Details
Original language | English |
---|---|
Title of host publication | The Apoplast of Higher Plants |
Subtitle of host publication | Compartment of Storage, Transport and Reactions: The Significance of the Apoplast for the Mineral Nutrition of Higher Plants |
Publisher | Springer Netherlands |
Pages | 307-321 |
Number of pages | 15 |
ISBN (electronic) | 9781402058431 |
ISBN (print) | 9781402058424 |
Publication status | Published - 2007 |
Abstract
First visible Mn toxicity symptoms are brown spots on older leaves, followed by chlorosis, necrosis and leaf shedding. The brown spots represent local accumulations of oxidized Mn (MnIV) and oxidized phenols in the cell wall, especially of the epidermis. Differences in Mn resistance between cv TVu 91 (Mn-sensitive) and cv TVu 1987 (Mntolerant) are due to higher Mn tissue tolerance. The physiological mechanism of Mn toxicity and Mn tolerance are still poorly understood. The apoplast was proposed to be the most important compartment for development of Mn toxicity and Mn tolerance. The detailed analysis and characterization of the proteome of the leaf apoplast confirm the particular role of PODs in the expression of Mn toxicity mediating H2O2 production/consumption and the oxidation of phenols in the leaf apoplast. The observed Mninduced release of pathogenesis-related like proteins (PR-like) is attributed to a general stress response. Since PR-like proteins are induced by various other abiotic and biotic stresses, a specific physiological role of these proteins in response to excess Mn supply remains to be established. From the apoplastic metabolites, particular the composition of phenolic compounds seemed to be crucial for the development and avoidance of Mn toxicity. Phenolic compounds affect POD activities causing a stimulation or inhibition of PODs in the apoplast. Furthermore, sequestration of Mn by phenolic compounds and thus rendering Mn physiologically inactive might enhance Mn tolerance. The analysis of the release of organic acids into the apoplast and translocation of Mn into the vacuoles did not support the hypothesis, that sequestration of Mn by organic acids in the apoplast and the vacuoles is crucial for Mn tolerance. Silicon alleviated Mn toxicity symptoms not only by a decrease of the apoplastic Mn concentration and an increased adsorption of Mn to the cell walls but also by the soluble Si in the apoplast. Although the antioxidant ascorbic acid proved to be beneficial for protecting the leaf tissue from Mn toxicity, it is not considered as the most important factor in Mn tolerance. The presented data confirm the importance of the apoplast for development and avoidance of Mn toxicity in the leaf tissue of cowpea. Conclusions about the chronology of Mn-induced physiological changes are difficult to draw. A more detailed study with emphasis on very early stages of Mn toxicity and a comparison of Mn-sensitive and Mn-tolerant leaves (genotype, Si nutrition, leaf age) is required.
Keywords
- Cowpea, Manganese, NADH peroxidase, Proteome, Tolerance, Toxicity
ASJC Scopus subject areas
- Agricultural and Biological Sciences(all)
- General Agricultural and Biological Sciences
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The Apoplast of Higher Plants: Compartment of Storage, Transport and Reactions: The Significance of the Apoplast for the Mineral Nutrition of Higher Plants. Springer Netherlands, 2007. p. 307-321.
Research output: Chapter in book/report/conference proceeding › Contribution to book/anthology › Research › peer review
}
TY - CHAP
T1 - The role of the leaf apoplast in manganese toxicity and tolerance in cowpea (Vigna Unguiculata L. Walp)
AU - Fecht-Christoffers, M. M.
AU - Maier, P.
AU - Iwasaki, K.
AU - Braun, H. P.
AU - Horst, W. J.
