in developing zebrafish epidermis.

Renuka Raman,Indraneel Damle,Shamik Banerjee,Chaitanya Dingare,Rahul Rote,Mahendra Sonawane

doi:10.1038/ncomms11643

Abstract

Epithelial cells exhibit apical membrane protrusions, which confer specific functions to epithelial tissues. Microridges are short actin protrusions that are laterally long and form a maze-like pattern in the apical domain. They are widely found on vertebrate squamous epithelia including epidermis and have functions in mucous retention, membrane storage and abrasion resistance. It is largely unknown how the formation of these laterally long actin projections is regulated. Here, we show that antagonistic interactions between aPKC and Lgl–regulators of apical and basolateral domain identity, respectively,–control the length of microridges in the zebrafish periderm, the outermost layer of the epidermis. aPKC regulates the levels of Lgl and the active form of non-muscle myosinII at the apical cortex to prevent actin polymerization-dependent precocious fusion and elongation of microridges. Our data unravels the functional significance of exclusion of Lgl from the apical domain in epithelial cells.

Highlights

Epithelial cells exhibit apical membrane protrusions, which confer specific functions to epithelial tissues
We found that Atypical protein kinase C (aPKC) localizes to the apical domain of peridermal cells at 48 h post fertilization (Fig. 1a; Supplementary Fig. 1a)
We show that functions of Lgl1/Lgl[2], pNMII and the process of actin polymerization are important for building microridges in the peridermal cells

Summary

Introduction

Epithelial cells exhibit apical membrane protrusions, which confer specific functions to epithelial tissues. Microridges are short actin protrusions that are laterally long and form a maze-like pattern in the apical domain They are widely found on vertebrate squamous epithelia including epidermis and have functions in mucous retention, membrane storage and abrasion resistance. It is largely unknown how the formation of these laterally long actin projections is regulated. In migrating cells, Lgl is known to regulate the localization of NMII and focal adhesion morphology to optimize cell migration and promote protrusion formation[30,32] It has remained unclear whether the elimination of Lgl from the apical domain by aPKC has any functional consequence in vertebrate epithelia. We propose that the formation of apical projections is under regulation of the mechanisms that control cell polarization

Methods

Results

Conclusion