Cleland R E
Department of Botany, University of Washington, Seattle, Washington 98195.
Plant Physiol. 1977 Nov;60(5):709-12. doi: 10.1104/pp.60.5.709.
The mechanism by which calcium ions inhibit cell elongation has been reinvestigated. Growth-inhibiting levels of calcium, when applied to isolated walls (in vitro treatment) do not decrease cell wall extensibility as measured by the Instron technique. Thus, the hypothesis that calcium inhibits growth by forming wall-stiffening calcium bridges must be abandoned. Treatment of living auxin-treated sections with calcium (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 calcium do not appreciably reduce the rate of auxin-enhanced H(+) excretion. Pretreatment with calcium does not reduce the capacity of walls to undergo acid-activated wall loosening in the absence of calcium. High concentrations of CaCl(2) (0.02 m) cause an initial elastic shrinkage of Avena 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. Calcium ions do inhibit H(+)-induced extension of frozen-thawed sections under tension. The growth-inhibitory effects of calcium, then, may be ascribed to a direct inhibition exerted by calcium ions on the H(+)-induced wall-loosening process.
钙离子抑制细胞伸长的机制已被重新研究。当将抑制生长水平的钙应用于分离的细胞壁（体外处理）时，通过英斯特朗技术测量，并不会降低细胞壁的伸展性。因此，钙通过形成使细胞壁变硬的钙桥来抑制生长这一假说必须被摒弃。用钙处理经生长素处理的活切片（体内处理）确实会导致随后测量的细胞壁伸展性降低，但这种下降似乎仅仅是生长抑制的结果而非其原因。抑制生长水平的钙不会明显降低生长素增强的H⁺排泄速率。在没有钙的情况下，用钙预处理不会降低细胞壁进行酸激活细胞壁松弛的能力。高浓度的CaCl₂（0.02 m）会导致燕麦切片最初出现弹性收缩，这与相同渗透压的甘露醇所引起的收缩相当，但随后的生长抑制过大，无法用渗透抑制来解释。钙离子确实会抑制在张力下冻融切片的H⁺诱导伸展。那么，钙的生长抑制作用可能归因于钙离子对H⁺诱导的细胞壁松弛过程的直接抑制。
