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Nitrogen‐stimulated potassium influx into maize roots: differential response of components resistant and sensitive to ambient ammonium 1
Author(s) -
VALE F. R.,
JACKSON W. A.,
VOLK R. J.
Publication year - 1988
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1111/j.1365-3040.1988.tb01788.x
Subject(s) - ammonium , potassium , chemistry , nitrogen , nitrate , stimulation , potassium nitrate , glutamine synthetase , biochemistry , ammonium nitrate , nuclear chemistry , inorganic chemistry , glutamine , endocrinology , biology , organic chemistry , amino acid
Potassium ( 86 Rb) influx from 200 mmol m −3 KCl into dark grown, decapitated maize seedlings 6 d old) was stimulated by nitrate pretreatment. The stimulus was clearly evident by 6h exposure to nitrate and required 12–24 h for maximal expression. Decay of the nitrate‐stimulated potassium influx was more than 50% complete within 3 h after transfer to nitrogen‐free solutions. The stimulation of potassium influx was entirely accounted for by an increase in the influx component that was resistant to inhibition by presence of 200 mmol m −3 ambient ammonium. In contrast, the component of potassium influx that was sensitive to inhibition by ambient ammonium was unaffected by nitrate pretreatment. Exposure to the glutamine synthetase inhibitor L‐methionine‐dl‐sulphoximine (MSX) during nitrate pretreatment stimulated the resistant component but the sensitive component was nearly eliminated. Pretreatment with ammonium increased the resistant component of potassium influx within 3 h, i.e. before it was increased by nitrate pretreatment, but the sensitive component was concomitantly restricted. The latter recovered partially during extended pretreatment with ammonium. The data indicate that the resistant component responded positively to increases in tissue ammonium concentrations whereas the sensitive component was unaffected by tissue ammonium except at concentrations in excess of 10μmol g −1 . Ammonium influx was also stimulated by nitrate pretreatment and to a greater extent than potassium influx. Presence of MSX with nitrate during pretreatment resulted in a further stimulation in ammonium influx. The parallel increases in root ammonium concentrations with the two pretreatments imply that part of the increase in ammonium influx was a consequnce of increased counter‐transport with endogenous ammonium.