PMID- 22049206
OWN - NLM
STAT- MEDLINE
DCOM- 20120325
LR  - 20211021
IS  - 1522-1563 (Electronic)
IS  - 0363-6143 (Print)
IS  - 0363-6143 (Linking)
VI  - 302
IP  - 3
DP  - 2012 Feb 1
TI  - Kinase activation of ClC-3 accelerates cytoplasmic condensation during mitotic 
      cell rounding.
PG  - C527-38
LID - 10.1152/ajpcell.00248.2011 [doi]
AB  - "Mitotic cell rounding" describes the rounding of mammalian cells before dividing 
      into two daughter cells. 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 Cl(-) via 
      ClC-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 ClC-3 by Ca(2+)/calmodulin-dependent protein 
      kinase II (CaMKII) in human glioma cells. Knockdown of endogenous ClC-3 protein 
      expression eliminated CaMKII-dependent Cl(-) currents in dividing cells and 
      impeded PMC. Thus, kinase-dependent changes in Cl(-) conductance contribute to an 
      outward osmotic pressure in dividing cells, which facilitates cytoplasmic 
      condensation preceding cell division.
FAU - Cuddapah, Vishnu Anand
AU  - Cuddapah VA
AD  - Dept. of Neurobiology, Univ. of Alabama, Birmingham, AL 35294, USA.
FAU - Habela, Christa W
AU  - Habela CW
FAU - Watkins, Stacey
AU  - Watkins S
FAU - Moore, Lindsay S
AU  - Moore LS
FAU - Barclay, Tia-Tabitha C
AU  - Barclay TT
FAU - Sontheimer, Harald
AU  - Sontheimer H
LA  - eng
GR  - R01 NS-36692/NS/NINDS NIH HHS/United States
GR  - R01 NS-52634/NS/NINDS NIH HHS/United States
GR  - R01 NS-31234/NS/NINDS NIH HHS/United States
GR  - F31 NS-73181/NS/NINDS NIH HHS/United States
GR  - F31 NS073181/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20111102
PL  - United States
TA  - Am J Physiol Cell Physiol
JT  - American journal of physiology. Cell physiology
JID - 100901225
RN  - 0 (Chloride Channels)
RN  - 0 (Chlorides)
RN  - 0 (ClC-3 channel)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
SB  - IM
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism
MH  - Cell Cycle
MH  - Cell Division
MH  - Cell Line, Tumor
MH  - Cell Membrane/metabolism
MH  - Cell Proliferation
MH  - Cell Shape
MH  - Chloride Channels/genetics/*metabolism
MH  - Chlorides
MH  - Cytoskeleton/metabolism
MH  - Gene Knockdown Techniques
MH  - Glioma
MH  - Humans
MH  - *Mitosis
MH  - Osmotic Pressure
MH  - Patch-Clamp Techniques
PMC - PMC3287156
EDAT- 2011/11/04 06:00
MHDA- 2012/03/27 06:00
PMCR- 2013/02/01
CRDT- 2011/11/04 06:00
PHST- 2011/11/04 06:00 [entrez]
PHST- 2011/11/04 06:00 [pubmed]
PHST- 2012/03/27 06:00 [medline]
PHST- 2013/02/01 00:00 [pmc-release]
AID - ajpcell.00248.2011 [pii]
AID - C-00248-2011 [pii]
AID - 10.1152/ajpcell.00248.2011 [doi]
PST - ppublish
SO  - Am J Physiol Cell Physiol. 2012 Feb 1;302(3):C527-38. doi: 
      10.1152/ajpcell.00248.2011. Epub 2011 Nov 2.