Calcium deficiency and plant ultrastructure

Hecht‐Buchholz, Ch.

doi:10.1080/00103627909366879

Cited by 34 publications

(14 citation statements)

References 10 publications

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“…This was very similar to changes described in Ca-deficient tissue [3,4]. The Al-induced changes in cell structure occurred in Dayton later (2--4 d) than in Kearney (24 h).…”

Section: Incipient Symptomssupporting

confidence: 78%

Effect of aluminium toxicity on root morphology of barley

Hecht‐Buchholz

Foy

1981

Plant Soil

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Light-and electronmicroscopic investigations were carried out in order to find the differences, in order to explain the differential A1 tolerance of two barley varieties [2], Kearney (Al-sensitive) and Dayton (Al-tolerant). The plants were exposed to 9 ppm AI in an acidified nutrient solution (pH 4,8). Typical symptoms RESULTS AND DISCUSSIONTypical symptoms of A1 toxicity I6] characterized by stunted brown root tips and inhibition of the newly emerging lateral roots occurred in the more tolerant Dayton some days later than in the Kearney. Incipient symptomsIncipient symptoms of AI toxicity in the root tips of both varieties observed with the light microscope also in wheat [5] and in maize [1] were: destruction of root cap cells, swelling and destruction of epidermis and cortex cells resulting in a disintegrated outer shape.Electronmicroscopic investigations revealed rapid autolysis of the Al-affected cells, beginning with the disorganization of the plasmalemma. This was very similar to changes described in Ca-deficient tissue [3,4]. The Al-induced changes in cell structure occurred in Dayton later (2--4 d) than in Kearney (24 h).93 Plant and Soil 63, 93-95 (1981

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“…This was very similar to changes described in Ca-deficient tissue [3,4]. The Al-induced changes in cell structure occurred in Dayton later (2--4 d) than in Kearney (24 h).…”

Section: Incipient Symptomssupporting

confidence: 78%

Effect of aluminium toxicity on root morphology of barley

Hecht‐Buchholz

Foy

1981

Plant Soil

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“…2; Hansson 1984) and may give a shortage of these ions at important sites in the plasma membrane. This explains why Al toxicity sometimes gives symptoms similar to Ca'^ deficiency (Hecht-Buchholz 1979). The selectivity of the plasma membrane afforded by Ca'* is disturbed by an increased binding of Al^*, which probably gives a more rigid membrane due to crosslinkages between negatively charged sites on adjacent headgroups (Clarkson 1984).…”

Section: Discussionmentioning

confidence: 99%

Influence of aluminium on phosphate and calcium uptake in beech (Fagus sylvatica) grown in nutrient solution and soil solution

Bengtsson

Asp

Jensen

et al. 1988

Physiologia Plantarum

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The effects of AICI3 on uptake of Ca2+ and phosphate in roots of intact beech (Fagus sylvatica L. provenance Maramures) plants were studied in nutrient solution and soil solution. Aluminium reduced the concentrations of Ca, Mg and P in plants and increased that of K. In short term experiments, uptake of Ca2+(45Ca) was reduced by exposure of the roots to Al. The effect of aluminium on Ca2+(45Ca) uptake was immediate and primarily of a competitive nature, preventing Ca2+ from being adsorbed. Uptake of 32P‐phosphate increased with increasing Al concentration up to 0.1 mM and then decreased at higher Al concentrations. The effect of Al on 32P‐phosphate uptake was most pronounced during the first hours of exposure. Growth of plants for 15 days in soil solution, collected from the upper A horizon of a beech forest soil, had no effect on uptake of Ca2+(45Ca) and 32P‐phosphate, probably because of a low concentration of labile bound monomeric Al and binding of Al to organic compounds. Soil solution from the deeper B horizon reduced Ca2+(45Ca) uptake and increased 32P‐phosphate uptake in a manner similar to that with Altreatment in nutrient solution. It is concluded that in soil solution from the deeper regions of the soil, mineral uptake by roots was affected by Al.

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“…Effects of aluminium on uptake of calcium Aluminium reduces accumulation of Ca in plant tissues to such an extent that symptoms of Al toxicity are often similar to those of Ca deficiency [leaf distortion and petiole collapse in Glycine max (Foy, Fleming & Armiger, 1969), rolled young leaves in small grains (Long & Foy, 1970), collapse of the midrib, terminal dieback and defoliation in Prunus persica seedlings (Edwards, Horton & Kirkpatrick, 1976), or reduced rate of wood formation and decreased amount of functional sapwood and live crown (Shortle & Smith, 1988)]. Symptoms of Al toxicity expressed either on whole roots (Horst, 1987;Kruger & SucofT, 1989) or root cell ultrastructure (Hecht-Buchholz, 1979) may also resemble symptoms of Ca deficiency. Root growth of Glycine max was similarly inhibited by either addition of Al or deprivation of Ca"^ .…”

Section: Uptake Into the Symplasmmentioning

confidence: 99%

Role of calcium in aluminium toxicity

1992

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summary Aluminium is the most important growth‐limiting factor in many acid soils throughout the world. Physiological effects of Al toxicity and mechanisms of tolerance are not well understood. An initial uptake of Al is confined to the apoplasm. Aluminium complexes (whose exact identification is beyond current experimental techniques) enter the cytosol slowly and only after prolonged exposure. Electrochemical properties of the cell wall Donnan free space as well as the plasma membrane of root cells are altered by the presence of Al ions that are polyvalent cations in acidic environments. The primary Al effects are very fast (taking only seconds to several minutes to develop) and may therefore occur while Al is still in the Donnan free space and on the apoplasmic side of the plasma membrane. Resumption of root growth upon removal of Al ions supports such a claim. Aluminium affects membrane permeability for both electrolytes and non‐electrolytes; it reduces accumulation of divalent cations (especially Ca and Mg) by interfering with the membrane transport. Aluminium alters the pattern of Ca2+ fluxes across the plasma membrane, thus supposedly disturbing symplasmic Ca2+ homeostasis. Supplemental Ca2+ can greatly alleviate deleterious Al effects. Frequently observed changes in the secretory activity of root cells exposed to Al are mediated through altered cell Ca2+ homeostasis; they result in cessation of cell wall growth and stoppage of root elongation. Involvement of calmodulin in the Al‐related phenomena is suggested to be indirect, at least in the initial stages of the Al treatment when Al is likely to be confined to the apoplasm. The role of growth substances, at least auxins and cytokinins, in the Al toxicity syndrome appears to be related to the Ca‐Al interactions that may alter the pattern of auxin transport as well as cytokinin biosynthesis and transport. Disturbance of the cell Ca2+ homeostasis appears to be an important feature of ion‐related environmental stresses in general (salt, heavy metals, aluminium).

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Calcium deficiency and plant ultrastructure

Cited by 34 publications

References 10 publications

Effect of aluminium toxicity on root morphology of barley

Effect of aluminium toxicity on root morphology of barley

Influence of aluminium on phosphate and calcium uptake in beech (Fagus sylvatica) grown in nutrient solution and soil solution

Role of calcium in aluminium toxicity

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