|
|
|
|
|
|
|
|
|||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | |||||
Journal of Cell Science, Vol 110, Issue 8 975-983, Copyright © 1997 by Company of Biologists
JOURNAL ARTICLES |
N Klauke and H Plattner
Faculty of Biology, University of Konstanz, Germany.
In Paramecium tetraurelia cells analysis of transient changes in Ca2+ concentration, [Ca2+]i, during aminoethyldextran (AED) stimulated synchronous (<1 second) trichocyst exocytosis has been hampered by various technical problems which we now have overcome. While Fura Red was found appropriate for quantitative double wavelength recordings, Fluo-3 allowed to follow, semi-quantitatively but with high time resolution, [Ca2+]i changes by rapid confocal laser scanning microscopy (CLSM). Resting values are between 50 and 70 nM in the strains analysed (7S wild type, as well as a non-discharge and a trichocyst-free mutant, nd9-28 degrees C and tl). In all strains [Ca2+]i first increases at the site of AED application, up to 10-fold above basal values, followed by a spillover into deeper cell regions. This might: (i) allow a vigorous Ca2+ flush during activation, and subsequently (ii) facilitate re-establishment of Ca2+ homeostasis within > or =20 seconds. Because of cell dislocation during vigorous trichocyst exocytosis, 7S cells could be reasonably analysed only by CLSM after Fluo-3 injection. In 7S cells cortical [Ca2+]i transients are strictly parallelled by trichocyst exocytosis, i.e. in the subsecond time range and precisely at the site of AED application. Injection of Ca2+ is a much less efficient trigger for exocytosis. Ca2+-buffer injections suggest a requirement of [Ca2+]i >1 to 10 microM for exocytosis to occur in response to AED. In conclusion, our data indicate: (i) correlation of cortical [Ca2+]i transients with exocytosis, as well as (ii) occurrence of a similar signal transduction mechanism in mutant cells where target structures may be defective or absent.
This article has been cited by other articles:
|
|
 |
|
  D. Vetter, R. Kissmehl, T. Treptau, K. Hauser, J. Kellermann, and H. Plattner Molecular Identification of a Calcium-Inhibited Catalytic Subunit of Casein Kinase Type 2 from Paramecium tetraurelia Eukaryot. Cell, December 1, 2003; 2(6): 1220 - 1233. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Iwadate Photolysis of caged calcium in cilia induces ciliary reversal in Paramecium caudatum J. Exp. Biol., April 1, 2003; 206(7): 1163 - 1170. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Momayezi, R. Kissmehl, and H. Plattner Quantitative Immunogold Localization of Protein Phosphatase 2B (Calcineurin) in Paramecium Cells J. Histochem. Cytochem., September 1, 2000; 48(9): 1269 - 1282. [Abstract] [Full Text]
|
|
|
|
|
|
H. Plattner, M. Flötenmeyer, R. Kissmehl, N. Pavlovic, K. Hauser, M. Momayezi, N. Braun, J. Tack, and L. Bachmann Microdomain Arrangement of the SERCA-type Ca2+ Pump (Ca2+-ATPase) in Subplasmalemmal Calcium Stores of Paramecium Cells J. Histochem. Cytochem., July 1, 1999; 47(7): 841 - 854. [Abstract] [Full Text]
|
|
|
|
 |
|
 K Hasegawa, H Kikuchi, S Ishizaki, A Tamura, Y Tsukahara, Y Nakaoka, E Iwai, and T Sato Simple fluctuation of Ca2+ elicits the complex circadian dynamics of cyclic AMP and cyclic GMP in Paramecium J. Cell Sci., January 1, 1999; 112(2): 201 - 207. [Abstract] [PDF]
|
|
|
|
|
|
B Constantin, K Meerschaert, J Vandekerckhove, and J Gettemans Disruption of the actin cytoskeleton of mammalian cells by the capping complex actin-fragmin is inhibited by actin phosphorylation and regulated by Ca2+ ions J. Cell Sci., January 6, 1998; 111(12): 1695 - 1706. [Abstract] [PDF]
|
|
