Calcium deficiency in potato (Solanum tuberosum ssp. tuberosum) leaves and its effects on the pectic composition of the apoplastic fluid

Potato plants (Solanum tuberosum ssp. tuberosum cv. Adelheid), multiplied in vitro, were cultivated in growth chambers on nutrient solution at calcium regimes of 1000, 90, 60 or 30 μM Ca. An absolute Ca deficiency, particularly at the low Ca-supply levels of 30 and 60 μM Ca, manifested itself initially in the form of marginal necrosis in younger, but not in the youngest, leaves of the potato plants. Further symptoms were rolling of the leaf lamina, browning of veins and roots, and finally necrosis also of the youngest leaves. Only in an advanced stage of Ca deficiency, the meristem of the shoots died. Ca-deficiency symptoms could be expected at a Ca content in the leaves of less than 5 mg Ca (g dry weight). However, there was no close negative correlation between the extent of leaf damage and the total Ca content of the leaves. In order to obtain information about the Ca concentration in the apoplast fluid of the leaves, apoplastic washing fluid was extracted by an infiltration-centrifugation technique. A low Ca supply reduced the Ca concentration both in the apoplast fluid of the leaves and in the cell walls. Up to 60% more diffusible pectin fragments were then found in the apoplast of younger leaves, as compared to the control supplied with an optimum Ca level of 1000 μM. The amount of diffusible pectins accounted for 1-2% of the total pectin content of younger potato leaves. The size of the existing pectin fragments varied depending on the Ca supply. Compared with an optimum Ca supply of 1000 μM, fewer monomers and up to 7 times more diffusible pectin fragments with a degree of polymerization 9-20 were present at the low Ca-supply level (30 μM). In addition, polygalacturonase activity in tissue homogenates increased remarkably with Ca deficiency. Thus it appears that one major effect of Ca deficiency was a stimulation of the activity of polygalacturonase, which could control the breakdown of pectic polysaccharides in the cell wall. Whether the release of potentially biologically active pectic fragments in cell walls might be involved in the occurrence of Ca-deficiency symptoms is discussed.