An ultrastructural study of the inhibition of mucilage secretion in the wheat root cap by aluminium

Puthota, Valentine; Cruz-Ortega, Rocío; Johnson, J. Morris; Ownby, James D.

doi:10.1007/978-94-011-3438-5_88

Cited by 23 publications

(13 citation statements)

References 26 publications

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“…The primary response to Al stress in plants occurs in roots, as reduced elongation at the tip, followed by swelling and distortion of differentiated cells, as well as root discolouration (Foy et al, 1978;Bergmann, 1992;Hossain et al, 2005). Within meristematic and root cap cells, Al toxicity is associated with an increased vacuolation and turnover of starch grains (de Lima and Copeland, 1994), as well as disruption of dictyosomes and their secretory function (Bennet et al, 1985;Puthota et al, 1991). The foliar symptoms in some plants resemble those of phosphorus deficiency manifested by overall stunting, small, dark green leaves, late maturity, purpling of stems, leaves and leaf veins, and yellowing and death of leaf tips (Foy, 1992).…”

Section: Symptom Of Al Toxicitymentioning

confidence: 99%

Aluminium tolerance in barley (Hordeum vulgare L.): Physiological mechanisms, genetics and screening methods

Wang

Raman

Zhang

et al. 2006

J. Zhejiang Univ. - Sci. B

120

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Aluminium (Al) toxicity is one of the major limiting factors for barley production on acid soils. It inhibits root cell division and elongation, thus reducing water and nutrient uptake, consequently resulting in poor plant growth and yield. Plants tolerate Al either through external resistance mechanisms, by which Al is excluded from plant tissues or internal tolerance mechanisms, conferring the ability of plants to tolerate Al ion in the plant symplasm where Al that has permeated the plasmalemma is sequestered or converted into an innocuous form. Barley is considered to be most sensitive to Al toxicity among cereal species. Al tolerance in barley has been assessed by several methods, such as nutrient solution culture, soil bioassay and field screening. Genetic and molecular mapping research has shown that Al tolerance in barley is controlled by a single locus which is located on chromosome 4H. Molecular markers linked with Al tolerance loci have been identified and validated in a range of diverse populations. This paper reviews the (1) screening methods for evaluating Al tolerance, (2) genetics and (3) mechanisms underlying Al tolerance in barley.

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Section: Symptom Of Al Toxicitymentioning

confidence: 99%

Aluminium tolerance in barley (Hordeum vulgare L.): Physiological mechanisms, genetics and screening methods

Wang

Raman

Zhang

et al. 2006

J. Zhejiang Univ. - Sci. B

120

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“…A protocol has been devised to remove mucilage from roots after the uptake period (Archambault et al,\996h); this procedure is to be follo-v\'ed when Al uptake by roots is quantified. It is especially important to remove mucilage when A\ uptake by different genotypes is compared because Puthota et al (1991) have shown that different T. aestivum genotypes differ in the production of mucilage, the fact that can result in differential apparent absorption of Al bv intact roots.…”

Section: Mucilagementioning

confidence: 99%

Uptake of aluminium by plant cells

1996

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SUMMARY The question of intracellular or extracellular primary lesion in the Al toxicity syndrome is unresolved. One of the crucial points for answering that question is quantification of Al fluxes across the plasma membrane within seconds or minutes of exposure of roots to Al, i.e. concurrent with or preceding the first symptoms of Al toxicity. A review of the available literature on Al uptake shows that there is abundant information on Al accumulation in root tissues only after the relatively prolonged uptake period, ranging from 30 min to over 24 h. Most of these reports either assume or claim explicitly that intracellular Al was measured, even though Al ions are bound strongly to negative charges in the apoplasm. Therefore, an effective and complete desorption of apoplasmic Al after the uptake period is crucial for measurements of intracellular Al. However, published studies do not seem to have desorbed cell‐wall‐bound Al appropriately. Recent studies with giant algal cells of Chara corallina, where physical separation of cell wall and cytoplasm after the uptake period can be achieved surgically, showed that desorption of Al from the apoplasm, even employing a wider variety of desorbents and more stringent conditions than in any of the previously published reports, cannot be achieved completely within 5 h. Consequently, measured rates of uptake of Al across the plasma membrane of intact Chara cells employing the cell wall/cytoplasm separation technique are up to several orders of magnitude lower than previously published values in which cell‐wall Al was attributed to the transmembrane uptake component. Although there is no doubt that Al does cross the plasma membrane, no information exists about which Al species or complexes take part in the transmembrane flux, mainly because of complexities inherent in Al speciation at the solution/ion exchanger (i.e. the cell wall and the membrane) interface. Similarly, it is not known which membrane transporters are involved in transport of Al across the plasma membrane. The Al‐resistant plant genotypes generally accumulate less Al in the root tips than do the Al‐sensitive genotypes. No direct relationship, however, appears to exist between increased organic acid extrusion as a mechanism of resistance to Al and decreased transmembrane flux of Al. Al‐accumulator plant species accumulate relatively large amounts of Al in their tissues without having a greater Al uptake rate than non‐accumulator genotypes. Progress in deciphering structural and functional aspects of transport of Al across the plasma membrane of intact plant cells will rely on using giant algal cells in which physical separation of the cell wall and the cytoplasm can be achieved, because, at present, there is no reliable quantitative method which can overcome problems presented by a relatively large apoplasmic Al pool remaining after desorption of intact root cells of higher plants.

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“…In addition, Al-related impairment of secretory function inhibited formation of mucilage around Triticum aestivum root tips (especially in Al-sensitive cultivars) (Puthota et al, 1991). It is indicative that the resumption of root elongation upon transfer of plants from Al-containing to Al-free media coincided with the recovery of secretory activity indicating a completely functional Golgi apparatus (Bennet & Breen, 1991 b) probably as a consequence of fully restored cell Ca^^ homeostasis.…”

Section: Cell Secretionmentioning

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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An ultrastructural study of the inhibition of mucilage secretion in the wheat root cap by aluminium

Cited by 23 publications

References 26 publications

Aluminium tolerance in barley (Hordeum vulgare L.): Physiological mechanisms, genetics and screening methods

Aluminium tolerance in barley (Hordeum vulgare L.): Physiological mechanisms, genetics and screening methods

Uptake of aluminium by plant cells

Role of calcium in aluminium toxicity

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