Abstract
The cascade of phospholipid signals, is one of the main systems of cellular transduction, and is related to other signal transduction mechanisms. These include the interaction between the generation of second messengers and different proteins such as ionic channels, protein kinase proteins, signaling proteins and transcription factors, among others. The result of this interaction could alter cellular metabolism. This phospholipid signal cascade is activated by the changes on the environment such as phosphate starvation, water and saline stress, as well as plant-pathogen interactions.
Because aluminum has been considered a main toxic factor for agriculture carried out in acid soils, many researches have focused on aluminum toxic mechanism in plants.1,2 We contribute by researching on the aluminum effects on phospholipids signalling. We focused on phosphatidic acid (PA), because its relevant role in signal cascades in plants. Also PA is the precursor of most of the phospholipids in their de novo biosynthesis. Our results show a dramatic inhibitory effects by aluminum on PA. The most important PA formation routes in plant signalling are: phospholipase C (PLC)/diacylglycerol kinase (DGK) and phospholipase D (PLD).3 We investigated which one of the pathways was affected by aluminum treatment and found that aluminum affects mainly the PLC/DGK route of PA formation. We conclude that Al3+ not only could generate a signal cascade in plants, but that it can also modulate other signal cascades generated by others stress. The aim of this addendum is to discuss the possible involvements of other phospholipids in the aluminum toxicity in plant cells.
Key Words: aluminum, phospholipids, plant signal transduction
It is well known that Al3+ assimilated by the roots is toxic for the agriculture in acid soils.4–6 Plants showing symptoms of aluminum toxicity are more sensitive to the changes in the environmental conditions,6 and this can be caused by aluminum-mediated effects on the signal transduction cascades.7–9
One of the main components of the phospholipid signaling are the polyphosphoinositides (PPI), which are involved in several processes of cellular signalling caused by different types of stress, such are saline stress, which causes a fast increase in the phosphatidylinositol 4,5-bisphosphate (PIP2) levels.10 In addition, PIP2 have a crucial function in several processes of cellular signaling.11
It has been reported previously8 that the incubation of Coffea arabica suspension cells with AlCl3 stimulates the activity of the phosphoinositide kinases (PIKs) quantified in vitro.
The main goal of this work was to investigate the effect of AlCl3 incubation of C. arabica cells on the endogenous levels of PIP2 and diacylglycerol pyrophoshate (DGPP) using a bio-labeling technique to obtain [32P]-phospholipids which were quantified. The results obtained in this work (Fig. 1) show that the amount of phospholipids was not affected by the incubation of the cells with AlCl3. We also examined the cellular effects of two activators of the phospholipid signal cascade in either absence or presence of AlCl3 (Fig. 1). The incubation of the cells with mastoparan-7 (mas-7) reduced slightly the amount of PIP2; this reduction was inhibited in cells incubated previously with Al3+.
Figure 1.

Effect of Al3+ incubation on PIP2 and DGPP formation. Prelabelend cells were incubates during 15 minutes in absence (□) o presence of AlCl3 100 µM (■). Then culture medium (control), mas-7 5 µM (mas-7) or NaCl 250 mM was added, after 15 minutes of incubation with the stimuls, phospholipids were extracted, and separated for quantification of PIP2 (A) and DGPP (B).
The incubation of the cells with AlCl3 also prevented the increase in PIP2 synthesis stimulated by NaCl. No effect of the incubation of the cells with AlCl3 was observed on the structural lipids such as phosphatidylcholine (PC) and phosphatidylethanolamine. Recently, DGPP has been considered as second messenger in plant signaling.12 This is the reason why we evaluated the production of this phospholipid in cells incubated with AlCl3. We did not find any effects on the production of this lipid at the basal state. On the other hand, in the cells that were incubated with mas-7 or NaCl, an increase in DGPP production was observed. This increase was inhibited when the cells were preincubated with AlCl3. Previously, it has been shown that Al3+ did not inhibit the enzyme that catalyzes the phosphorylation of PA to produce DGPP.8
In summary our data show that Al can modulate the levels of phopholipids either in the presence or absence of a stimulus, perhaps generating per se a phospholipid signal transduction cascade. Also we have provided evidence that Al can affect this signal cascade (Fig. 2), with the final modification of several physiological and biochemical processes.
Figure 2.
Model of Al3+ effect on phospholipid signalling, and its possible consequence on other cell signaling components (X, inhibition of the pathway by Al3+).
Acknowledgements
This work was supported by Consejo Nacional de Ciencia y Tecnología grant to S.M.T.H.-S. (45798-2), and a fellowship to A.R.-D. (165087).
Footnotes
Previously published online as a Plant Signaling & Behavior E-publication: http://www.landesbioscience.com/journals/psb/article/3871
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