Abstract
The effect of 10 mm K+ on the HCO3− influx in Chara corallina has been used to distinguish a Ca2+-dependent membrane integrity site from the HCO3− transport site which is also Ca2+-dependent (Lucas and Dainty, Plant Physiology 1977 60: 862-867).
In the presence of 0.2 mm Ca2+ at pH 9, 10 mm K+ inhibits the HCO3− influx and depolarizes the membrane potential. Inhibition of the HCO3− influx may be prevented by raising the Ca2+ concentration in the solution or by addition of Mg2+, Sr2+, or Mn2+. Protection is also afforded by 20 mm Na+ and Cs+ but not by Rb+ which acts as a weak analog of K+ in producing inhibition of the HCO3− influx and depolarization of the membrane potential. With the exception of Na+, ions which prevent inhibition of the influx also prevent depolarization of the membrane potential.
Once inhibited by 10 mm K+, HCO3− transport cannot be restored by addition of Ca2+, Mg2+, or Sr2+ in less than 3 hours. Addition of Mn2+, however, results in a progressive restoration of the proportion of cells with influxes equal to the control value. Mn2+ also produces an increase in the membrane potential with a sharp hyperpolarization occurring at a threshold of about—180 mv. This sudden recovery of the HCO3− influx in individual cells contrasts with the gradual recovery observed when the K+ concentration is reduced to 0.2 mm. Since Mn2+ cannot substitute for Ca2+ at the HCO3− transport site, restoration of HCO3− transport by Mn2+ involving the membrane integrity site, as evidenced by the effect on the membrane potential and resistance, is clearly separate. The other divalent cations were able to restore HCO3− transport if applied at a concentration of 2 mm for 14 hours.
The OH− efflux is also inhibited by 10 mm KCl. It is postulated that voltage dependency of the OH− or HCO3− transport systems may account for the observed effects of 10 mm K+ on the HCO3− influx.
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Selected References
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