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Cyclic expression of the voltage‐gated potassium channel K V 10.1 promotes disassembly of the primary cilium
Author(s) -
Sánchez Araceli,
Urrego Diana,
Pardo Luis A
Publication year - 2016
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201541082
Subject(s) - ciliogenesis , cilium , centrosome , microbiology and biotechnology , biology , potassium channel , cell cycle , mitosis , gene knockdown , cell growth , cell , cell culture , endocrinology , genetics
The primary cilium, critical for morphogenic and growth factor signaling, is assembled upon cell cycle exit, but the links between ciliogenesis and cell cycle progression are unclear. K V 10.1 is a voltage‐gated potassium channel frequently overexpressed in tumors. We have previously reported that expression of K V 10.1 is temporally restricted to a time period immediately prior to mitosis in healthy cells. Here, we provide microscopical and biochemical evidence that K V 10.1 localizes to the centrosome and the primary cilium and promotes ciliary disassembly. Interference with K V 10.1 ciliary localization abolishes not only the effects on ciliary disassembly, but also K V 10.1‐induced tumor progression in vivo . Conversely, upon knockdown of K V 10.1, ciliary disassembly is impaired, proliferation is delayed, and proliferating cells show prominent primary cilia. Thus, modulation of ciliogenesis by K V 10.1 can explain the influence of K V 10.1 expression on the proliferation of normal cells and is likely to be a major mechanism underlying its tumorigenic effects.