Aluminum ions inhibit phospholipase D in a microtubule-dependent manner
Language English Country Great Britain, England Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
18164219
DOI
10.1016/j.cellbi.2007.11.008
PII: S1065-6995(07)00258-2
Knihovny.cz E-resources
- MeSH
- Cell Line MeSH
- Aluminum Chloride MeSH
- Chlorides toxicity MeSH
- Phospholipase D antagonists & inhibitors metabolism MeSH
- Phosphatidic Acids metabolism MeSH
- Soil Pollutants toxicity MeSH
- Microtubules metabolism MeSH
- Aluminum Compounds toxicity MeSH
- Nicotiana drug effects enzymology MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Aluminum Chloride MeSH
- Chlorides MeSH
- Phospholipase D MeSH
- Phosphatidic Acids MeSH
- Soil Pollutants MeSH
- Aluminum Compounds MeSH
Aluminum is a highly cytotoxic metal to plants, but the molecular base and the primary target of Al toxicity are still unknown. The most important physiological consequence of Al toxicity is a cessation of root growth and changes in root morphology suggesting a role of the root cytoskeleton as a target structure. The important role of phospholipid degrading enzyme phospholipase D in regulation of cytoskeleton remodelling in both animal and plant organisms is now evident. Both the phospholipid pathway and the cytoskeleton are influenced by Al(3+), but their relationship with Al stress remains to be explored. Therefore, we tested the possibility that Al stress could be sensed by plants through microtubules in close interaction with phospholipases. We have shown that Al(3+) reduced the formation of phosphatidic acid in vivo, inhibited activity of phosphatidylinositol-4,5-bisphosphate-dependent phospholipase D in vitro and that the phosphatidic acid production is modified by microtubule dynamics.
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