Affordable Access

deepdyve-link
Publisher Website

Polarizing intestinal epithelial cells electrically through Ror2.

Authors
  • L, Cao
  • Cd, Mccaig
  • Rh, Scott
  • S, Zhao
  • G, Milne
  • H, Clevers
  • Min Zhao
  • J, Pu
Type
Published Article
Journal
Journal of Cell Science
Publisher
The Company of Biologists
Volume
127
Issue
Pt 15
Pages
3233–3233
Identifiers
DOI: 10.1242/jcs.146357
Source
zhaolab-ucdavis dermatology-ucdavis
License
Unknown

Abstract

The apicobasal polarity of enterocytes determines where the brush border membrane (apical membrane) will form, but how this apical membrane faces the lumen is not well understood. The electrical signal across the epithelium could serve as a coordinating cue, orienting and polarizing enterocytes. Here, we show that applying a physiological electric field to intestinal epithelial cells, to mimic the natural electric field created by the transepithelial potential difference, polarized phosphorylation of the actin-binding protein ezrin, increased expression of intestinal alkaline phosphatase (ALPI, a differentiation marker) and remodeled the actin cytoskeleton selectively on the cathode side. In addition, an applied electric field also activated ERK1/2 and LKB1 (also known as STK11), key molecules in apical membrane formation. Disruption of the tyrosine protein kinase transmembrane receptor Ror2 suppressed activation of ERK1/2 and LKB1 significantly, and subsequently inhibited apical membrane formation in enterocytes. Our findings indicate that the endogenous electric field created by the transepithelial potential difference might act as an essential coordinating signal for apical membrane formation at a tissue level, through activation of LKB1 mediated by Ror2-ERK signaling.

Report this publication

Statistics

Seen <100 times