The planar cell polarity effector protein Wdpcp (Fritz) controls epithelial cell cortex dynamics via septins and actomyosin.

Citation data:

Biochemical and biophysical research communications, ISSN: 1090-2104, Vol: 456, Issue: 2, Page: 562-6

Publication Year:
2015
Usage 28
Abstract Views 28
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Readers 35
Citations 4
Citation Indexes 4
Repository URL:
http://scholarworks.unist.ac.kr/handle/201301/9529
PMID:
25436430
DOI:
10.1016/j.bbrc.2014.11.078
PMCID:
PMC4429777
Author(s):
Park, Tae Joo; Kim, Su Kyoung; Wallingford, John B.
Publisher(s):
Elsevier BV; ACADEMIC PRESS INC ELSEVIER SCIENCE
Tags:
Biochemistry, Genetics and Molecular Biology; Medicine; Wdpcp; Fritz; Septin; Actomyosin; Cilia; Planar cell polarity
article description
Planar cell polarity (PCP) signaling controls polarized behaviors in diverse tissues, including the collective cell movements of gastrulation and the planar polarized beating of motile cilia. A major question in PCP signaling concerns the mechanisms linking this signaling cascade with more general cytoskeletal elements to drive polarized behavior. Previously, we reported that the PCP effector protein Wdpcp (formerly known as Fritz) interacts with septins and is critical for collective cell migration and cilia formation. Here, we report that Wdpcp is broadly involved in maintaining cortical tension in epithelial cells. In vivo 3D time-lapse imaging revealed that Wdpcp is necessary for basolateral plasma membrane stability in epithelial tissues, and we further show that Wdpcp controls cortical septin localization to maintain cortical rigidity in mucociliary epithelial cells. Finally, we show that Wdpcp acts via actomyosin to maintain balanced cortical tension in the epithelium. These data suggest that, in addition to its role in controlling plasma membrane dynamics in collective mesenchymal cell movements, Wdpcp is also essential for normal cell cortex stability during epithelial homeostasis.