On the nature and origin of the calcium asymmetry arising during gravitropic response in etiolated pea epicotyls.
Seven day old etiolated pea epicotyls were loaded symmetrically with 3H-indole 3-acetic acid (IAA) or 45Ca2+, then subjected to 1.5 hours of 1g gravistimulation.  Epidermal peels taken from top and bottom surfaces after 90 minutes showed an increase in IAA on the lower side and of Ca2+ on the upper side.  Inhibitors of IAA movement (TIBA, 9-hydroxyfluorene carboxylic acid) block the development of both IAA and Ca2+ asymmetries, but substances known to interfere with normal Ca2+ transport (nitrendipine, nisoldipine, Bay K 8644, A 23187) do not significantly alter either IAA or Ca2+ asymmetries.  These substances, however, are active in modifying both Ca2+ uptake and efflux through oat and pea leaf protoplast membranes.  We conclude that the 45Ca2+ fed to pea epicotyls occurs largely in the cell wall, and that auxin movement is primary and Ca2+ movement secondary in gravitropism.  We hypothesize that apoplastic Ca2+ changes during graviresponse because it is displaced by H+ secreted through auxin-induced proton release.  This proposed mechanism is supported by localized pH experiments, in which filter paper soaked in various buffers was applied to one side of a carborundum-abraded epicotyls.  Buffer at pH 3 increases calcium loss from the side to which it is applied, whereas pH 7 buffer decreases it.  Moreover, 10 micromolar IAA and 1 micromolar  fusicoccin, which promote H+ efflux, increase Ca2+ release from pea epicotyl segments, whereas cycloheximide, which inhibits H+ efflux, has the reverse effect.  We suggest that Ca2+ does not redistribute actively during gravitropism: the asymmetry arises because of its release from the wall adjacent to the region of high IAA concentration, proton secretion, and growth.  Thus, the asymmetric distribution of Ca2+ appears to be a consequence of growth stimulation, not a critical step in the early phase of the graviresponse.
Migliaccio
F
F
Department of Biology, Yale University, New Haven, Connecticut 06511-8112, USA.
Galston
A W
AW
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D001692:Biological Transport / Q000187:drug effects / Q000502:physiology; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000493:pharmacokinetics* / Q000502:physiology; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D003513:Cycloheximide / Q000494:pharmacology; D006027:Glycosides / Q000494:pharmacology; D006112:Gravitation; D018522:Gravitropism / Q000502:physiology*; D006863:Hydrogen-Ion Concentration; D007210:Indoleacetic Acids / Q000037:antagonists & inhibitors / Q000493:pharmacokinetics*; D007476:Ionophores / Q000494:pharmacology; D015737:Nisoldipine / Q000494:pharmacology; D009568:Nitrendipine / Q000494:pharmacology; D018532:Pisum sativum / Q000187:drug effects / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D010937:Plant Growth Regulators / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000493:pharmacokinetics*; D018520:Plant Shoots / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism* / Q000502:physiology; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D011523:Protoplasts / Q000378:metabolism
D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D006027:Glycosides; D007210:Indoleacetic Acids; D007476:Ionophores; D010937:Plant Growth Regulators; D011500:Protein Synthesis Inhibitors; C007808:fusicoccin; D000001:Calcimycin; D015737:Nisoldipine; C030737:indoleacetic acid; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D003513:Cycloheximide; D009568:Nitrendipine; D002118:Calcium