학술논문

Kinase activation of ClC-3 accelerates cytoplasmic condensation during mitotic cell rounding
Document Type
Author abstract
Report
Source
American Journal of Physiology (Consolidated). Feb 2012, Vol. 302 Issue 2, pC527, 12 p.
Subject
United States
Language
English
ISSN
0002-9513
Abstract
"Mitotic cell rounding" describes the rounding of mammalian cells before dividing into two daughter ceils. This shape change requires coordinated cytoskeletal contraction and changes in osmotic pressure. While considerable research has been devoted to understanding mechanisms underlying cytoskeletal contraction, little is known about how osmotic gradients are involved in cell division. Here we describe cytoplasmic condensation preceding cell division, termed "premitotic condensation" (PMC), which involves cells extruding osmotically active [C1.sup.-] via CIC-3, a voltage-gated channel/transporter. This leads to a decrease in cytoplasmic volume during mitotic cell rounding and cell division. Using a combination of time-lapse microscopy and biophysical measurements, we demonstrate that PMC involves the activation of C1C-3 by [Ca.sup.2+]/ calmodulin-dependent protein kinase II (CaMKII) in human glioma cells. Knockdown of endogenous C1C-3 protein expression eliminated CaMKII-dependent [C1.sup.-] currents in dividing cells and impeded PMC. Thus, kinase-dependent changes in [C1.sup.-] conductance contribute to an outward osmotic pressure in dividing cells, which facilitates cytoplasmic condensation preceding cell division. glioma; chloride channel doi: 10.1152/ajpcell.00248.2011.

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