PY - 2007
Y1 - 2007
N2 - First visible Mn toxicity symptoms are brown spots on older leaves, followed by chlorosis, necrosis and leaf shedding. The brown spots represent local accumulations of oxidized Mn (MnIV) and oxidized phenols in the cell wall, especially of the epidermis. Differences in Mn resistance between cv TVu 91 (Mn-sensitive) and cv TVu 1987 (Mntolerant) are due to higher Mn tissue tolerance. The physiological mechanism of Mn toxicity and Mn tolerance are still poorly understood. The apoplast was proposed to be the most important compartment for development of Mn toxicity and Mn tolerance. The detailed analysis and characterization of the proteome of the leaf apoplast confirm the particular role of PODs in the expression of Mn toxicity mediating H2O2 production/consumption and the oxidation of phenols in the leaf apoplast. The observed Mninduced release of pathogenesis-related like proteins (PR-like) is attributed to a general stress response. Since PR-like proteins are induced by various other abiotic and biotic stresses, a specific physiological role of these proteins in response to excess Mn supply remains to be established. From the apoplastic metabolites, particular the composition of phenolic compounds seemed to be crucial for the development and avoidance of Mn toxicity. Phenolic compounds affect POD activities causing a stimulation or inhibition of PODs in the apoplast. Furthermore, sequestration of Mn by phenolic compounds and thus rendering Mn physiologically inactive might enhance Mn tolerance. The analysis of the release of organic acids into the apoplast and translocation of Mn into the vacuoles did not support the hypothesis, that sequestration of Mn by organic acids in the apoplast and the vacuoles is crucial for Mn tolerance. Silicon alleviated Mn toxicity symptoms not only by a decrease of the apoplastic Mn concentration and an increased adsorption of Mn to the cell walls but also by the soluble Si in the apoplast. Although the antioxidant ascorbic acid proved to be beneficial for protecting the leaf tissue from Mn toxicity, it is not considered as the most important factor in Mn tolerance. The presented data confirm the importance of the apoplast for development and avoidance of Mn toxicity in the leaf tissue of cowpea. Conclusions about the chronology of Mn-induced physiological changes are difficult to draw. A more detailed study with emphasis on very early stages of Mn toxicity and a comparison of Mn-sensitive and Mn-tolerant leaves (genotype, Si nutrition, leaf age) is required.
AB - First visible Mn toxicity symptoms are brown spots on older leaves, followed by chlorosis, necrosis and leaf shedding. The brown spots represent local accumulations of oxidized Mn (MnIV) and oxidized phenols in the cell wall, especially of the epidermis. Differences in Mn resistance between cv TVu 91 (Mn-sensitive) and cv TVu 1987 (Mntolerant) are due to higher Mn tissue tolerance. The physiological mechanism of Mn toxicity and Mn tolerance are still poorly understood. The apoplast was proposed to be the most important compartment for development of Mn toxicity and Mn tolerance. The detailed analysis and characterization of the proteome of the leaf apoplast confirm the particular role of PODs in the expression of Mn toxicity mediating H2O2 production/consumption and the oxidation of phenols in the leaf apoplast. The observed Mninduced release of pathogenesis-related like proteins (PR-like) is attributed to a general stress response. Since PR-like proteins are induced by various other abiotic and biotic stresses, a specific physiological role of these proteins in response to excess Mn supply remains to be established. From the apoplastic metabolites, particular the composition of phenolic compounds seemed to be crucial for the development and avoidance of Mn toxicity. Phenolic compounds affect POD activities causing a stimulation or inhibition of PODs in the apoplast. Furthermore, sequestration of Mn by phenolic compounds and thus rendering Mn physiologically inactive might enhance Mn tolerance. The analysis of the release of organic acids into the apoplast and translocation of Mn into the vacuoles did not support the hypothesis, that sequestration of Mn by organic acids in the apoplast and the vacuoles is crucial for Mn tolerance. Silicon alleviated Mn toxicity symptoms not only by a decrease of the apoplastic Mn concentration and an increased adsorption of Mn to the cell walls but also by the soluble Si in the apoplast. Although the antioxidant ascorbic acid proved to be beneficial for protecting the leaf tissue from Mn toxicity, it is not considered as the most important factor in Mn tolerance. The presented data confirm the importance of the apoplast for development and avoidance of Mn toxicity in the leaf tissue of cowpea. Conclusions about the chronology of Mn-induced physiological changes are difficult to draw. A more detailed study with emphasis on very early stages of Mn toxicity and a comparison of Mn-sensitive and Mn-tolerant leaves (genotype, Si nutrition, leaf age) is required.
KW - Cowpea
KW - Manganese
KW - NADH peroxidase
KW - Proteome
KW - Tolerance
KW - Toxicity
UR - http://www.scopus.com/inward/record.url?scp=84919706022&partnerID=8YFLogxK
U2 - 10.1007/978-1-4020-5843-1_23
DO - 10.1007/978-1-4020-5843-1_23
M3 - Contribution to book/anthology
AN - SCOPUS:84919706022
SN - 9781402058424
SP - 307
EP - 321
BT - The Apoplast of Higher Plants
PB - Springer Netherlands
ER -