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Vacuoles are large intracellular storage organelles in plants cells. In addition to the ion channels in the plasma membrane, vacuolar ion channels have important functions in regulation of stomatal opening and closure because vacuoles can occupy up to 90% of guard cell’s volume. Therefore, a majority of ions are released from vacuoles when stomata are closed. Vascuolar K+ (VK) channels and fast vacuolar channels can mediate K+ release from vacuoles. Vacuolar K+ (VK) channels are activated by elevation in the intracellular calcium concentration. Another type of calcium-activated channel, is the slow vacuolar (SV) channel. SV channels have been shown to function as cation channels that are permeable to Ca2+ ions, but their exact functions are not yet known in plants.

Guard cells control gas exchange and ion exchange through opening and closing. K+ is one ion that flows both into and out of the cell, causing a positive charge to develop. Malate is one of the main anions used to counteract this positive charge, and it is moved through the AtALMT6 ion channel. AtALMT6 is an aluminum-activated malate transporter that is found in guard cells, specifically in the vacuoles. This transport channel was found to cause either an influx or efflux of malate depending on the concentrations of calcium. In a study by Meyer et al, patch clamp experiments were conducted on mesophyll vacuoles from arabidopsis rdr6-11 (WT) and arabidopsis that were overexpressing AtALMT6-GFP. It was found from these experiments that in the WT there were only small currents when calcium ions were introduced, while in the AtALMT6-GFP mutant a huge inward rectifying current was observed. When the transporter is knocked out from guard cell vacuoles there is a significant reduction in malate flow current. The current goes from a huge inward current to not much different than the WT, and Meyer et al hypothesized that this is due to residual malate concentrations in the vacuole. There is also a similar response in the knockout mutants to drought as in the WT. There was no phenotypic difference observed between the knockout mutants, the wild type, or the AtALMT6-GFP mutants, and the exact cause for this is not fully known.