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1.  The role of the root apoplast in aluminium-induced inhibition of root elongation and in aluminium resistance of plants: a review 
Annals of Botany  2010;106(1):185-197.
Background
Aluminium (Al) toxicity is the most important soil constraint for plant growth and development in acid soils. The mechanism of Al-induced inhibition of root elongation is still not well understood, and it is a matter of debate whether the primary lesions of Al toxicity are apoplastic or symplastic.
Scope
The present review focuses on the role of the apoplast in Al toxicity and resistance, summarizing evidence from our own experimental work and other evidence published since 1995.
Conclusions
The binding of Al in the cell wall particularly to the pectic matrix and to the apoplastic face of the plasma membrane in the most Al-sensitive root zone of the root apex thus impairing apoplastic and symplastic cell functions is a major factor leading to Al-induced inhibition of root elongation. Although symplastic lesions of Al toxicity cannot be excluded, the protection of the root apoplast appears to be a prerequisite for Al resistance in both Al-tolerant and Al-accumulating plant species. In many plant species the release of organic acid anions complexing Al, thus protecting the root apoplast from Al binding, is a most important Al resistance mechanism. However, there is increasing physiological, biochemical and, most recently also, molecular evidence showing that the modification of the binding properties of the root apoplast contributes to Al resistance. A further in-depth characterization of the Al-induced apoplastic reaction in the most Al-sensitive zone of the root apex is urgently required, particularly to understand the Al resistance of the most Al-resistant plant species.
doi:10.1093/aob/mcq053
PMCID: PMC2889789  PMID: 20237112
Aluminium; aluminum; resistance; apoplast; cell wall; pectin; root elongation
2.  Physiological and proteomic characterization of manganese sensitivity and tolerance in rice (Oryza sativa) in comparison with barley (Hordeum vulgare) 
Annals of Botany  2010;105(7):1129-1140.
Background and Aims
Research on manganese (Mn) toxicity and tolerance indicates that Mn toxicity develops apoplastically through increased peroxidase activities mediated by phenolics and Mn, and Mn tolerance could be conferred by sequestration of Mn in inert cell compartments. This comparative study focuses on Mn-sensitive barley (Hordeum vulgare) and Mn-tolerant rice (Oryza sativa) as model organisms to unravel the mechanisms of Mn toxicity and/or tolerance in monocots.
Methods
Bulk leaf Mn concentrations as well as peroxidase activities and protein concentrations were analysed in apoplastic washing fluid (AWF) in both species. In rice, Mn distribution between leaf compartments and the leaf proteome using 2D isoelectic focusing IEF/SDS–PAGE and 2D Blue native BN/SDS–PAGE was studied.
Key Results
The Mn sensitivity of barley was confirmed since the formation of brown spots on older leaves was induced by low bulk leaf and AWF Mn concentrations and exhibited strongly enhanced H2O2-producing and consuming peroxidase activities. In contrast, by a factor of 50, higher Mn concentrations did not produce Mn toxicity symptoms on older leaves in rice. Peroxidase activities, lower by a factor of about 100 in the rice leaf AWF compared with barley, support the view of a central role for these peroxidases in the apoplastic expression of Mn toxicity. The high Mn tolerance of old rice leaves could be related to a high Mn binding capacity of the cell walls. Proteomic studies suggest that the lower Mn tolerance of young rice leaves could be related to Mn excess-induced displacement of Mg and Fe from essential metabolic functions.
Conclusions
The results provide evidence that Mn toxicity in barley involves apoplastic lesions mediated by peroxidases. The high Mn tolerance of old leaves of rice involves a high Mn binding capacity of the cell walls, whereas Mn toxicity in less Mn-tolerant young leaves is related to Mn-induced Mg and Fe deficiencies.
doi:10.1093/aob/mcq046
PMCID: PMC2887067  PMID: 20237113
Apoplast; compartmentation; Hordeum vulgare ‘Baroness’; Mn sensitivity; Mn tolerance; Oryza sativa var. japonica ‘Guara’; proteome; photosynthesis
3.  Transcriptomic analysis reveals differential gene expression in response to aluminium in common bean (Phaseolus vulgaris) genotypes 
Annals of Botany  2010;105(7):1119-1128.
Background and Aims
Aluminium (Al) resistance in common bean is known to be due to exudation of citrate from the root after a lag phase, indicating the induction of gene transcription and protein synthesis. The aims of this study were to identify Al-induced differentially expressed genes and to analyse the expression of candidate genes conferring Al resistance in bean.
Methods
The suppression subtractive hybridization (SSH) method was used to identify differentially expressed genes in an Al-resistant bean genotype (‘Quimbaya’) during the induction period. Using quantitative real-time PCR the expression patterns of selected genes were compared between an Al-resistant and an Al-sensitive genotype (‘VAX 1’) treated with Al for up to 24 h.
Key Results
Short-term Al treatment resulted in up-regulation of stress-induced genes and down-regulation of genes involved in metabolism. However, the expressions of genes encoding enzymes involved in citrate metabolism were not significantly affected by Al. Al treatment dramatically increased the expression of common bean expressed sequence tags belonging to the citrate transporter gene family MATE (multidrug and toxin extrusion family protein) in both the Al-resistant and -sensitive genotype in close agreement with Al-induced citrate exudation.
Conclusions
The expression of a citrate transporter MATE gene is crucial for citrate exudation in common bean. However, although the expression of the citrate transporter is a prerequisite for citrate exudation, genotypic Al resistance in common bean particularly depends on the capacity to sustain the synthesis of citrate for maintaining the cytosolic citrate pool that enables exudation.
doi:10.1093/aob/mcq049
PMCID: PMC2887069  PMID: 20237115
Aluminium resistance; aluminum; citrate exudation; common bean; MATE; Phaseolus vulgaris; transcriptomic analysis; differential gene expression

Results 1-3 (3)