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Disturbance of cell Ca 2+ homeostasis as a primary trigger of Al toxicity syndrome
Author(s) -
RENGEL Z.
Publication year - 1992
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1111/j.1365-3040.1992.tb01025.x
Subject(s) - calmodulin , cytosol , biophysics , mitosis , microbiology and biotechnology , chemistry , homeostasis , second messenger system , calcium , biology , biochemistry , intracellular , organic chemistry , enzyme
The primary toxic effects of Al are fast (taking only seconds to several minutes to develop). These effects may be due to the presence of Al ions on the apoplasmic side of the plasma membrane; Al ions may not need to enter the cytosol for a range of primary deleterious Al effects to occur. Aluminium may disturb the symplasmic Ca 2+ homeostasis by altering the pattern of Ca 2+ fluxes across the plasma membrane. Disturbance of transmembrane Ca 2+ fluxes may prevent an increase in cytosolic Ca 2+ activity necessary to trigger spindle formation during prophase as well as to initiate the metaphase/anaphase transition. The mechanism behind Al‐related inhibition of mitosis and polar cell growth is suggested to be disturbance of stimulus/response coupling effected through Ca 2+ as a second messenger. Involvement of calmodulin in the Al‐related phenomena could be indirect, at least in the initial stages of the Al treatment when Al is probably confined to the apoplasm only. Al‐related disturbance of the Ca 2+ homeostasis in the cytosol would alter the patterns of Ca 2+ ‐calmodulin binding, resulting in the absence of activation or only partial activation of calmodulin.