The alleviating effect of silicon (Si) supply on aluminum (Al) toxicity was suggested to be based on ex or in planta mechanisms. In our experiments with the Al-sensitive maize (Zea mays) cultivar Lixis, Si treatment but not Si pretreatment ameliorated Alinduced root injury as revealed by less root-growth inhibition and callose formation. Si treatment did not affect monomeric Al concentrations in the nutrient solution, suggesting an in planta effect of Si on Al resistance. A fractionated analysis of Si and Al in the 1-cm root apices revealed that more than 85% of the root-tip Al was bound in the cell wall. Al contents in the apoplastic sap, the symplastic sap, and the cell wall did not differ between 2Si and 1Si plants. Si did not affect the Al-induced exudation of organic acid anions and phenols from the root apices. However, Al treatment greatly enhanced Si accumulation in the cell wall fraction, reducing the mobility of apoplastic Al. From our data we conclude that Si treatment leads to the formation of hydroxyaluminumsilicates in the apoplast of the root apex, thus detoxifying Al.Aluminum (Al) toxicity is one of the main factors limiting plant growth and crop yields in acid soils. Although much progress has been made during recent years, the mechanisms of Al-induced inhibition of root elongation and Al resistance are still not well understood. There are a number of excellent reviews in recent years summarizing the state of knowledge and addressing knowledge gaps (Kochian, 1995;Taylor, 1995;Delhaize and Ryan, 1995;Matsumoto, 2000;Kochian et al., 2002). Particularly, the relative importance of symplastic versus apoplastic lesions of Al toxicity remains a matter of debate. Rengel (1996) and especially Horst (1995) focused the attention on the role of the apoplast in Al toxicity regarding short-term inhibition of root elongation by Al.Silicon (Si) is a beneficial mineral element for plants and even a plant nutrient for some plant species (Epstein, 1999). The role of Si in plant resistance against biotic and abiotic stresses has been attributed particularly to modification of cell wall properties (Chérif et al., 1992;Horst et al., 1999a;Fawe et al., 2001;Lux et al., 2002). Iwasaki et al. (2002aIwasaki et al. ( , 2002b and Rogalla and Rö mheld (2002) showed that Si-enhanced manganeseleaf tolerance is related to a reduction in the concentration of Mn 21 in the leaf apoplastic washing fluid in cowpea (Vigna unguiculata) and cucumber (Cucumis sativus), respectively. Si has been reported to alleviate Al toxicity in conifers (Ryder et al., 2003), barley (Hordeum vulgare; Hammond et al., 1995), soybean (Glycine max; Baylis et al., 1994), maize (Zea mays; Barceló et al., 1993), and sorghum (Sorghum bicolor; Galvez et al., 1987). Little or no effect of Si on Al resistance has been found in wheat (Triticum aestivum), pea (Pisum sativum; Hodson and Evans, 1995), and cotton (Gossypium hirsutum; Li et al., 1989), but this may have been due to methodological shortcomings (Ryder et al., 2003). The beneficial role of Si has been...

Cell-wall (CW) pectin content and its degree of methylation in root apices of selected maize cultivars were studied in relation to genotypic Al resistance. Maize cultivars differing in Al resistance were grown in nutrient solution treated with or without Al, and pectin content of the root tips was determined. Control plants did not differ in pectin content in the 5 mm root apex. Al treatment increased the pectin content of the root apex in all cultivars but more prominently in the Al-sensitive cultivars. Pectin and Al contents in 1 mm root sections decreased from the apex to the 3-4 mm zone. Pectin contents of the apical root sections were consistently higher although significantly different only in the 1-2 mm zone in the Al-sensitive cv Lixis. Al contents in most root sections were significantly higher in cv Lixis than in Al-resistant cv ATP-Y. Localization of pectins by immunofluorescence revealed that Al-sensitive cv. Lixis has a higher proportion of low-methylated pectin and thus a higher negativity of the cell wall than Al-resistant cv ATP-Y. This is in agreement with the higher Al content and Al sensitivity of cv Lixis. It is concluded that differences in CW pectin and its degree of methylation contribute to genotypic differences in Al resistance in maize in addition to the release of organic acid anions previously reported.

Morin is a fluorochrome which forms a fluorescent complex with aluminium (Al) and is thus used to localize Al in plant tissues. However, reports about the cellular distribution of Al-apoplastic versus symplastic-based on morin staining are often conflicting. The objective of this work was to investigate whether Al localization with morin staining can show the proper cellular distribution of Al. Fresh root cross-sections were made from root apices of maize (cv. Lixis) treated with 25 muM Al for 6 h and stained with morin. Fluorescence microscopic investigation showed Al-morin fluorescence in the cytosol, but not in the cell wall. This is in contrast to the growing evidence which shows that Al mainly accumulates in the cell wall, especially bound to the pectin matrix. Therefore, in vitro analyses were carried out to study whether morin can form a fluorescent complex with Al, which is bound to pectin, cell wall, and other Al-binding ligands such as phosphate, galacturonate, DNA, and ATP. Compared with the control treatment without Al-binding ligands, fluorescence intensity was reduced by about 10-fold in the presence of pectin and isolated cell walls, but fairly unaffected in the presence of phosphate and galacturonate. Al associated with DNA and ATP also formed a fluorescent complex with morin. This implies that, although Al is mainly accumulated in the cell wall, it cannot be detected with morin as it is tightly bound to cell-wall pectin. Thus, morin staining should not be used to study the distribution of Al between cell compartments.

The interaction of boron (B) and aluminium (Al) was investigated in 5-day-old seedlings of soybean cv. Maple Arrow. Al treatment inhibited root elongation and callose formation in root tips particularly after 4-h Al treatment. After 10 and 24 h, both parameters indicated increasing recovery from Al stress. B deficiency aggravated Al toxicity compared with B sufficiency. B deficiency did lead to an increase in unmethylated pectin in the first 3 mm of the root tip. This increase in potential binding sites is reflected in generally higher Al contents in root tips of B-deficient plants. A fractionated extraction of Al from the root tips showed that citrate-exchangeable and non-exchangeable Al steeply increased up to 4 h, but then decreased after 10- and 24-h Al treatment faster in B-sufficient than in B-deficient plants. This decrease of Al contents can be explained by an Al-enhanced release of citrate from the root tips after 10-h Al treatment. However, the citrate exudation rate was the same (after 10 h) or even lower (after 24 h) in B-sufficient plants and thus cannot explain the faster decrease in Al contents of the root tips compared with the B-deficient plants. We, therefore, propose that under B deficiency, Al is more strongly bound by the pectic network of the cell wall of the root tips, which delays or prevents the recovery from initial Al stress through exudation of citrate, and thus explains the greater Al sensitivity of B-deficient common bean roots.

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