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Plant Physiol, April 2001, Vol. 125, pp. 2120-2128
Abscisic Acid-Induced Actin Reorganization in Guard Cells of
Dayflower Is Mediated by Cytosolic Calcium Levels and by Protein Kinase
and Protein Phosphatase Activities1
Jae-Ung
Hwang and
Youngsook
Lee*
Division of Molecular Life Science, Pohang University of Science
and Technology, Pohang 790-784, Republic of Korea
In guard cells of open stomata under daylight, long actin filaments
are arranged at the cortex, radiating out from the stomatal pore.
Abscisic acid (ABA), a signal for stomatal closure, induces rapid
depolymerization of cortical actin filaments and the slower formation
of a new type of actin that is randomly oriented throughout the cell.
This change in actin organization has been suggested to be important in
signaling pathways involved in stomatal closing movement, since actin
antagonists interfere with normal stomatal closing responses to ABA.
Here we present evidence that the actin changes induced by ABA in guard
cells of dayflower (Commelina communis) are
mediated by cytosolic calcium levels and by protein phosphatase and
protein kinase activities. Treatment of guard cells with
CaCl2 induced changes in actin organization similar to
those induced by ABA. Removal of extracellular calcium with EGTA
inhibited ABA-induced actin changes. These results suggest that
Ca2+ acts as a signal mediator in actin reorganization
during guard cell response to ABA. A protein kinase inhibitor,
staurosporine, inhibited actin reorganization in guard cells treated
with ABA or CaCl2, and also increased the population of
cells with long radial cortical actin filaments in untreated control
cells. A protein phosphatase inhibitor, calyculin A, induced
fragmentation of actin filaments in ABA- or CaCl2-treated
cells and in control cells, and inhibited the formation of randomly
oriented long actin filaments induced by ABA or CaCl2.
These results suggest that protein kinase(s) and phosphatase(s)
participate in actin remodeling in guard cells during ABA-induced
stomatal closure.
1
This work was supported by the Science and
Engineering Foundation of Korea (grant no. 98-0401-07-3 to
Y.L.).
*
Corresponding author; e-mail ylee{at}postech.ac.kr; fax
82-54-279-2199.
© 2001 American Society of Plant Physiologists
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