Hypo-osmotic shock of tobacco cells stimulates Ca2+ fluxes deriving first from external and then internal Ca2+ stores.
Hypo-osmotic shock of aequorin-transformed tobacco cells induces a biphasic cytosolic Ca2+ influx. Because both phases of Ca2+ entry are readily blocked by Ca2+ channel inhibitors, we conclude that the Ca2+ transients are mediated by Ca2+ channels. Evidence that the first but not second Ca2+ transient derives from external Ca2+ stores is that the first but not second influx is (i) eliminated by membrane-impermeable Ca2+ chelators, (ii) enlarged by supplementation of the medium with excess Ca2+, and (iii) reduced by the addition of competitive cations such as Mg2+ and Mn2+. Furthermore, entry of 45Ca during osmotic shock is prevented by inhibitors of the first but not second phase of Ca2+ entry. Evidence that the second wave of Ca2+ influx stems from release of intracellular Ca2+ is based on the above data plus observations that probable modulators of intracellular Ca2+ channels selectively block this phase of Ca2+ influx. Finally, a mechanism of communication between the two Ca2+ release pathways has become apparent, since perturbations that elevate or reduce the first Ca2+ transient lead to a compensating diminution/elevation of the second and vice versa. These data thus suggest that osmotic shock leads to the sequential opening of extracellular followed by intracellular Ca2+ stores and that these Ca2+ release pathways are internally compensated.
Cessna
S G
SG
Department of Chemistry, Purdue University, West Lafayette, Indiana 47907-1393, USA.
Chandra
S
S
Low
P S
PS
D000331:Aequorin; D001692:Biological Transport; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D020013:Calcium Signaling; D002451:Cell Compartmentation; D003600:Cytosol / Q000378:metabolism; D004533:Egtazic Acid / Q000494:pharmacology; D007473:Ion Channels / Q000378:metabolism; D007700:Kinetics; D007811:Lanthanum / Q000494:pharmacology; D008274:Magnesium / Q000494:pharmacology; D009544:Niflumic Acid / Q000494:pharmacology; D009997:Osmotic Pressure; D010947:Plants, Toxic; D016897:Respiratory Burst; D014026:Nicotiana / Q000166:cytology / Q000378:metabolism*
D015220:Calcium Channels; D007473:Ion Channels; D002110:Caffeine; D009544:Niflumic Acid; D000331:Aequorin; D004533:Egtazic Acid; D007811:Lanthanum; D008274:Magnesium; D002118:Calcium