The sensing of salt

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The sensing of salt

How  plants sense salt has at last been deciphered by the group of Zhen-Ming Pei. For their last publication in Nature they went on the hunt for mutants that did not show salt induced Ca²⁺ spikes. This resulted in the identification of a mutant they named moca1 for monocation-induced [Ca²⁺]_i increases 1.  moca1 is hypersensitive to salt stress. One of the reasons is that, unlike wildtype plants who through activation of the SOS-pathway try to actively export Na⁺ from the cell,  moca1 plants don’t do this.

They found that moca1 had a mutation in a gene encoding for an enzyme in the pathway of the biosynthesis of membrane lipid called glycosyl inositol phosphorylceramide or GIPC for short. GIPCs are located at the outside of the plasma membrane and have a negative charge. Analysing the levels of GIPC in moca1 plants showed that they were reduced. However, when grown under optimal conditions it was not possible to distinguish moca1 from wildtype, only under salt stress conditions moca1 showed a phenotype. This suggested that while the levels of GIPC in moca1 plants were low, they were high enough to survive under normal conditions. But that under salt stress conditions higher levels of GIPC are needed.

Being puzzled by this, the researches subsequently analysed how GIPC could play a role in salt-induced increases of Ca²⁺ in the cell. Revealing that in the abcense of GIPC the cell-surface potential is not affected by NaCl, while NaCl does have an effect on the viability of the cells. Furthermore, they show that Na⁺ bind to GIPC outside the cell. The combination of these results they link to the opening of Ca²⁺ channels needed for the observed Ca²⁺ influx upon NaCl perception. Although, upto date it is not exactly know how the opening of Ca²⁺ channels in plants is regulated.

In the accompanying review of this article an alternative model was suggested that the binding of Na⁺ to GIPC would result in the formation of a microdomain in the plasma membrane. This microdomain would contain in addition to GIPC, Ca²⁺ channels also signalling proteins. In the alternative model it was proposed that some of these signalling proteins then activate the Ca²⁺ channel.

While it is possible that the binding of Na⁺ to GIPC leads to microdomain formation,  it adds one extra step to the process.  And as Occam’s razor reminds us, the simplest option is often the best.  Therefore, if there needs to be an alternative model to that of the authors mine would be that under non-stress conditions GIPC is bound to Ca²⁺ channels, thereby inactivating them. However when Na⁺ levels rise Na+ outcompetes the Ca²⁺ channels for GIPC binding. Releasing the inhibition from the Ca²⁺ channels, allowing them to open.

Whatever model turns out to be true, the groups of James Siedow and Zhen-Ming Pei have done great work to show us how Na⁺ is perceived by the plant and that disruption of this perception results in an absence of the Ca²⁺ signal needed to alert the rest of the plant that it is under salt stress.