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Extracellular hexacyanoferrate III inhibits cytoplasmic streaming in the alga Lamprothamnium papulosum
Author(s) -
THIEL GERHARD,
KIRST GUNTER O.
Publication year - 1990
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/j.1469-8137.1990.tb00489.x
Subject(s) - extracellular , cytoplasm , biophysics , depolarization , membrane potential , cytoplasmic streaming , chemistry , redox , euryhaline , ion transporter , membrane transport , biochemistry , membrane , biology , inorganic chemistry , fishery , fish <actinopterygii>
summary Internodal cells of the euryhaline charophyte Lamprothamnium papulosum exhibited a transient slow down of the cytoplasmic streaming when transferred to a medium containing hexacyanoferrate III (HCF III). The reduced form, hexacyanoferrate II, was without effect. The extent of the streaming inhibition, which appeared with a time lag of ≃ 3 min after addition of the redox reactant, was a function of the HCF III concentration. The inhibition could be prevented by preconditioning cells in the Ca 2+ ‐channel antagonist LaCl 3 or by lowering the Ca 2+ concentration in the external medium even though these treatments did not greatly affect the rate of extracellular HCF III reduction. We therefore conclude that HCF III generates a Ca 2+ influx into the cytoplasm. The resulting transient increase in cytoplasmic free Ca 2+ inhibits the Ca 2+ ‐sensitive streaming mechanism. Streaming inhibition was observed in acid (pH 55) and alkaline (pH 8) media. Because HCF III induced only a marked depolarization in alkaline medium, Ca 2+ influx is not a consequence of a decrease in transmembrane voltage. The treatments that protected cytoplasmic streaming from inhibition by HCF III did not affect the decrease in membrane resistance caused by the redox reactant. Ca 2+ influx is therefore unlikely to be a major mechanism by which HCF III affects membrane transport pathways.