S. Seling et al., Calcium deficiency in potato (Solanum tuberosum ssp tuberosum) leaves and its effects on the pectic composition of the apoplastic fluid, PHYSL PLANT, 109(1), 2000, pp. 44-50
Potato plants (Solanum tuberosum ssp, tuberosum cv, Adelheld), multiplied i
n vitro, mere cultivated in growth chambers on nutrient solution at calcium
regimes of 1000, 90, 60 or 30 mu M Ca. An absolute Ca deficiency, particul
arly at the Iom Ca-supply levels of 30 and 60 mu M Ca, manifested itself in
itially in tbe form of marginal necrosis in younger, but not in the younges
t, leaves of the potato plants. Further symptoms mere rolling of the leaf l
amina, browning of veins and roots, and finally necrosis also of the younge
st 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 th
e leaves of less than 5 mg Ca (g dry weight)(-1) However, there was no clos
e negative correlation between the extent of leaf damage and the total Ca c
ontent of the leaves. In order to obtain information about tbe Ca concentra
tion in the apoplast fluid of the leaves, apoplastic mashing fluid mas extr
acted by an infiltration-centrifugation technique. A low Ca supply reduced
the Ca concentration both in the apoplast fluid of the leaves and in the ce
ll walls. Up to 60% more diffusible pectin fragments mere then found in the
apoplast of younger leaves, as compared to the control supplied with an op
timum Ca level of 1000 mu M 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 mu M; fewer monomers and up to 7 times more di
ffusible pectin fragments with a degree of polymerization 9-20 were present
at the low Ca-supply level (30 mu M). In addition, polygalacturonase activ
ity in tissue homogenates increased remarkably with Ca deficiency. Thus it
appears that one major effect of Ca deficiency was a stimulation of the act
ivity of polygalacturonase, which could control the breakdown of pectic pol
ysaccharides in the cell wall. Whether the release of potentially biologica
lly active pectic fragments in cell malls might be involved in the occurren
ce of Ca-deficiency symptoms is discussed.