Reevaluation of the Effect of Calcium Ions on Auxin-induced Elongation

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Abstract
The mechanism by which Ca ions inhibit cell elongation was reinvestigated. Growth-inhibiting levels of Ca, when applied to isolated walls (in vitro treatment) do not decrease cell wall extensibility as measured by the Instron technique. Thus, the hypothesis that Ca inhibits growth by forming wall-stiffening Ca bridges must be abandoned. Treatment of living auxin-treated sections with Ca (in vivo treatment) does cause a decrease in the subsequently measured wall extensibility, but this decline appears to be simply a consequence of the growth inhibition rather than its cause. Growth-inhibiting levels of Ca do not appreciably reduce the rate of auxin-enhanced H+ excretion. Pretreatment with Ca does not reduce the capacity of walls to undergo acid-activated wall loosening in the absence of Ca. High concentrations of CaCl2 (0.02 M) cause an initial elastic shrinkage of Avena [sativa] sections comparable to that caused by the same osmolarity of mannitol, but the subsequent growth inhibition is too great to be explained by an osmotic inhibition. Ca ions do inhibit H+-induced extension of frozen-thawed sections under tension. The growth-inhibitory effects of Ca may be ascribed to a direct inhibition exerted by Ca ions on the H+-induced wall-loosening process.